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Sample records for increase lung cancer

  1. Lung cancer

    SciTech Connect

    Aisner, J.

    1985-01-01

    This book contains 13 chapters. Some of the chapter titles are: The Pathology of Lung Cancer; Radiotherapy for Non-Small-Cell Cancer of the Lung; Chemotherapy for Non-Small-Cell Lung Cancer; Immunotherapy in the Management of Lung Cancer; Preoperative Staging and Surgery for Non-Small-Cell Lung Cancer; and Prognostic Factors in Lung Cancer.

  2. Lung Cancer

    MedlinePlus

    ... version of this page please turn Javascript on. Lung Cancer What is Lung Cancer? How Tumors Form The body is made ... button on your keyboard.) Two Major Types of Lung Cancer There are two major types of lung ...

  3. ALX1 promotes migration and invasion of lung cancer cells through increasing snail expression

    PubMed Central

    Yao, Wei; Liu, Yong; Zhang, Zhuo; Li, Guoquan; Xu, Xiaoying; Zou, Kun; Xu, Yinghui; Zou, Lijuan

    2015-01-01

    Lung cancer is one of the main causes in cancer-related death. Here we reported a novel functional role of Aristaless-like homeobox1 (ALX1) in lung carcinogenesis. Analysis of ALX1 in lung cancer specimens confirms upregulation of ALX1 in lung cancer, especially these with distant metastasis. Moreover, higher level of ALX1 expression is associated with poorer prognosis of lung cancer patients. Ectopic expression of ALX1 significantly promotes lung cancer cell proliferation, migration and invasion, while ALX1 silencing by siRNA significantly inhibits these abilities of lung cancer cells. The functional role of ALX1 is dependent on increasing Snail expression and knockdown of Snail could restrain the role of ALX1. Collectively, we identify critical roles of ALX1 in lung cancer development and progression. These findings may serve as a framework for future investigations designed to more comprehensive determination of ALX1 as a potential therapeutic target. PMID:26722397

  4. Lung Cancer

    MedlinePlus

    Lung cancer is one of the most common cancers in the world. It is a leading cause of ... in the United States. Cigarette smoking causes most lung cancers. The more cigarettes you smoke per day and ...

  5. Inhibition of thromboxane synthase induces lung cancer cell death via increasing the nuclear p27

    SciTech Connect

    Leung, Kin Chung; Hsin, Michael K.Y.; Chan, Joey S.Y.; Yip, Johnson H.Y.; Li, Mingyue; Leung, Billy C.S.; Mok, Tony S.K.; Warner, Timothy D.; Underwood, Malcolm J.; Chen, George G.

    2009-10-15

    The role of thromboxane in lung carcinogenesis is not clearly known, though thromboxane B2 (TXB{sub 2}) level is increased and antagonists of thromboxane receptors or TXA2 can induce apoptosis of lung cancer cells. p27, an atypical tumor suppressor, is normally sequestered in the nucleus. The increased nuclear p27 may result in apoptosis of tumor cells. We hypothesize that the inhibition of thromboxane synthase (TXS) induces the death of lung cancer cells and that such inhibition is associated with the nuclear p27 level. Our experiment showed that the inhibition of TXS significantly induced the death or apoptosis in lung cancer cells. The activity of TXS was increased in lung cancer. The nuclear p27 was remarkably reduced in lung cancer tissues. The inhibition of TXS caused the cell death and apoptosis of lung cancer cells, likely via the elevation of the nuclear p27 since the TXS inhibition promoted the nuclear p27 level and the inhibition of p27 by its siRNA recovered the cell death induced by TXS inhibition. Collectively, lung cancer cells produce high levels of TXB{sub 2} but their nuclear p27 is markedly reduced. The inhibition of TXS results in the p27-related induction of cell death in lung cancer cells.

  6. Increased risk for lung cancer and for cancer of the gastrointestinal tract among Geneva professional drivers.

    PubMed

    Gubéran, E; Usel, M; Raymond, L; Bolay, J; Fioretta, G; Puissant, J

    1992-05-01

    A historical prospective cohort study of 6630 drivers from the Canton of Geneva was carried out to evaluate mortality and incidence of cancer in this occupation. The study population was all men (of all vocations) who held in 1949 a special licence for driving lorries, taxis, buses, or coaches and all new licence holders in the period 1949-61. Men born before 1900 and those with only an ordinary driving licence were excluded. According to the occupation registered on their licence, the 6630 drivers were distributed into three groups: (1) professional drivers (n = 1726), (2) non-professional drivers "more exposed" to exhaust gas and fumes (this group included occupations such as vehicle mechanic, policeman, road sweeper; n = 712), and (3) non-professional drivers "less exposed," composed of all other occupations (n = 4192). The cohort was followed up from 1949 to December 1986 and the trace of 197 men (3%) was lost. Compared with the general population of the Canton of Geneva, professional drivers experienced significant excess risks, taking into account 15 years of latency, for all causes of death (standardised mortality ratio (SMR) 115, 90% confidence interval (90% CI) 107-123) and for all malignant neoplasms (SMR 125, 90% CI 112-140; standardised incidence ratio (SIR) 128, 90% CI 115-142). Cause specific analysis showed significant excesses for lung cancer (SMR 150, 90% CI 123-181; SIR 161, 90% CI 129-198), oesophageal cancer (SMR 183, 90% CI 108-291), stomach cancer (SMR 179, 90% CI 117-263; SIR233, 90% CI 156-336), rectal cancer (SMR 258, 90% CIU 162-392; SIR 200, 90% CI 127-300), and cirrhosis of the liver (SMR 145, 90% CI 104-198). Risk of lung cancer increased significantly with time from first exposure. Among non-professional drivers no significant excess risk was found except for lung cancer mortality among the "less exposed" group (SMR 121, 90% CI 103-140), and for incidence of lung cancer among the "more exposed" group (SIR 161, 90% CI 111-227). The

  7. Lung cancer burden has increased during the last 40 years in Hebei Province, China

    PubMed Central

    He, Yutong; Li, Daojuan; Song, Guohui; Li, Yongwei; Liang, Di; Jin, Jing; Wen, Denggui

    2016-01-01

    Abstract Background In 2011, Hebei Province, located in North China with a population of 71 794 239, accounted for approximately 6% of the national population. It is well known as a heavily air polluted area. This study reports the lung cancer burden and mortality trend in Hebei Province from 1973 to 2011. Methods Eight cancer registries in Hebei Province submitted data to the Hebei Provincial Cancer Registry Center. Pooled data were stratified by area (urban/rural), gender, and age group. The proportions, cumulative incidence/mortality rates, and median age at death of lung cancer were calculated. Lung cancer mortality data of 1973–1975, 1990–1992, and 2004–2005 were extracted from national death surveys. Data of lung cancer from Cixian and Shexian were obtained from population‐based cancer registries in each county. Results The estimated numbers of newly diagnosed lung cancer cases and deaths in 2011 in Hebei Province were 32 623 and 27 612, respectively. The crude incidence rate of lung cancer was 45.44/100 000. The age‐standardized incidence rate by world standard population was 39.01/100 000, ranking second among all cancers. The lung cancer mortality rate was 38.46/100 000, ranking first among all cancer deaths, with a significantly increasing trend in Hebei Province from 1973–1975 to 2010–2011, with an increased rate of 189.15%. Conclusion Hebei Province suffers a heavy disease burden of lung cancer and an obvious increasing trend has been observed over the past 40 years. Preventive and control strategies should be encouraged. PMID:27148418

  8. Lung cancer

    PubMed Central

    Dong, Jie; Kislinger, Thomas; Jurisica, Igor; Wigle, Dennis A.

    2010-01-01

    High-throughput genomic data for both lung development and lung cancer continue to accumulate. Significant molecular intersection between these two processes has been hypothesized due to overlap in phenotypes and genomic variation. Examining the network biology of both cancer and development of the lung may shed functional light on the individual signaling modules involved. Stem cell biology may explain a portion of this network intersection and consequently studying lung organogenesis may have relevance for understanding lung cancer. This review summarizes our understanding of the potential overlapping mechanisms involved in lung development and lung tumorigenesis. PMID:19202349

  9. Lung Cancer

    MedlinePlus

    Lung cancer is one of the most common cancers in the world. It is a leading cause of cancer death in men and women in the United States. Cigarette smoking causes most lung cancers. The more cigarettes you smoke per day and ...

  10. S100P interacts with integrin α7 and increases cancer cell migration and invasion in lung cancer.

    PubMed

    Hsu, Ya-Ling; Hung, Jen-Yu; Liang, Yung-Yu; Lin, Yi-Shiuan; Tsai, Ming-Ju; Chou, Shah-Hwa; Lu, Chi-Yu; Kuo, Po-Lin

    2015-10-01

    S100P, a Ca2+ binding protein, has been shown to be overexpressed in various cancers. However, its functional character in lung cancer remains largely unknown. In this study, we show that S100P increases cancer migration, invasion and metastasis in lung cancer cells. Ectopic expression of S100P increases migration, invasion and EMT in less invasive CL1-0 lung cancer cells. Conversely, knockdown of S100P suppressed migration and invasion, and caused a reversion of EMT in highly invasive lung cancer cells. These effects were transduced by increasing the interaction of S100P with integrin α7, which activated focal adhesion kinase (FAK) and AKT. Blocking FAK significantly decreased S100P-induced migration by decreasing Src and AKT activation, whereas inhibiting AKT reduced S100P upregulation on ZEB1 expression. Further study has indicated that S100P knockdown prevents the spread of highly metastatic human lung cancer in animal models. This study therefore suggests that S100P represents a critical activator of lung cancer metastasis. Detection and targeted treatment of S100P-expressing cancer is an attractive therapeutic strategy in treating lung cancer. PMID:26320193

  11. S100P interacts with integrin α7 and increases cancer cell migration and invasion in lung cancer

    PubMed Central

    Hsu, Ya-Ling; Hung, Jen-Yu; Liang, Yung-Yu; Lin, Yi-Shiuan; Tsai, Ming-Ju; Chou, Shah-Hwa; Lu, Chi-Yu; Kuo, Po-Lin

    2015-01-01

    S100P, a Ca2+ binding protein, has been shown to be overexpressed in various cancers. However, its functional character in lung cancer remains largely unknown. In this study, we show that S100P increases cancer migration, invasion and metastasis in lung cancer cells. Ectopic expression of S100P increases migration, invasion and EMT in less invasive CL1-0 lung cancer cells. Conversely, knockdown of S100P suppressed migration and invasion, and caused a reversion of EMT in highly invasive lung cancer cells. These effects were transduced by increasing the interaction of S100P with integrin α7, which activated focal adhesion kinase (FAK) and AKT. Blocking FAK significantly decreased S100P-induced migration by decreasing Src and AKT activation, whereas inhibiting AKT reduced S100P upregulation on ZEB1 expression. Further study has indicated that S100P knockdown prevents the spread of highly metastatic human lung cancer in animal models. This study therefore suggests that S100P represents a critical activator of lung cancer metastasis. Detection and targeted treatment of S100P-expressing cancer is an attractive therapeutic strategy in treating lung cancer. PMID:26320193

  12. Increasing physical activity and exercise in lung cancer: reviewing safety, benefits, and application.

    PubMed

    Bade, Brett C; Thomas, D David; Scott, JoAnn B; Silvestri, Gerard A

    2015-06-01

    Lung cancer continues to be a difficult disease frequently diagnosed in late stages with a high mortality and symptom burden. In part because of frequent lung comorbidity, even lung cancer survivors often remain symptomatic and functionally limited. Though targeted therapy continues to increase treatment options for advanced-stage disease, symptom burden remains high with few therapeutic options. In the last several decades, exercise and physical activity have arisen as therapeutic options for obstructive lung disease and lung cancer. To date, exercise has been shown to reduce symptoms, increase exercise tolerance, improve quality of life, and potentially reduce length of stay and postoperative complications. Multiple small trials have been performed in perioperative non-small-cell lung cancer patients, although fewer studies are available for patients with advanced-stage disease. Despite the increased interest in this subject over the last few years, a validated exercise regimen has not been established for perioperative or advanced-stage disease. Clinicians underutilize exercise and pulmonary rehabilitation as a therapy, in part because of the lack of evidence-based consensus as to how and when to implement increasing physical activity. This review summarizes the existing evidence on exercise in lung cancer patients. PMID:25831230

  13. What Is Lung Cancer?

    MedlinePlus

    ... starts in the lungs, it is called lung cancer. Lung cancer begins in the lungs and may spread ... lung cancer. For more information, visit the National Cancer Institute’s Lung Cancer. Previous Basic Information Basic Information Basic Information ...

  14. Intakes of red meat, processed meat, and meat-mutagens increase lung cancer risk

    PubMed Central

    Lam, Tram Kim; Cross, Amanda J.; Consonni, Dario; Randi, Giorgia; Bagnardi, Vincenzo; Bertazzi, Pier Alberto; Caporaso, Neil E.; Sinha, Rashmi; Subar, Amy F.; Landi, Maria Teresa

    2009-01-01

    Red and processed meat intake may increase lung cancer risk. However, the epidemiologic evidence is inconsistent and few studies have evaluated the role of meat-mutagens formed during high cooking temperatures. We investigated the association of red meat, processed meat, and meat-mutagen intake with lung cancer risk in Environment And Genetics in Lung cancer Etiology (EAGLE), a population-based case-control study. Primary lung cancer cases (n=2101) were recruited from 13 hospitals within the Lombardy region of Italy examining ~80% of the cases from the area. Non-cancer population controls (n=2120), matched to cases on gender, residence, and age, were randomly selected from the same catchment area. Diet was assessed in 1903 cases and 2073 controls, and used in conjunction with a meat-mutagen database to estimate intake of heterocyclic amines and benzo[a]pyrene. Multivariable odds ratios (ORs) and 95% confidence intervals (CIs) for sex-specific tertiles of intake were calculated using unconditional logistic regression. Red and processed meat were positively associated with lung cancer risk (highest-versus-lowest tertile: OR=1.8; 95% CI=1.5–2.2; p-trend<0.001 and OR=1.7; 95% CI=1.4–2.1; p-trend<0.001, respectively); the risks were strongest among never smokers (OR=2.4, 95% CI=1.4–4.0, p-trend=0.001 and OR=2.5, 95% CI=1.5–4.2, p-trend=0.001, respectively). Heterocyclic amines and benzo[a]pyrene were significantly associated with increased risk of lung cancer. When separated by histology, significant positive associations for both meat groups were restricted to adenocarcinoma and squamous cell carcinoma, but not small cell carcinoma of the lung. In summary, red meat, processed meat, and meat-mutagens were independently associated with increased risk of lung cancer. PMID:19141639

  15. Epidemiology of Lung Cancer

    PubMed Central

    Brock, Malcolm V.; Ford, Jean G.; Samet, Jonathan M.; Spivack, Simon D.

    2013-01-01

    Background: Ever since a lung cancer epidemic emerged in the mid-1900s, the epidemiology of lung cancer has been intensively investigated to characterize its causes and patterns of occurrence. This report summarizes the key findings of this research. Methods: A detailed literature search provided the basis for a narrative review, identifying and summarizing key reports on population patterns and factors that affect lung cancer risk. Results: Established environmental risk factors for lung cancer include smoking cigarettes and other tobacco products and exposure to secondhand tobacco smoke, occupational lung carcinogens, radiation, and indoor and outdoor air pollution. Cigarette smoking is the predominant cause of lung cancer and the leading worldwide cause of cancer death. Smoking prevalence in developing nations has increased, starting new lung cancer epidemics in these nations. A positive family history and acquired lung disease are examples of host factors that are clinically useful risk indicators. Risk prediction models based on lung cancer risk factors have been developed, but further refinement is needed to provide clinically useful risk stratification. Promising biomarkers of lung cancer risk and early detection have been identified, but none are ready for broad clinical application. Conclusions: Almost all lung cancer deaths are caused by cigarette smoking, underscoring the need for ongoing efforts at tobacco control throughout the world. Further research is needed into the reasons underlying lung cancer disparities, the causes of lung cancer in never smokers, the potential role of HIV in lung carcinogenesis, and the development of biomarkers. PMID:23649439

  16. Smad4 loss promotes lung cancer formation but increases sensitivity to DNA topoisomerase inhibitors.

    PubMed

    Haeger, S M; Thompson, J J; Kalra, S; Cleaver, T G; Merrick, D; Wang, X-J; Malkoski, S P

    2016-02-01

    Non-small-cell lung cancer (NSCLC) is a common malignancy with a poor prognosis. Despite progress targeting oncogenic drivers, there are no therapies targeting tumor-suppressor loss. Smad4 is an established tumor suppressor in pancreatic and colon cancer; however, the consequences of Smad4 loss in lung cancer are largely unknown. We evaluated Smad4 expression in human NSCLC samples and examined Smad4 alterations in large NSCLC data sets and found that reduced Smad4 expression is common in human NSCLC and occurs through a variety of mechanisms, including mutation, homozygous deletion and heterozygous loss. We modeled Smad4 loss in lung cancer by deleting Smad4 in airway epithelial cells and found that Smad4 deletion both initiates and promotes lung tumor development. Interestingly, both Smad4(-/-) mouse tumors and human NSCLC samples with reduced Smad4 expression demonstrated increased DNA damage, whereas Smad4 knockdown in lung cancer cells reduced DNA repair and increased apoptosis after DNA damage. In addition, Smad4-deficient NSCLC cells demonstrated increased sensitivity to both chemotherapeutics that inhibit DNA topoisomerase and drugs that block double-strand DNA break repair by non-homologous end joining. In sum, these studies establish Smad4 as a lung tumor suppressor and suggest that the defective DNA repair phenotype of Smad4-deficient tumors can be exploited by specific therapeutic strategies. PMID:25893305

  17. Reduced Fatalism and Increased Prevention Behavior After Two High-Profile Lung Cancer Events

    PubMed Central

    PORTNOY, DAVID B.; LEACH, CORINNE R.; KAUFMAN, ANNETTE R.; MOSER, RICHARD P.; ALFANO, CATHERINE M.

    2015-01-01

    The positive impact of media coverage of high-profile cancer events on cancer prevention behaviors is well-established. However, less work has focused on potential adverse psychological reactions to such events, such as fatalism. Conducting 3 studies, the authors explored how the lung cancer death of Peter Jennings and diagnosis of Dana Reeve in 2005 related to fatalism. Analysis of a national media sample in Study 1 found that media coverage of these events often focused on reiterating the typical profile of those diagnosed with lung cancer; 38% of the media mentioned at least 1 known risk factor for lung cancer, most often smoking. Data from a nationally representative survey in Study 2 found that respondents reported lower lung cancer fatalism, after, compared with before, the events (OR = 0.16, 95% CI [0.03, 0.93]). A sustained increase in call volume to the national tobacco Quitline after these events was found in Study 3. These results suggest that there is a temporal association between high-profile cancer events, the subsequent media coverage, psychological outcomes, and cancer prevention behaviors. These results suggest that high-profile cancer events could be leveraged as an opportunity for large-scale public heath communication campaigns through the dissemination of cancer prevention messages and services. PMID:24274730

  18. Occupational lung cancer.

    PubMed

    Cone, J E

    1987-01-01

    The author addresses the attribution of lung cancer to cigarette smoking and the problems of confounding synergistic effects of occupational and other carcinogenic risk factors, as well as the divergent trends of declining smoking rates and increasing rates of lung cancer. He also reviews the existing literature to document associations between lung cancer and occupational exposures. Finally, interventions for prevention of occupational lung cancer are discussed. PMID:3303381

  19. Occupational lung cancer

    SciTech Connect

    Cone, J.E.

    1987-04-01

    The author addresses the attribution of lung cancer to cigarette smoking and the problems of confounding synergistic effects of occupational and other carcinogenic risk factors, as well as the divergent trends of declining smoking rates and increasing rates of lung cancer. He also reviews the existing literature to document associations between lung cancer and occupational exposures. Finally, interventions for prevention of occupational lung cancer are discussed.

  20. Lung cancer in women.

    PubMed

    Coscio, Angela M; Garst, Jennifer

    2006-07-01

    Lung cancer is the most common cancer in both men and women; however, there are some clear gender-based differences. As the incidence of lung cancer is declining in men, the incidence of lung cancer is increasing in women. Women are more likely than men to have adenocarcinoma, a histologic subtype that correlates with worsened prognosis, but women have improved survival compared with men. Genetic predisposition and the presence of estrogen receptors in lung cancer cells may predispose women to developing lung cancer. Further studies are needed to understand the mechanism and significance of these findings. PMID:17254523

  1. Lung cancer chemotherapy agents increase procoagulant activity via protein disulfide isomerase-dependent tissue factor decryption.

    PubMed

    Lysov, Zakhar; Swystun, Laura L; Kuruvilla, Sara; Arnold, Andrew; Liaw, Patricia C

    2015-01-01

    Lung cancer patients undergoing chemotherapy have an elevated risk for thrombosis. However, the mechanisms by which chemotherapy agents increase the risk for thrombosis remains unclear. The aim of this study was to determine the mechanism(s) by which lung cancer chemotherapy agents cisplatin, carboplatin, gemcitabine, and paclitaxel elicit increased tissue factor activity on endothelial cells, A549 cells, and monocytes. Tissue factor activity, tissue factor antigen, and phosphatidylserine exposure were measured on chemotherapy-treated human umbilical vein endothelial cells (HUVEC), A549 cells, and monocytes. Cell surface protein disulfide isomerase (PDI) and cell surface free thiol levels were measured on HUVEC and A549 non-small cell lung carcinoma cells. Treatment of HUVECs, A549 cells, and monocytes with lung cancer chemotherapy significantly increased cell surface tissue factor activity. However, elevated tissue factor antigen levels were observed only on cisplatin-treated and gemcitabine-treated monocytes. Cell surface levels of phosphatidylserine were increased on HUVEC and monocytes treated with cisplatin/gemcitabine combination therapy. Chemotherapy also resulted in increased cell surface levels of PDI and reduced cell surface free thiol levels. Glutathione treatment and PDI inhibition, but not phosphatidylserine inhibition, attenuated tissue factor activity. Furthermore, increased tissue factor activity was reversed by reducing cysteines with dithiothreitol. These studies are the first to demonstrate that lung cancer chemotherapy agents increase procoagulant activity on endothelial cells and A549 cells by tissue factor decryption through a disulfide bond formation in a PDI-dependent mechanism. PMID:24911456

  2. Lung cancer.

    PubMed

    Akhurst, Tim; MacManus, Michael; Hicks, Rodney J

    2015-04-01

    (18)F-fluorodeoxyglucose-positron emission tomography/computed tomography (FDG-PET/CT) plays a key role in the evaluation of undiagnosed lung nodules, when primary lung cancer is strongly suspected, or when it has already been diagnosed by other techniques. Although technical factors may compromise characterization of small or highly mobile lesions, lesions without apparent FDG uptake can generally be safely observed, whereas FDG-avid lung nodules almost always need further evaluation. FDG-PET/CT is now the primary staging imaging modality for patients with lung cancer who are being considered for curative therapy with either surgery or definitive radiation therapy. PMID:25829084

  3. Increased risk of lung cancer, non-Hodgkin's lymphoma, and leukemia following Hodgkin's disease

    SciTech Connect

    van Leeuwen, F.E.; Somers, R.; Taal, B.G.; van Heerde, P.; Coster, B.; Dozeman, T.; Huisman, S.J.; Hart, A.A.

    1989-08-01

    The risk of second cancers (SCs) was assessed in 744 patients with Hodgkin's disease (HD) admitted to The Netherlands Cancer Institute from 1966 to 1983. Sixty-nine SCs were observed one month or more after start of first treatment. These included 14 cases of lung cancer, nine cases of non-Hodgkin's lymphoma (NHL), 16 cases of leukemia, and six cases of the myelodysplastic syndrome (MDS). The median interval between the diagnosis of HD and that of second lung cancer, NHL, and leukemia was 8.1, 13.3, and 5.7 years, respectively. The overall relative risks (RR) (observed/expected (O/E) ratios) of developing lung cancer, NHL, and leukemia were 4.9 (95% confidence limit (CL), 2.7 to 8.2), 31.0 (95% CL, 14.2 to 58.9) and 45.7 (95% CL, 26.1 to 74.2), respectively. At 15 years the cumulative risk of developing an SC amounted to 20.6% +/- 2.9%. The 15-year estimates of lung cancer, NHL, and leukemia were 6.2% +/- 1.9%, 5.9% +/- 2.1% and 6.3% +/- 1.7%, respectively. Increased lung cancer risk following HD has not frequently been clearly demonstrated before; that we were able to demonstrate such risk may be due to the completeness of follow-up over long periods that could be achieved in this study. Excess lung cancer risk was only noted in treatment regimens with radiotherapy (RT); also, all lung cancers arose in irradiation fields. Excess risk of leukemia was only found in treatment regimens involving chemotherapy (CT). For NHL, combined modality treatment was shown to be the most important risk factor. Risk of lung cancer and NHL increased with time since diagnosis. A time-dependent covariate analysis (Cox model) performed on leukemia and MDS showed an increasing risk with intensity of CT, age (greater than 40 years), and a splenectomy.

  4. Lung cancer: is the increasing incidence due to radioactive polonium in cigarettes

    SciTech Connect

    Marmorstein, J.

    1986-02-01

    This paper presents clinical, experimental, and epidemiologic evidence to help explain the rapidly increasing incidence of primary lung cancer, with recently observed reversal in leading cell type from squamous cell to adenocarcinoma. It postulates that this may be due to changes in modern cigarettes, with or without filters, which allow inhalation of increased amounts of radioactive lead and polonium and decreased amounts of benzopyrene. This hypothesis is based upon measurements of increased concentrations of radioactive polonium in the lungs of cigarette smokers, in modern tobaccos grown since 1950, and in high-phosphate fertilizers used for tobacco farming in industrialized countries. Critical support for this thesis is based upon experimental animal studies in which lung cancers that resemble adenocarcinomas are induced with as little as 15 rads of radioactive polonium, equal to one fifth the dosage inhaled by cigarette smokers who average two packs a day during a 25-year period.

  5. Do inhaled corticosteroids increase the risk of Pneumocystis pneumonia in people with lung cancer?

    PubMed Central

    Msaad, Sameh; Yangui, Ilhem; Bahloul, Najla; Abid, Narjes; Koubaa, Makram; Hentati, Yosr; Ben Jemaa, Mounir; Kammoun, Samy

    2015-01-01

    Pneumocystis pneumonia (PCP) is a life-threatening infection in immunocompromised patients. It is relatively uncommon in patients with lung cancer. We report a case of PCP in a 59-year-old man with a past medical history of chronic obstructive pulmonary disease treated with formoterol and a moderate daily dose of inhaled budesonide. He had also advanced stage non-small lung cancer treated with concurrent chemo-radiation with a cisplatin-etoposide containing regimen. The diagnosis of PCP was suspected based on the context of rapidly increasing dyspnea, lymphopenia and the imaging findings. Polymerase chain reaction testing on an induced sputum specimen was positive for Pneumocystis jirovecii. The patient was treated with oral trimethoprim-sulfamethoxazole and systemic corticotherapy and had showed clinical and radiological improvement. Six months after the PCP diagnosis, he developed a malignant pleural effusion and expired on hospice care. Through this case, we remind the importance of screening for PCP in lung cancer patients under chemotherapeutic regimens and with increasing dyspnea. In addition, we alert to the fact that long-term inhaled corticosteroids may be a risk factor for PCP in patients with lung cancer. Despite intensive treatment, the mortality of PCP remains high, hence the importance of chemoprophylaxis should be considered. PMID:26380833

  6. Lung cancer - small cell

    MedlinePlus

    Cancer - lung - small cell; Small cell lung cancer; SCLC ... About 15% of all lung cancer cases are SCLC. Small cell lung cancer is slightly more common in men than women. Almost all cases of SCLC ...

  7. Lung cancer - small cell

    MedlinePlus

    Cancer - lung - small cell; Small cell lung cancer; SCLC ... About 15% of all lung cancer cases are SCLC. Small cell lung cancer is slightly more common in men than women. Almost all cases of SCLC are ...

  8. Epidemiology of Lung Cancer.

    PubMed

    Schwartz, Ann G; Cote, Michele L

    2016-01-01

    Lung cancer continues to be one of the most common causes of cancer death despite understanding the major cause of the disease: cigarette smoking. Smoking increases lung cancer risk 5- to 10-fold with a clear dose-response relationship. Exposure to environmental tobacco smoke among nonsmokers increases lung cancer risk about 20%. Risks for marijuana and hookah use, and the new e-cigarettes, are yet to be consistently defined and will be important areas for continued research as use of these products increases. Other known environmental risk factors include exposures to radon, asbestos, diesel, and ionizing radiation. Host factors have also been associated with lung cancer risk, including family history of lung cancer, history of chronic obstructive pulmonary disease and infections. Studies to identify genes associated with lung cancer susceptibility have consistently identified chromosomal regions on 15q25, 6p21 and 5p15 associated with lung cancer risk. Risk prediction models for lung cancer typically include age, sex, cigarette smoking intensity and/or duration, medical history, and occupational exposures, however there is not yet a risk prediction model currently recommended for general use. As lung cancer screening becomes more widespread, a validated model will be needed to better define risk groups to inform screening guidelines. PMID:26667337

  9. Metabolic alterations in lung cancer-associated fibroblasts correlated with increased glycolytic metabolism of the tumor

    PubMed Central

    Chaudhri, Virendra K.; Salzler, Gregory G.; Dick, Salihah A.; Buckman, Melanie S.; Sordella, Raffaella; Karoly, Edward D.; Mohney, Robert; Stiles, Brendon M.; Elemento, Olivier; Altorki, Nasser K.; McGraw, Timothy E.

    2013-01-01

    SUMMARY Cancer cells undergo a metabolic reprogramming but little is known about metabolic alterations of other cells within tumors. We use mass spectrometry-based profiling and a metabolic pathway-based systems analysis to compare 21 primary human lung tumor cancer-associated fibroblast lines (CAFs) to “normal” fibroblast lines (NFs) generated from adjacent non-neoplastic lung tissue. CAFs are pro-tumorigenic, although the mechanisms by which CAFs support tumors have not been elucidated. We have identified several pathways whose metabolite abundance globally distinguished CAFs from NFs, suggesting that metabolic alterations are not limited to cancer cells. In addition, we found metabolic differences between CAFs from high and low glycolytic tumors that might reflect distinct roles of CAFs related to the tumor’s glycolytic capacity. One such change was an increase of dipeptides in CAFs. Dipeptides primarily arise from the breakdown of proteins. We found in CAFs an increase in basal macroautophagy which likely accounts for the increase in dipeptides. Furthermore, we demonstrate a difference between CAFs and NFs in the induction of autophagy promoted by reduced glucose. In sum, our data suggest increased autophagy may account for metabolic differences between CAFs and NFs and may play additional as yet undetermined roles in lung cancer. PMID:23475953

  10. Murine Lung Cancer Increases CD4+ T Cell Apoptosis and Decreases Gut Proliferative Capacity in Sepsis

    PubMed Central

    Lyons, John D.; Mittal, Rohit; Fay, Katherine T.; Chen, Ching-Wen; Liang, Zhe; Margoles, Lindsay M.; Burd, Eileen M.; Farris, Alton B.

    2016-01-01

    Background Mortality is significantly higher in septic patients with cancer than in septic patients without a history of cancer. We have previously described a model of pancreatic cancer followed by sepsis from Pseudomonas aeruginosa pneumonia in which cancer septic mice have higher mortality than previously healthy septic mice, associated with increased gut epithelial apoptosis and decreased T cell apoptosis. The purpose of this study was to determine whether this represents a common host response by creating a new model in which both the type of cancer and the model of sepsis are altered. Methods C57Bl/6 mice received an injection of 250,000 cells of the lung cancer line LLC-1 into their right thigh and were followed three weeks for development of palpable tumors. Mice with cancer and mice without cancer were then subjected to cecal ligation and puncture and sacrificed 24 hours after the onset of sepsis or followed 7 days for survival. Results Cancer septic mice had a higher mortality than previously healthy septic mice (60% vs. 18%, p = 0.003). Cancer septic mice had decreased number and frequency of splenic CD4+ lymphocytes secondary to increased apoptosis without changes in splenic CD8+ numbers. Intestinal proliferation was also decreased in cancer septic mice. Cancer septic mice had a higher bacterial burden in the peritoneal cavity, but this was not associated with alterations in local cytokine, neutrophil or dendritic cell responses. Cancer septic mice had biochemical evidence of worsened renal function, but there was no histologic evidence of renal injury. Conclusions Animals with cancer have a significantly higher mortality than previously healthy animals following sepsis. The potential mechanisms associated with this elevated mortality differ significantly based upon the model of cancer and sepsis utilized. While lymphocyte apoptosis and intestinal integrity are both altered by the combination of cancer and sepsis, the patterns of these alterations vary

  11. Post-Inhaled Corticosteroid Pulmonary Tuberculosis Increases Lung Cancer in Patients with Asthma

    PubMed Central

    Lin, Frank Cheau-Feng; Nfor, Oswald Ndi; Jhang, Kai-Ming; Ku, Wen-Yuan; Ho, Chien-Chang; Lung, Chia-Chi; Pan, Hui-Hsien; Wu, Min-Chen; Wu, Ming-Fang; Liaw, Yung-Po

    2016-01-01

    Purpose To evaluate the association between post-inhaled corticosteroid (ICS) pulmonary tuberculosis (TB), pneumonia and lung cancer in patients with asthma. Methods The study samples were collected from the National Health Insurance Database. Asthmatic patients who were first-time users of ICS between 2003 and 2005 were identified as cases. For each case, 4 control individuals were randomly matched for sex, age and date of ICS use. Cases and matched controls were followed up until the end of 2010. Cox proportional hazard regression was used to determine the hazard ratio for pulmonary infections and lung cancer risk in the ICS users and non-users. Results A total of 10,904 first-time users of ICS were matched with 43,616 controls. The hazard ratios for lung cancer were: 2.52 (95% confidence interval [CI], 1.22–5.22; p = 0.012) for individuals with post-ICS TB, 1.28 (95%CI, 0.73–2.26; p = 0.389) for post-ICS pneumonia, 2.31(95%CI, 0.84–6.38; p = 0.105) for post-ICS pneumonia+TB, 1.08 (95%CI, 0.57–2.03; p = 0.815) for TB, 0.99 (95%CI, 0.63–1.55; p = 0.970) for pneumonia, and 0.32 (95%CI, 0.05–2.32; p = 0.261) for pneumonia+ TB, respectively. Conclusions Post-ICS TB increased lung cancer risk in patients with asthma. Because of the high mortality associated with lung cancer, screening tests are recommended for patients with post-ICS TB. PMID:27448321

  12. 6 Common Cancers - Lung Cancer

    MedlinePlus

    ... Home Current Issue Past Issues 6 Common Cancers - Lung Cancer Past Issues / Spring 2007 Table of Contents For ... for Desperate Housewives. (Photo ©2005 Kathy Hutchins / Hutchins) Lung Cancer Lung cancer causes more deaths than the next ...

  13. 6 Common Cancers - Lung Cancer

    MedlinePlus

    ... Bar Home Current Issue Past Issues 6 Common Cancers - Lung Cancer Past Issues / Spring 2007 Table of Contents For ... Desperate Housewives. (Photo ©2005 Kathy Hutchins / Hutchins) Lung Cancer Lung cancer causes more deaths than the next ...

  14. Lung Cancer Screening

    MedlinePlus

    ... Cancer Treatment Small Cell Lung Cancer Treatment Lung cancer is the leading cause of cancer death in the United States. Lung cancer is ... non- skin cancer in the United States. Lung cancer is the leading cause of cancer death in men and in women. ...

  15. Expression of Nemo-like kinase was increased and negatively correlated with the expression of TCF4 in lung cancers

    PubMed Central

    Zhang, Xiu-Wei; Chen, Song-Yan; Xue, Dong-Wei; Xu, Hui-Hui; Yang, Lian-He; Xu, Hong-Tao; Wang, En-Hua

    2015-01-01

    Nemo-like kinase (NLK), as a mitogen activated protein kinase (MAPK)-like kinase, is involved in the development of several human cancers. In this study, we explored the expression of NLK in lung squamous cell carcinoma (SCC) and adenocarcinoma tissues, and investigated the associations among NLK, β-catenin, T-cell factor 4 (TCF4), and the clinicopathological factors of lung cancers. The expressions of NLK, β-catenin, TCF4 were examined in 109 cases of lung cancers using immunohistochemistry method. The expression of NLK was observed in the nuclei of lung cancer tissues, and was significantly higher in lung cancer tissues than that in corresponding normal lung tissues (t = 21.636, n = 109, P < 0.001). The high expression of NLK was found in 45 cases of lung SCCs (45/49, 91.84%), which was much more than that in adenocarcinomas (38/60, 63.33%) (P = 0.001). Furthermore, the high expression of NLK was negatively correlated with TCF4 expression and positively correlated with the membranous expression of β-catenin. In conclusion, the present study demonstrated that the expression of NLK was localized in nucleus and significantly increased in lung cancers. The expression of NLK was negatively correlated with TCF4 expression and positively correlated with β-catenin membranous expression in lung cancers. PMID:26823848

  16. TUBERCULOSIS AND LUNG CANCER.

    PubMed

    Tamura, Atsuhisa

    2016-01-01

    The occurrence of pulmonary tuberculosis (PTB) and lung cancer as comorbidities has been extensively discussed in many studies. In the past, it was well known that lung cancer is a specific epidemiological successor of PTB and that lung cancer often develops in scars caused by PTB. In recent years, the relevance of the two diseases has drawn attention in terms of the close epidemiological connection and chronic inflammation-associated carcinogenesis. In Japanese case series studies, most lung cancer patients with tuberculous sequelae received supportive care alone in the past, but more recently, the use of aggressive lung cancer treatment is increasing. Many studies on PTB and lung cancer as comorbidities have revealed that active PTB is noted in 2-5% of lung cancer cases, whereas lung cancer is noted in 1-2% of active PTB cases. In such instances of comorbidity, many active PTB cases showed Type II (non-extensively cavitary disease) and Spread 2-3 (intermediate-extensive diseases) on chest X-rays, but standard anti-tuberculosis treatment easily eradicates negative conversion of sputum culture for M. tuberculosis; lung cancer cases were often stage III- IV and squamous cell carcinoma predominant, and the administration of aggressive treatment for lung cancer is increasing. The major clinical problems associated with PTB and lung cancer as comorbidities include delay in diagnosis (doctor's delay) and therapeutic limitations. The former involves two factors of radiographic interpretation: the principles of parsimony (Occam's razor) and visual search; the latter involves three factors of lung cancer treatment: infectivity of M.tuberculosis, anatomical limitation due to lung damage by tuberculosis, and drug-drug interactions between rifampicin and anti-cancer drugs, especially molecularly targeted drugs. The comorbidity of these two diseases is an important health-related issue in Japan. In the treatment of PTB, the possibility of concurrent lung cancer should be kept

  17. Lung cancer diagnosis and staging in the minimally invasive age with increasing demands for tissue analysis

    PubMed Central

    Costa, Daniel B.; Wright, Jeffrey; VanderLaan, Paul A.

    2015-01-01

    The diagnosis and staging of patients with lung cancer in recent decades has increasingly relied on minimally invasive tissue sampling techniques, such as endobronchial ultrasound (EBUS) or endoscopic ultrasound (EUS) needle aspiration, transbronchial biopsy, and transthoracic image guided core needle biopsy. These modalities have been shown to have low complication rates, and provide adequate cellular material for pathologic diagnosis and necessary ancillary molecular testing. As an important component to a multidisciplinary team approach in the care of patients with lung cancer, these minimally invasive modalities have proven invaluable for the rapid and safe acquisition of tissue used for the diagnosis, staging, and molecular testing of tumors to identify the best evidence-based treatment plan. The continuous evolution of the field of lung cancer staging and treatment has translated into improvements in survival and quality of life for patients. Although differences in clinical practice between academic and community hospital settings still exist, improvements in physician education and training as well as adoption of technological advancements should help narrow this gap going forward. PMID:26380180

  18. CYP24, the enzyme that catabolizes the antiproliferative agent vitamin D, is increased in lung cancer.

    PubMed

    Parise, Robert A; Egorin, Merrill J; Kanterewicz, Beatriz; Taimi, Mohammed; Petkovich, Martin; Lew, April M; Chuang, Samuel S; Nichols, Mark; El-Hefnawy, Talal; Hershberger, Pamela A

    2006-10-15

    1Alpha,25-dihydroxyvitamin D3 (1,25D3) displays potent antiproliferative activity in a variety of tumor model systems and is currently under investigation in clinical trials in cancer. Studies were initiated to explore its potential in nonsmall cell lung cancer (NSCLC), as effective approaches to the treatment of that disease are needed. In evaluating factors that may affect activity in NSCLC, the authors found that CYP24 (25-hydroxyvitamin D3-24-hydroxylase), the enzyme that catabolizes 1,25D3, is frequently expressed in NSCLC cell lines but not in the nontumorigenic bronchial epithelial cell line, Beas2B. CYP24 expression by RT-PCR was also detected in 10/18 primary lung tumors but in only 1/11 normal lung tissue specimens. Tumor-specific CYP24 upregulation was confirmed at the protein level via immunoblot analysis of patient-matched normal lung tissue and lung tumor extracts. Enzymatically active CYP24 is expected to desensitize NSCLC cells to 1,25D3. The authors therefore implemented a high performance liquid chromatography-tandem mass spectrometry (HPLC-MS/MS) assay for 1,25D3 and its CYP24-generated metabolites to determine whether NSCLC cells express active enzyme. Analysis of NSCLC cell cultures revealed time-dependent loss of 1,25D3 coincident with the appearance of CYP24-generated metabolites. MK-24(S)-S(O)(NH)-Ph-1, a specific inhibitor of CYP24, slowed the loss of 1,25D3 and increased 1,25D3 half-life. Furthermore, combination of 1,25D3 with MK-24(S)-S(O)(NH)-Ph-1 resulted in a significant decrease in the concentration of 1,25D3 required to achieve maximum growth inhibition in NSCLC cells. These data suggest that increased CYP24 expression in lung tumors restricts 1,25D3 activity and support the preclinical evaluation of CYP24 inhibitors for lung cancer treatment. PMID:16708384

  19. Lung Cancer Prevention

    MedlinePlus

    ... from the breakdown of uranium in rocks and soil. It seeps up through the ground, and leaks ... substances increases the risk of lung cancer: Asbestos . Arsenic . Chromium. Nickel. Beryllium. Cadmium . Tar and soot. These ...

  20. A message of hope: creation of the Faces of Lung Cancer project for increasing awareness of clinical trials.

    PubMed

    Quinn, G P; Bell-Ellison, B A; Bell, M Y; Caraway, V D; Conforte, D; Graci, L B; Lewandowski, A; Reynolds, B; Shaffer, A; Powell-Stafford, V L; Sapp, A L; Shimizu, C O; Vadaparampil, S; Vaughn, E J; Williams, C; Bepler, G

    2008-11-01

    In 2002, the Thoracic Oncology Advocacy Program at H. Lee Moffitt Cancer Center and Research Institute was created with a mission to contribute to the prevention and cure of lung cancer by embracing the patient perspective. In an effort to increase awareness of clinical trials (CTs) and to humanize the CT process, members of the advocacy programme were involved in the creation of the Faces of Lung Cancer project. Twelve lung cancer patients who participated in a CT, four caregivers of patients who had been on a trial and four thoracic health care professionals were interviewed and photographed by a professional photographer with prior experience in photo-documentary work. Preliminary results indicate just the process of participating in the Faces of Lung Cancer project and creating the photo essay has had a positive impact on the lives of cancer patients and their caregivers. Formal evaluation of the Faces of Lung Cancer project is underway; however, preliminary results indicate that the project is viewed as successful in terms of conveying a message of hope and increasing awareness. By including visual displays, in conjunction with patient interviews, the photo essay is able to generate and blend powerful information and images that provide a richer, more complete portrayal of the context of a patient's experience. PMID:18771536

  1. Lung cancer.

    PubMed

    Frödin, J E

    1996-01-01

    This synthesis of the literature on radiotherapy for lung cancer is based on 80 scientific articles, including 2 meta-analyses, 29 randomized studies, 19 prospective studies, and 21 retrospective studies. These studies involve 28172 patients. Basic treatment for limited-stage small cell lung cancer (SCLC), is chemotherapy. Addition of radiotherapy to the primary tumor and mediastinum reduces local recurrence, prolongs long-term survival, and is often indicated. Current, and future, studies can be expected to show successive improvements in results for SCLC by optimizing the combination of radiotherapy and chemotherapy. Should these treatments be given simultaneously or sequentially, and in which order? Which fractionation is best? Probably, no change in resource requirements for radiotherapy will be necessary, with the possible exception of changes in fractionation. Surgery constitutes primary treatment for nonsmall cell lung cancer (NSCLC) stages I and II. Radiotherapy may provide an alternative for patients who are inoperable for medical reasons. The value of radiotherapy following radical surgery for NSCLC remains to be shown. It is not indicated based on current knowledge. For NSCLC stage III, radiotherapy shrinks tumors and prolongs survival at 2 and 3 years. Whether it influences long-term survival after 5 years has not been shown. Considering the side effects of treatment, one must question whether limited improvements in survival motivate routine radiotherapy in these patients. Earlier attempts to add chemotherapy to radiotherapy to improve treatment results of NSCLC have not yielded convincing results. Several studies are currently on-going. Prophylactic cranial irradiation (PCI) greatly reduces the risk for brain metastases from SCLC. However, it has little influence on survival. Many treatment centers give PCI to SCLC patients who have achieved complete remission. This practice may be questioned since PCI is associated with serious complications. PCI is

  2. [Chemoprevention of lung cancer].

    PubMed

    Tsuchida, Takaaki; Saito, Makoto; Honda, Hidetoshi; Hirata, Takeshi; Kato, Harubumi

    2003-02-01

    Since a high concentration of beta-carotene in blood reduces the risk of lung cancer, a large-scale intervention examination containing beta-carotene was conducted, mainly by the National Cancer Institute. The results showed that the risk of lung cancer increased with administration of beta-carotene. This result demonstrates that continuation of smoking is an important factor in the increased risk, and not smoking is confirmed to be the most important prevention method. The authors examined the treatment effect of raising the concentration of folic acid and vitamin B12 in blood on bronchial dysplasia as a pre-cancerous lesion. A significant medical treatment effect was see in the folic acid and vitamin B12 medication groups, which seems promising for the chemoprevention of lung cancer. PMID:12610863

  3. Increased APOBEC3B Predicts Worse Outcomes in Lung Cancer: A Comprehensive Retrospective Study

    PubMed Central

    Yan, Shumei; He, Fan; Gao, Bei; Wu, Huini; Li, Mei; Huang, Liyun; Liang, Jianzhong; Wu, Qiuliang; Li, Yong

    2016-01-01

    Lung cancer ranks as the most common and lethal malignancy in America and worldwide. APOBEC3B is a newly identified DNA cytosine deaminase, which is supposed to function as a major source of DNA mutation in many different tumors. In this study, we combine the data of online databases and two hundred and twenty-one primary non-small-cell lung carcinoma (NSCLC) specimens from Sun Yat-sen University Cancer Center to investigate, for the first time, the clinical role of APOBEC3B in lung cancer. We found that the APOBEC3 expression was commonly elevated in NSCLC tissues and overexpression of APOBEC3B was correlated with unfavorable prognosis of the patients with NSCLC. Furthermore, APOBEC3B expression was associated with nodal status, TNM staging and adjuvant chemotherapy of the patients with NSCLC. Further research is warranted. PMID:27076842

  4. Radon and lung cancer.

    PubMed

    Sethi, Tarsheen K; El-Ghamry, Moataz N; Kloecker, Goetz H

    2012-03-01

    Lung cancer is the leading cause of cancer-related deaths worldwide. Radon exposure is the second leading cause of lung cancer, following tobacco smoke. Radon is not only an independent risk factor; it also increases the risk of lung cancer in smokers. Numerous cohort, case-control, and experimental studies have established the carcinogenic potential of radon. The possibility of radon having a causative effect on other cancers has been explored but not yet proven. One of the postulated mechanisms of carcinogenesis is DNA damage by alpha particles mediated by the production of reactive oxygen species. The latter are also thought to constitute one of the common mechanisms underlying the synergistic effect of radon and tobacco smoke. With an estimated 21,000 lung cancer deaths attributable to radon in the United States annually, the need for radon mitigation is well acknowledged. The Environmental Protection Agency (EPA) has established an indoor limit of 4 picocuries (pCi)/L, and various methods are available for indoor radon reduction when testing shows higher levels. Radon mitigation should accompany smoking cessation measures in lung cancer prevention efforts. PMID:22402423

  5. Celecoxib increases lung cancer cell lysis by lymphokine-activated killer cells via upregulation of ICAM-1

    PubMed Central

    Frank, Marcus; Linnebacher, Michael; Hinz, Burkhard

    2015-01-01

    The antitumorigenic mechanism of the selective cyclooxygenase-2 (COX-2) inhibitor celecoxib is still a matter of debate. Using lung cancer cell lines (A549, H460) and metastatic cells derived from a lung cancer patient, the present study investigates the impact of celecoxib on the expression of intercellular adhesion molecule 1 (ICAM-1) and cancer cell lysis by lymphokine-activated killer (LAK) cells. Celecoxib, but not other structurally related selective COX-2 inhibitors (i.e., etoricoxib, rofecoxib, valdecoxib), was found to cause a substantial upregulation of ICAM-1 protein levels. Likewise, ICAM-1 mRNA expression was increased by celecoxib. Celecoxib enhanced the susceptibility of cancer cells to be lysed by LAK cells with the respective effect being reversed by a neutralizing ICAM-1 antibody. In addition, enhanced killing of celecoxib-treated cancer cells was reversed by preincubation of LAK cells with an antibody to lymphocyte function associated antigen 1 (LFA-1), suggesting intercellular ICAM-1/LFA-1 crosslink as crucial event within this process. Finally, celecoxib elicited no significant increase of LAK cell-mediated lysis of non-tumor bronchial epithelial cells, BEAS-2B, associated with a far less ICAM-1 induction as compared to cancer cells. Altogether, our data demonstrate celecoxib-induced upregulation of ICAM-1 on lung cancer cells to be responsible for intercellular ICAM-1/LFA-1 crosslink that confers increased cancer cell lysis by LAK cells. These findings provide proof for a novel antitumorigenic mechanism of celecoxib. PMID:26513172

  6. Lung Cancer in Never Smokers.

    PubMed

    Rivera, Gabriel Alberto; Wakelee, Heather

    2016-01-01

    Lung cancer is predominantly associated with cigarette smoking; however, a substantial minority of patients with the disease have never smoked. In the US it is estimated there are 17,000-26,000 annual deaths from lung cancer in never smokers, which as a separate entity would be the seventh leading cause of cancer mortality. Controversy surrounds the question of whether or not the incidence of lung cancer in never-smokers is increasing, with more data to support this observation in Asia. There are several factors associated with an increased risk of developing lung cancer in never smokers including second hand smoke, indoor air pollution, occupational exposures, and genetic susceptibility among others. Adenocarcinoma is the most common histology of lung cancer in never smokers and in comparison to lung cancer in smokers appears less complex with a higher likelihood to have targetable driver mutations. PMID:26667338

  7. Epidemiology of Lung Cancer

    PubMed Central

    Ridge, Carole A.; McErlean, Aoife M.; Ginsberg, Michelle S.

    2013-01-01

    Incidence and mortality attributed to lung cancer has risen steadily since the 1930s. Efforts to improve outcomes have not only led to a greater understanding of the etiology of lung cancer, but also the histologic and molecular characteristics of individual lung tumors. This article describes this evolution by discussing the extent of the current lung cancer epidemic including contemporary incidence and mortality trends, the risk factors for development of lung cancer, and details of promising molecular targets for treatment. PMID:24436524

  8. Lung cancer prevention.

    PubMed

    Slatore, Christopher; Sockrider, Marianna

    2014-11-15

    Lung cancer is a common form of cancer.There are things you can do to lower your risk of lung cancer. Stop smoking tobacco. Ask your health care provider for help in quitting, including use of medicines to help with nicotine dependence. discuss with your healthcare provider,what you are taking or doing to decrease your risk for lung cancer PMID:25398122

  9. Epidemiology of Lung Cancer.

    PubMed

    Mao, Yousheng; Yang, Ding; He, Jie; Krasna, Mark J

    2016-07-01

    Lung cancer has been transformed from a rare disease into a global problem and public health issue. The etiologic factors of lung cancer become more complex along with industrialization, urbanization, and environmental pollution around the world. Currently, the control of lung cancer has attracted worldwide attention. Studies on the epidemiologic characteristics of lung cancer and its relative risk factors have played an important role in the tertiary prevention of lung cancer and in exploring new ways of diagnosis and treatment. This article reviews the current evolution of the epidemiology of lung cancer. PMID:27261907

  10. [Smoking and lung cancer].

    PubMed

    Postmus, P E

    1999-11-01

    Since fifty years it is clear now that smoking of tobacco products is responsible for the lung cancer epidemic that is currently in progress worldwide. Although in the Western world a small decrease of lung cancer in males is found, the number of female patients is steadily increasing. Changes in tobacco production have resulted in exposition of smokers to other carcinogens. This is probably the cause of the change in the histological pattern with an increase of adenocarcinoma and stabilisation of squamous cell lung cancer. Despite the bad prognosis there is some hope that with improvement of early detection methods more patients can be cured. However, for a real change it is necessary to discourage smoking by all means. PMID:11930407

  11. The Expression of the Ubiquitin Ligase SIAH2 (Seven In Absentia Homolog 2) Is Increased in Human Lung Cancer

    PubMed Central

    Moreno, Paula; Lara-Chica, Maribel; Soler-Torronteras, Rafael; Caro, Teresa; Medina, Manuel; Álvarez, Antonio; Salvatierra, Ángel; Muñoz, Eduardo; Calzado, Marco A.

    2015-01-01

    Objectives Lung cancer is the leading cause of cancer-related deaths worldwide. Overall 5-year survival has shown little improvement over the last decades. Seven in absentia homolog (SIAH) proteins are E3 ubiquitin ligases that mediate proteasomal protein degradation by poly-ubiquitination. Even though SIAH proteins play a key role in several biological processes, their role in human cancer remains controversial. The aim of the study was to document SIAH2 expression pattern at different levels (mRNA, protein level and immunohistochemistry) in human non-small cell lung cancer (NSCLC) samples compared to surrounding healthy tissue from the same patient, and to analyse the association with clinicopathological features. Materials and Methods One hundred and fifty-two samples from a patient cohort treated surgically for primary lung cancer were obtained for the study. Genic and protein expression levels of SIAH2 were analysed and compared with clinic-pathologic variables. Results The present study is the first to analyze the SIAH2 expression pattern at different levels (RNA, protein expression and immunohistochemistry) in non-small cell lung cancer (NSCLC). We found that SIAH2 protein expression is significantly enhanced in human lung adenocarcinoma (ADC) and squamous cell lung cancer (SCC). Paradoxically, non-significant changes at RNA level were found, suggesting a post-traductional regulatory mechanism. More importantly, an increased correlation between SIAH2 expression and tumor grade was detected, suggesting that this protein could be used as a prognostic biomarker to predict lung cancer progression. Likewise, SIAH2 protein expression showed a strong positive correlation with fluorodeoxyglucose (2-deoxy-2(18F)fluoro-D-glucose) uptake in primary NSCLC, which may assist clinicians in stratifying patients at increased overall risk of poor survival. Additionally, we described an inverse correlation between the expression of SIAH2 and the levels of one of its substrates

  12. Controversies in Lung Cancer Screening.

    PubMed

    Gill, Ritu R; Jaklitsch, Michael T; Jacobson, Francine L

    2016-02-01

    There remains an extensive debate over lung cancer screening, with lobbying for and against screening for very compelling reasons. The National Lung Screening Trial, International Early Lung Cancer Program, and other major screening studies favor screening with low-dose CT scans and have shown a reduction in lung cancer-specific mortality. The increasing incidence of lung cancer and the dismal survival rate for advanced disease despite improved multimodality therapy have sparked an interest in the implementation of national lung cancer screening. Concerns over imaging workflow, radiation dose, management of small nodules, overdiagnosis bias, lead-time and length-time bias, emerging new technologies, and cost-effectiveness continue to be debated. The authors address each of these issues as they relate to radiologic practice. PMID:26846531

  13. Metastatic cancer to the lung

    MedlinePlus

    ... Bladder cancer Breast cancer Colon cancer Kidney cancer Neuroblastoma Prostate cancer Sarcoma Wilms tumor Symptoms Symptoms may ... Breast cancer Cancer Chemotherapy Colon cancer Lung cancer Neuroblastoma Prostate cancer Radiation therapy Wilms tumor Update Date ...

  14. Risks of Lung Cancer Screening

    MedlinePlus

    ... Cancer Treatment Small Cell Lung Cancer Treatment Lung cancer is the leading cause of cancer death in the United States. Lung cancer is ... non- skin cancer in the United States. Lung cancer is the leading cause of cancer death in men and in women. ...

  15. Lung cancer

    MedlinePlus

    ... any symptoms. Symptoms depend on the type of cancer you have, but may include: Chest pain Cough that does not go away Coughing up blood Fatigue Losing weight without trying Loss of appetite Shortness of breath ...

  16. Drugs Approved for Lung Cancer

    MedlinePlus

    ... Professionals Questions to Ask about Your Treatment Research Drugs Approved for Lung Cancer This page lists cancer ... in lung cancer that are not listed here. Drugs Approved for Non-Small Cell Lung Cancer Abitrexate ( ...

  17. Increased cytosine DNA-methyltransferase activity is target-cell-specific and an early event in lung cancer.

    PubMed Central

    Belinsky, S A; Nikula, K J; Baylin, S B; Issa, J P

    1996-01-01

    The association between increased DNA-methyltransferase (DNA-MTase) activity and tumor development suggest a fundamental role for this enzyme in the initiation and progression of cancer. A true functional role for DNA-MTase in the neoplastic process would be further substantiated if the target cells affected by the initiating carcinogen exhibit changes in enzyme activity. This hypothesis was addressed by examining DNA-MTase activity in alveolar type II (target) and Clara (nontarget) cells from A/J and C3H mice that exhibit high and low susceptibility, respectively, for lung tumor formation. Increased DNA-MTase activity was found only in the target alveolar type II cells of the susceptible A/J mouse and caused a marked increase in overall DNA methylation in these cells. Both DNA-MTase and DNA methylation changes were detected 7 days after carcinogen exposure and, thus, were early events in neoplastic evolution. Increased gene expression was also detected by RNA in situ hybridization in hypertrophic alveolar type II cells of carcinogen-treated A/J mice, indicating that elevated levels of expression may be a biomarker for premalignancy. Enzyme activity increased incrementally during lung cancer progression and coincided with increased expression of the DNA-MTase activity are strongly associated with neoplastic development and constitute a key step in carcinogenesis. The detection of premalignant lung disease through increased DNA-MTase expression and the possibility of blocking the deleterious effects of this change with specific inhibitors will offer new intervention strategies for lung cancer. Images Fig. 2 PMID:8633014

  18. [The epidemiology of lung cancer].

    PubMed

    Kosacka, Monika; Jankowska, Renata

    2007-01-01

    Lung cancer is currently most frequently diagnosed neoplasm in males and the fifth most frequent cancer in females. In developed countries only breast cancer is diagnosed more often in women. Worldwide, lung cancer is the most common cause of cancer mortality in males and females. In the Europe lung cancer accounts for 21% of all cancer cases in males and 29% of all cancer deaths. The rapid increase in lung cancer incidence was observed the since beginning of the XX century till 1990-1994. The incidence in males decreased recently, but still increases in females, especially in young women. The changes in frequency of various histological subtypes of lung cancer are observed too. Despite many clinical trials, modern diagnostic techniques and improved supportive care, the prognosis remains unfavourable and long-term survival almost did not change. In Poland the incidence of lung cancer in 2002 was 81.9/100 000 in males and 22.2/100 000 in females. In both genders 1-year and 5-year survivals time are one of the shortest in Europe. PMID:17541915

  19. Epidemiology of lung cancer in China

    PubMed Central

    Chen, Wanqing; Zheng, Rongshou; Zeng, Hongmei; Zhang, Siwei

    2015-01-01

    Background Lung cancer is the most common cancer and the leading cause of cancer death in China. Along with socioeconomic development, environmental problems have intensified and the burden of lung cancer continues to increase. Methods In this study, national cancer registry data was used for evaluating incidence, mortality, time trend, and prediction. Results In China in 2010, 605 900 patients were diagnosed and 486 600 patients died of lung cancer. Throughout the last three decades, the mortality of lung cancer has dramatically increased, as shown in national death surveys. From 2000 to 2010, age specific incidence of lung cancer increased in most age groups. It is estimated that in 2015, the total number of new cases of lung cancer will reach 733 300. Conclusions Lung cancer is a serious disease affecting public health and an effective control strategy is needed in China. PMID:26273360

  20. Rare lung cancers.

    PubMed

    2015-12-01

    There are several different kinds of lung cancer, often referred to as lung cancer subtypes. Some of these occur more often than others. In this factsheet we will specifically look at the subtypes of cancers that do not happen very often and are considered 'rare'. PMID:27066129

  1. Lung Cancer Indicators Recurrence

    Cancer.gov

    This study describes prognostic factors for lung cancer spread and recurrence, as well as subsequent risk of death from the disease. The investigators observed that regardless of cancer stage, grade, or type of lung cancer, patients in the study were more

  2. Lung Cancer Screening.

    PubMed

    Wu, Geena X; Raz, Dan J

    2016-01-01

    Lung cancer is the leading cause of cancer mortality in the United States and worldwide. Since lung cancer outcomes are dependent on stage at diagnosis with early disease resulting in longer survival, the goal of screening is to capture lung cancer in its early stages when it can be treated and cured. Multiple studies have evaluated the use of chest X-ray (CXR) with or without sputum cytologic examination for lung cancer screening, but none has demonstrated a mortality benefit. In contrast, the multicenter National Lung Screening Trial (NLST) from the United States found a 20 % reduction in lung cancer mortality following three consecutive screenings with low-dose computed tomography (LDCT) in high-risk current and former smokers. Data from European trials are not yet available. In addition to a mortality benefit, lung cancer screening with LDCT also offers a unique opportunity to promote smoking cessation and abstinence and may lead to the diagnoses of treatable chronic diseases, thus decreasing the overall disease burden. The risks of lung cancer screening include overdiagnosis, radiation exposure, and false-positive results leading to unnecessary testing and possible patient anxiety and distress. However, the reduction in lung cancer mortality is a benefit that outweighs the risks and major health organizations currently recommend lung cancer screening using age, smoking history, and quit time criteria derived from the NLST. Although more research is needed to clearly define and understand the application and utility of lung cancer screening in the general population, current data support that lung cancer screening is effective and should be offered to eligible beneficiaries. PMID:27535387

  3. Immunotherapy for lung cancer.

    PubMed

    Steven, Antonius; Fisher, Scott A; Robinson, Bruce W

    2016-07-01

    Treatment of lung cancer remains a challenge, and lung cancer is still the leading cause of cancer-related mortality. Immunotherapy has previously failed in lung cancer but has recently emerged as a very effective new therapy, and there is now growing worldwide enthusiasm in cancer immunotherapy. We summarize why immune checkpoint blockade therapies have generated efficacious and durable responses in clinical trials and why this has reignited interest in this field. Cancer vaccines have also been explored in the past with marginal success. Identification of optimal candidate neoantigens may improve cancer vaccine efficacy and may pave the way to personalized immunotherapy, alone or in combination with other immunotherapy such as immune checkpoint blockade. Understanding the steps in immune recognition and eradication of cancer cells is vital to understanding why previous immunotherapies failed and how current therapies can be used optimally. We hold an optimistic view for the future prospect in lung cancer immunotherapy. PMID:27101251

  4. Genetics Home Reference: lung cancer

    MedlinePlus

    ... Me Understand Genetics Home Health Conditions lung cancer lung cancer Enable Javascript to view the expand/collapse boxes. Download PDF Open All Close All Description Lung cancer is a disease in which certain cells ...

  5. Increased Lung and Bladder Cancer Incidence In Adults After In Utero and Early-Life Arsenic Exposure

    PubMed Central

    Steinmaus, Craig; Ferreccio, Catterina; Acevedo, Johanna; Yuan, Yan; Liaw, Jane; Durán, Viviana; Cuevas, Susana; García, José; Meza, Rodrigo; Valdés, Rodrigo; Valdés, Gustavo; Benítez, Hugo; VanderLinde, Vania; Villagra, Vania; Cantor, Kenneth P; Moore, Lee E; Perez, Saida G; Steinmaus, Scott; Smith, Allan H

    2014-01-01

    Background From 1958–70, >100,000 people in northern Chile were exposed to a well-documented, distinct period of high drinking water arsenic concentrations. We previously reported ecological evidence suggesting that early-life exposure in this population resulted in increased mortality in adults from several outcomes including lung and bladder cancer. Methods We have now completed the first study ever assessing incident cancer cases after early-life arsenic exposure, and the first study on this topic with individual participant exposure and confounding factor data. Subjects included 221 lung and 160 bladder cancer cases diagnosed in northern Chile from 2007–2010, and 508 age and gender-matched controls. Results Odds ratios (ORs) adjusted for age, sex, and smoking in those only exposed in early-life to arsenic water concentrations of ≤110, 110–800, and >800 μg/L were 1.00, 1.88 (95% confidence interval (CI), 0.96–3.71), and 5.24 (3.05–9.00) (p-trend<0.001) for lung cancer, and 1.00, 2.94 (1.29–6.70), and 8.11 (4.31–15.25) (p-trend<0.001) for bladder cancer. ORs were lower in those not exposed until adulthood. The highest category (>800 μg/L) involved exposures which started 49–52 years before, and ended 37–40 years before the cancer cases were diagnosed. Conclusion Lung and bladder cancer incidence in adults was markedly increased following exposure to arsenic in early-life, even up to 40 years after high exposures ceased. Findings like these have not been identified before for any environmental exposure, and suggest that humans are extraordinarily susceptible to early-life arsenic exposure. Impact Policies aimed at reducing early-life exposure may help reduce the long-term risks of arsenic-related disease. PMID:24859871

  6. E-Cadherin repression increases amount of cancer stem cells in human A549 lung adenocarcinoma and stimulates tumor growth.

    PubMed

    Farmakovskaya, M; Khromova, N; Rybko, V; Dugina, V; Kopnin, B; Kopnin, P

    2016-04-17

    Here we show that cancer stem cells amount in human lung adenocarcinoma cell line A549 depends on E-cadherin expression. In fact, downregulation of E-cadherin expression enhanced expression of pluripotent genes (c-MYC, NESTIN, OCT3/4 and SOX2) and enriched cell population with the cells possessing the properties of so-called 'cancer stem cells' via activation of Wnt/β-catenin signaling. Repression of E-cadherin also stimulated cell proliferation and migration in vitro, decreased cell amount essential for xenografts formation in nude mice, increased tumors vascularization and growth. On the other hand, E-cadherin upregulation caused opposite effects i.e. diminished the number of cancer stem cells, decreased xenograft vascularization and decelerated tumor growth. Therefore, agents restoring E-cadherin expression may be useful in anticancer therapy. PMID:26940223

  7. Staging of Lung Cancer

    MedlinePlus

    ... of N2 means cancer has spread to the middle part of the chest (called the mediastinum). A rating ... so that the surgeon can remove the cancerous part of the lung and/or lymph node ... biopsied are your lungs, bones, and brain. These types of biopsies can be done with ...

  8. Matrix Metalloproteinase-19 Promotes Metastatic Behavior In Vitro and Is Associated with Increased Mortality in Non–Small Cell Lung Cancer

    PubMed Central

    Yu, Guoying; Herazo-Maya, Jose D.; Nukui, Tomoko; Romkes, Marjorie; Parwani, Anil; Juan-Guardela, Brenda M.; Robertson, Jennifer; Gauldie, Jack; Siegfried, Jill M.; Kaminski, Naftali

    2014-01-01

    Rationale: Lung cancer is the leading cause of cancer death in both men and women in the United States and worldwide. Matrix metalloproteinases (MMPs) have been implicated in the development and progression of lung cancer, but their role in the molecular pathogenesis of lung cancer remains unclear. We have found that MMP19, a relatively novel member of the MMP family, is overexpressed in lung tumors when compared with control subjects. Objectives: To test the hypothesis that MMP19 plays a significant role in the development and progression of non–small cell lung cancer (NSCLC). Methods: We have analyzed lung cancer gene expression data, immunostained lung tumors for MMP19, and performed in vitro assays to test the effects of MMP19 in NSCLC cells. Measurements and Main Results: We found that MMP19 gene and protein expression is increased in lung cancer tumors compared with adjacent and histologically normal lung tissues. In three independent datasets, increased MMP19 gene expression conferred a poorer prognosis in NSCLC. In vitro, we found that overexpression of MMP19 promotes epithelial–mesenchymal transition, migration, and invasiveness in multiple NSCLC cell lines. Overexpression of MMP19 with a mutation at the catalytic site did not impair epithelial–mesenchymal transition or expression of prometastasis genes. We also found that miR-30 isoforms, a microRNA family predicted to target MMP19, is markedly down-regulated in human lung cancer and regulates MMP19 expression. Conclusions: Taken together, these findings suggest that MMP19 is associated with the development and progression of NSCLC and may be a potential biomarker of disease severity and outcome. PMID:25250855

  9. Occupational lung cancer

    SciTech Connect

    Coultas, D.B.; Samet, J.M. )

    1992-06-01

    The overall importance of occupational agents as a cause of lung cancer has been a controversial subject since the 1970s. A federal report, released in the late 1970s, projected a surprisingly high burden of occupational lung cancer; for asbestos and four other agents, from 61,000 to 98,000 cases annually were attributed to these agents alone. Many estimates followed, some much more conservative. For example, Doll and Peto estimated that 15% of lung cancer in men and 5% in women could be attributed to occupational exposures. A number of population-based case-control studies also provide relevant estimates. In a recent literature review, Vineis and Simonato cited attributable risk estimates for occupation and lung cancer that ranged from 4% to 40%; for asbestos alone, the estimates ranged from 1% to 5%. These estimates would be expected to vary across locations and over time. Nevertheless, these recent estimates indicate that occupation remains an important cause of lung cancer. Approaches to Prevention. Prevention of lung cancer mortality among workers exposed to agents or industrial processes that cause lung cancer may involve several strategies, including eliminating or reducing exposures, smoking cessation, screening, and chemo-prevention. For example, changes in industrial processes that have eliminated or reduced exposures to chloromethyl ethers and nickel compounds have provided evidence of reduced risk of lung cancer following these changes. Although occupational exposures are important causes of lung cancer, cigarette smoking is the most important preventable cause of lung cancer. For adults, the work site offers an important location to target smoking cessation efforts. In fact, the work site may be the only place to reach many smokers.

  10. Genetic variants associated with longer telomere length are associated with increased lung cancer risk among never-smoking women in Asia: a report from the female lung cancer consortium in Asia.

    PubMed

    Machiela, Mitchell J; Hsiung, Chao Agnes; Shu, Xiao-Ou; Seow, Wei Jie; Wang, Zhaoming; Matsuo, Keitaro; Hong, Yun-Chul; Seow, Adeline; Wu, Chen; Hosgood, H Dean; Chen, Kexin; Wang, Jiu-Cun; Wen, Wanqing; Cawthon, Richard; Chatterjee, Nilanjan; Hu, Wei; Caporaso, Neil E; Park, Jae Yong; Chen, Chien-Jen; Kim, Yeul Hong; Kim, Young Tae; Landi, Maria Teresa; Shen, Hongbing; Lawrence, Charles; Burdett, Laurie; Yeager, Meredith; Chang, I-Shou; Mitsudomi, Tetsuya; Kim, Hee Nam; Chang, Gee-Chen; Bassig, Bryan A; Tucker, Margaret; Wei, Fusheng; Yin, Zhihua; An, She-Juan; Qian, Biyun; Lee, Victor Ho Fun; Lu, Daru; Liu, Jianjun; Jeon, Hyo-Sung; Hsiao, Chin-Fu; Sung, Jae Sook; Kim, Jin Hee; Gao, Yu-Tang; Tsai, Ying-Huang; Jung, Yoo Jin; Guo, Huan; Hu, Zhibin; Hutchinson, Amy; Wang, Wen-Chang; Klein, Robert J; Chung, Charles C; Oh, In-Jae; Chen, Kuan-Yu; Berndt, Sonja I; Wu, Wei; Chang, Jiang; Zhang, Xu-Chao; Huang, Ming-Shyan; Zheng, Hong; Wang, Junwen; Zhao, Xueying; Li, Yuqing; Choi, Jin Eun; Su, Wu-Chou; Park, Kyong Hwa; Sung, Sook Whan; Chen, Yuh-Min; Liu, Li; Kang, Chang Hyun; Hu, Lingmin; Chen, Chung-Hsing; Pao, William; Kim, Young-Chul; Yang, Tsung-Ying; Xu, Jun; Guan, Peng; Tan, Wen; Su, Jian; Wang, Chih-Liang; Li, Haixin; Sihoe, Alan Dart Loon; Zhao, Zhenhong; Chen, Ying; Choi, Yi Young; Hung, Jen-Yu; Kim, Jun Suk; Yoon, Ho-Il; Cai, Qiuyin; Lin, Chien-Chung; Park, In Kyu; Xu, Ping; Dong, Jing; Kim, Christopher; He, Qincheng; Perng, Reury-Perng; Kohno, Takashi; Kweon, Sun-Seog; Chen, Chih-Yi; Vermeulen, Roel C H; Wu, Junjie; Lim, Wei-Yen; Chen, Kun-Chieh; Chow, Wong-Ho; Ji, Bu-Tian; Chan, John K C; Chu, Minjie; Li, Yao-Jen; Yokota, Jun; Li, Jihua; Chen, Hongyan; Xiang, Yong-Bing; Yu, Chong-Jen; Kunitoh, Hideo; Wu, Guoping; Jin, Li; Lo, Yen-Li; Shiraishi, Kouya; Chen, Ying-Hsiang; Lin, Hsien-Chih; Wu, Tangchun; Wong, Maria Pik; Wu, Yi-Long; Yang, Pan-Chyr; Zhou, Baosen; Shin, Min-Ho; Fraumeni, Joseph F; Zheng, Wei; Lin, Dongxin; Chanock, Stephen J; Rothman, Nathaniel; Lan, Qing

    2015-07-15

    Recent evidence from several relatively small nested case-control studies in prospective cohorts shows an association between longer telomere length measured phenotypically in peripheral white blood cell (WBC) DNA and increased lung cancer risk. We sought to further explore this relationship by examining a panel of seven telomere-length associated genetic variants in a large study of 5,457 never-smoking female Asian lung cancer cases and 4,493 never-smoking female Asian controls using data from a previously reported genome-wide association study. Using a group of 1,536 individuals with phenotypically measured telomere length in WBCs in the prospective Shanghai Women's Health study, we demonstrated the utility of a genetic risk score (GRS) of seven telomere-length associated variants to predict telomere length in an Asian population. We then found that GRSs used as instrumental variables to predict longer telomere length were associated with increased lung cancer risk (OR = 1.51 (95% CI = 1.34-1.69) for upper vs. lower quartile of the weighted GRS, p value = 4.54 × 10(-14) ) even after removing rs2736100 (p value = 4.81 × 10(-3) ), a SNP in the TERT locus robustly associated with lung cancer risk in prior association studies. Stratified analyses suggested the effect of the telomere-associated GRS is strongest among younger individuals. We found no difference in GRS effect between adenocarcinoma and squamous cell subtypes. Our results indicate that a genetic background that favors longer telomere length may increase lung cancer risk, which is consistent with earlier prospective studies relating longer telomere length with increased lung cancer risk. PMID:25516442

  11. Genetic variants associated with longer telomere length are associated with increased lung cancer risk among never-smoking women in Asia: A report from the Female Lung Cancer Consortium in Asia

    PubMed Central

    Machiela, Mitchell J; Hsiung, Chao Agnes; Shu, Xiao-Ou; Seow, Wei Jie; Wang, Zhaoming; Matsuo, Keitaro; Hong, Yun-Chul; Seow, Adeline; Wu, Chen; Hosgood, H Dean; Chen, Kexin; Wang, Jiu-Cun; Wen, Wanqing; Cawthon, Richard; Chatterjee, Nilanjan; Hu, Wei; Caporaso, Neil E; Park, Jae Yong; Chen, Chien-Jen; Kim, Yeul Hong; Kim, Young Tae; Landi, Maria Teresa; Shen, Hongbing; Lawrence, Charles; Burdett, Laurie; Yeager, Meredith; Chang, I-Shou; Mitsudomi, Tetsuya; Kim, Hee Nam; Chang, Gee-Chen; Bassig, Bryan A; Tucker, Margaret; Wei, Fusheng; Yin, Zhihua; An, She-Juan; Qian, Biyun; Lee, Victor Ho Fun; Lu, Daru; Liu, Jianjun; Jeon, Hyo-Sung; Hsiao, Chin-Fu; Sung, Jae Sook; Kim, Jin Hee; Gao, Yu-Tang; Tsai, Ying-Huang; Jung, Yoo Jin; Guo, Huan; Hu, Zhibin; Hutchinson, Amy; Wang, Wen-Chang; Klein, Robert J; Chung, Charles C; Oh, In-Jae; Chen, Kuan-Yu; Berndt, Sonja I; Wu, Wei; Chang, Jiang; Zhang, Xu-Chao; Huang, Ming-Shyan; Zheng, Hong; Wang, Junwen; Zhao, Xueying; Li, Yuqing; Choi, Jin Eun; Su, Wu-Chou; Park, Kyong Hwa; Sung, Sook Whan; Chen, Yuh-Min; Liu, Li; Kang, Chang Hyun; Hu, Lingmin; Chen, Chung-Hsing; Pao, William; Kim, Young-Chul; Yang, Tsung-Ying; Xu, Jun; Guan, Peng; Tan, Wen; Su, Jian; Wang, Chih-Liang; Li, Haixin; Sihoe, Alan Dart Loon; Zhao, Zhenhong; Chen, Ying; Choi, Yi Young; Hung, Jen-Yu; Kim, Jun Suk; Yoon, Ho-Il; Cai, Qiuyin; Lin, Chien-Chung; Park, In Kyu; Xu, Ping; Dong, Jing; Kim, Christopher; He, Qincheng; Perng, Reury-Perng; Kohno, Takashi; Kweon, Sun-Seog; Chen, Chih-Yi; Vermeulen, Roel C H; Wu, Junjie; Lim, Wei-Yen; Chen, Kun-Chieh; Chow, Wong-Ho; Ji, Bu-Tian; Chan, John K C; Chu, Minjie; Li, Yao-Jen; Yokota, Jun; Li, Jihua; Chen, Hongyan; Xiang, Yong-Bing; Yu, Chong-Jen; Kunitoh, Hideo; Wu, Guoping; Jin, Li; Lo, Yen-Li; Shiraishi, Kouya; Chen, Ying-Hsiang; Lin, Hsien-Chih; Wu, Tangchun; Wong, Maria Pik; Wu, Yi-Long; Yang, Pan-Chyr; Zhou, Baosen; Shin, Min-Ho; Fraumeni, Joseph F; Zheng, Wei; Lin, Dongxin; Chanock, Stephen J; Rothman, Nathaniel; Lan, Qing

    2016-01-01

    Recent evidence from several relatively small nested case-control studies in prospective cohorts shows an association between longer telomere length measured phenotypically in peripheral white blood cell (WBC) DNA and increased lung cancer risk. We sought to further explore this relationship by examining a panel of 7 telomere-length associated genetic variants in a large study of 5,457 never-smoking female Asian lung cancer cases and 4,493 never-smoking female Asian controls using data from a previously reported genome-wide association study. Using a group of 1,536 individuals with phenotypically measured telomere length in WBCs in the prospective Shanghai Women’s Health study, we demonstrated the utility of a genetic risk score (GRS) of 7 telomere-length associated variants to predict telomere length in an Asian population. We then found that GRSs used as instrumental variables to predict longer telomere length were associated with increased lung cancer risk (OR = 1.51 (95% CI=1.34–1.69) for upper vs. lower quartile of the weighted GRS, P-value=4.54×10−14) even after removing rs2736100 (P-value=4.81×10−3), a SNP in the TERT locus robustly associated with lung cancer risk in prior association studies. Stratified analyses suggested the effect of the telomere-associated GRS is strongest among younger individuals. We found no difference in GRS effect between adenocarcinoma and squamous cell subtypes. Our results indicate that a genetic background that favors longer telomere length may increase lung cancer risk, which is consistent with earlier prospective studies relating longer telomere length with increased lung cancer risk. PMID:25516442

  12. Target Therapy in Lung Cancer.

    PubMed

    Cafarotti, Stefano; Lococo, Filippo; Froesh, Patrizia; Zappa, Francesco; Andrè, Dutly

    2016-01-01

    Lung cancer is an extremely heterogeneous disease, with well over 50 different histological variants recognized under the fourth revision of the World Health Organization (WHO) typing system. Because these variants have differing genetic and biological properties correct classification of lung cancer is necessary to assure that lung cancer patients receive optimum management. Due to the recent understanding that histologic typing and EGFR mutation status are important for target the therapy in lung adenocarcinoma patients there was a great need for a new classification that addresses diagnostic issues and strategic management to allow for molecular testing in small biopsy and cytology specimens. For this reason and in order to address advances in lung cancer treatment an international multidisciplinary classification was proposed by the International Association for the Study of Lung Cancer (IASLC), American Thoracic Society (ATS), and European Respiratory Society (ERS), further increasing the histological heterogeneity and improving the existing WHO-classification. Is now the beginning of personalized therapy era that is ideally finalized to treat each individual case of lung cancer in different way. PMID:26667341

  13. Lung tumor-associated dendritic cell-derived resistin promoted cancer progression by increasing Wolf-Hirschhorn syndrome candidate 1/Twist pathway.

    PubMed

    Kuo, Chih-Hsin; Chen, Kuei-Fang; Chou, Shah-Hwa; Huang, Ya-Fang; Wu, Cheng-Ying; Cheng, Da-En; Chen, Yu-Wen; Yang, Chih-Jen; Hung, Jen-Yu; Huang, Ming-Shyan

    2013-11-01

    The interaction between tumors and their microenvironments leads to a vicious cycle, which strengthens both immune suppression and cancer progression. The present study demonstrates for the first time that tumor-associated dendritic cells (TADCs) are a source of resistin, which is responsible for increasing lung cancer epithelial-to-mesenchymal transition. In addition, large amounts of resistin in the condition medium (CM) of TADCs increase cell migration and invasion, as well as the osteolytic bone metastatic properties of lung cancer cells. Neutralization of resistin from TADC-CM prevents the advanced malignancy-inducing features of TADC-CM. Significantly elevated levels of resistin have been observed in mice transplanted with lung cancer cells, tumor-infiltrating CD11c(+) DCs in human lung cancer samples and lung cancer patients' sera. Induction of lung cancer progression by TADC-derived resistin is associated with increased expression of Wolf-Hirschhorn syndrome candidate 1 (WHSC1), a histone methyltransferase. Resistin-induced WHSC1 increases the dimethylation of histone 3 at lysine 36 and decreases the trimethylation of histone 3 at lysine 27 on the promoter of Twist, resulting in an enhancement of the expression of Twist. Knockdown of WHSC1 by small interfering RNA transfection significantly decreases resistin-mediated cancer progression by decreasing the upregulation of Twist, suggesting that WHSC1 plays a critical role in the regulation of Twist by epigenetic modification. Furthermore, mice that received antiresistin antibodies showed a decreased incidence of cancer development and metastasis. These findings suggest that TADC-derived resistin may be a novel candidate in promoting the development of lung cancer. PMID:23955539

  14. Afatinib increases sensitivity to radiation in non-small cell lung cancer cells with acquired EGFR T790M mutation

    PubMed Central

    Huang, Haixiu; Wu, Kan; Wang, Bing; Chen, Xufeng; Ma, Shenglin

    2015-01-01

    Afatinib is a second-generation of epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor and has shown a significant clinical benefit in non-small cell lung cancer (NSCLC) patients with EGFR-activating mutations. However, the potential therapeutic effects of afatinib combining with other modalities, including ionizing radiation (IR), are not well understood. In this study, we developed a gefitinib-resistant cell subline (PC-9-GR) with a secondary EGFR mutation (T790M) from NSCLC PC-9 cells after chronic exposures to increasing doses of gefitinib. The presence of afatinib significantly increases the cell killing effect of radiation in PC-9-GR cells harboring acquired T790M, but not in H1975 cells with de novo T790M or in H460 cells that express wild-type EGFR. In PC-9-GR cells, afatinib remarkable blocks baseline of EGFR and ERK phosphorylations, and causes delay of IR-induced AKT phosphorylation. Afatinib treatment also leads to increased apoptosis and suppressed DNA damage repair in irradiated PC-9-GR cells, and enhanced tumor growth inhibition when combined with IR in PC-9-GR xenografts. Our findings suggest a potential therapeutic impact of afatinib as a radiation sensitizer in lung cancer cells harboring acquired T790M mutation, providing a rationale for a clinical trial with combination of afatinib and radiation in NSCLCs with EGFR T790M mutation. PMID:25714021

  15. Inactivation of TGF-{beta} signaling in lung cancer results in increased CDK4 activity that can be rescued by ELF

    SciTech Connect

    Baek, Hye Jung; Kim, Sang Soo; Silva, Fabio May da; Volpe, Eugene A.; Evans, Stephen; Mishra, Bibhuti; Mishra, Lopa . E-mail: lopamishra@yahoo.com; Blair Marshall, M. . E-mail: mbm5@gunet.georgetown.edu

    2006-08-11

    Escape from TGF-{beta} inhibition of proliferation is a hallmark of multiple cancers including lung cancer. We explored the role of ELF, crucial TGF-{beta} adaptor protein identified from endodermal progenitor cells, in lung carcinogenesis and cell-cycle regulation. Interestingly, elf {sup -/-} mice develop multiple defects that include lung, liver, and cardiac abnormalities. Four out of 6 lung cancer and mesothelioma cell lines displayed deficiency of ELF expression with increased CDK4 expression. Immunohistochemistry and Western blot analysis of primary human lung cancers also showed decreased ELF expression and overexpression of CDK4. Moreover, rescue of ELF in ELF-deficient cell lines decreased the expression of CDK4 and resulted in accumulation of G1/S checkpoint arrested cells. These results suggest that disruption in TGF-{beta} signaling mediated by loss of ELF in lung cancer leads to cell-cycle deregulation by modulating CDK4 and ELF highlights a key role of TGF-{beta} adaptor protein in suppressing early lung cancer.

  16. Stathmin1 increases radioresistance by enhancing autophagy in non-small-cell lung cancer cells

    PubMed Central

    Zhang, Xi; Ji, Jingfen; Yang, Yu; Zhang, Juan; Shen, Liangfang

    2016-01-01

    Radioresistance has been demonstrated to be involved in the poor prognosis of patients with non-small-cell lung cancer (NSCLC). However, the underlying mechanism remains largely unclear. Investigation on special therapeutic targets associated with radioresistance shows promises for the enhancement of clinical radiotherapy effect toward NSCLC. This study aimed to reveal the role of Stathmin1 (STMN1) in radioresistance in NSCLC as well as the underlying mechanism. Our data showed that the protein levels of STMN1 were significantly upregulated in NSCLC cells subjected to radiation, accompanied with the activation of autophagy. Knockdown of STMN1 expression enhanced the sensitivity of NSCLC cells to X-ray, and the radiation-induced autophagy was also inhibited. Molecular mechanism investigation showed that knockdown of STMN1 expression upregulated the activity of phosphoinositide 3-kinase (PI3K)/mammalian target of rapamycin (mTOR) signaling pathway in NSCLC cells. Moreover, the activation of PI3K/mTOR signaling showed an inhibitory effect on the autophagy and radioresistance induced by STMN1 in NSCLC cells. In addition, luciferase reporter assay data indicated that STMN1 was a direct target gene of miR-101, which had been reported to be an inhibitor of autophagy. Based on these data, we suggest that as a target gene of miR-101, STMN1 promotes the radioresistance by induction of autophagy through PI3K/mTOR signaling pathway in NSCLC. Therefore, STMN1 may become a potential therapeutic target for NSCLC radiotherapy. PMID:27199567

  17. Silence of fibronectin 1 increases cisplatin sensitivity of non-small cell lung cancer cell line.

    PubMed

    Gao, Weiwei; Liu, Ying; Qin, Ruiling; Liu, Daijian; Feng, Qingqing

    2016-07-15

    Fibronectin 1 (FN1) is a member of the glycoprotein family which is widely expressed by multiple cell types and involved in cellular adhesion and migration processes. Recent studies have reported that FN1 might have a role in regulating chemoresistance in tumors. However, the regulation of FN1 on cisplatin resistance in non-small cell lung cancer (NSCLC) has not been investigated. The present study aims to illustrate the effect of FN1 on cisplatin resistance in NSCLC and explore potential mechanisms. In the present study, the mRNA and protein expression levels of FN1 were investigated by RT-PCR and Western blot analysis, respectively, and the 50% inhibitory concentration (IC50) value of cisplatin was measured by MTT assay. Apoptotic ratio and migration were determined using an annexin V-FITC/PI detection kit and a Transwell assay, respectively. The interaction between FN1 and integrin-β1 was evaluated by co-immunoprecipitation assay. The protein expression of β-catenin, cyclin D1 and c-myc were tested using Western blot analysis. The results showed that FN1 was more highly expressed in A549/DDP than in A549 cells, and significantly upregulated by cisplatin treatment in H1299 cells. Knockdown of FN1 reduced the IC50 value of cisplatin, inhibited cell migration and promoted apoptosis. FN1 and integrin-β1 protein directly interacted with each other both in A549 and A549/DDP cells. FN1 silencing suppressed the Wnt/β-catenin signaling pathway, and this effect was dampened by integrin-β1-blocking antibody. Taken together, our findings first suggest that FN1 plays a role in the development of cisplatin resistance in NSCLC, possibly by modulation of β-catenin signaling through interaction with integrin-β1 in NSCLC. PMID:27207836

  18. Stathmin1 increases radioresistance by enhancing autophagy in non-small-cell lung cancer cells.

    PubMed

    Zhang, Xi; Ji, Jingfen; Yang, Yu; Zhang, Juan; Shen, Liangfang

    2016-01-01

    Radioresistance has been demonstrated to be involved in the poor prognosis of patients with non-small-cell lung cancer (NSCLC). However, the underlying mechanism remains largely unclear. Investigation on special therapeutic targets associated with radioresistance shows promises for the enhancement of clinical radiotherapy effect toward NSCLC. This study aimed to reveal the role of Stathmin1 (STMN1) in radioresistance in NSCLC as well as the underlying mechanism. Our data showed that the protein levels of STMN1 were significantly upregulated in NSCLC cells subjected to radiation, accompanied with the activation of autophagy. Knockdown of STMN1 expression enhanced the sensitivity of NSCLC cells to X-ray, and the radiation-induced autophagy was also inhibited. Molecular mechanism investigation showed that knockdown of STMN1 expression upregulated the activity of phosphoinositide 3-kinase (PI3K)/mammalian target of rapamycin (mTOR) signaling pathway in NSCLC cells. Moreover, the activation of PI3K/mTOR signaling showed an inhibitory effect on the autophagy and radioresistance induced by STMN1 in NSCLC cells. In addition, luciferase reporter assay data indicated that STMN1 was a direct target gene of miR-101, which had been reported to be an inhibitor of autophagy. Based on these data, we suggest that as a target gene of miR-101, STMN1 promotes the radioresistance by induction of autophagy through PI3K/mTOR signaling pathway in NSCLC. Therefore, STMN1 may become a potential therapeutic target for NSCLC radiotherapy. PMID:27199567

  19. Lung cancer in Australia.

    PubMed

    McLennan, G; Roder, D M

    1989-02-20

    Lung cancer is the leading cause of death of cancer in Australian men and the third leading cause in Australian women. Efforts are being made to reduce the incidence of this disease by smoking-cessation programmes and improved industrial hygiene, and these measures need to be encouraged strongly by all sectors of the community. On a population basis, insufficient evidence is available to justify screening procedures for the early detection of lung cancer in "at-risk" groups. Cure is possible by surgical resection in early cases. Improvements in therapeutic results with traditional cancer treatments largely have reached a plateau, but a number of newer therapies, and combinations of standard therapies, currently are being evaluated. Of particular interest is concurrent radiotherapy and chemotherapy in localized non-small-cell lung cancer; laser "debulking" in conjunction with radiotherapy in non-small-cell lung cancer, and biological response-modifying agents in non-small-cell and small-cell lung cancer. It is important that data be collected adequately to define epidemiological changes and to evaluate treatment results (including repeat bronchoscopy, to assess local control of tumour), and that the quality of life is recorded and reported in the evaluation process. Finally, phase-III studies in lung-cancer treatments require adequate numbers of subjects to enable meaningful conclusions to be achieve objectives within a reasonable study period. PMID:2469943

  20. Laricitrin suppresses increased benzo(a)pyrene-induced lung tumor-associated monocyte-derived dendritic cell cancer progression

    PubMed Central

    CHANG, WEI-AN; HUNG, JEN-YU; TSAI, YING-MING; HSU, YA-LING; CHIANG, HUNG-HSING; CHOU, SHAH-HWA; HUANG, MING-SHYAN; KUO, PO-LIN

    2016-01-01

    Benzo(a)pyrene (BaP) stimulates lung cancer cells, promoting monocyte-derived dendritic cells to secrete soluble factors, including heparin binding-epidermal growth factor and C-X-C motif chemokine 5. The secretions from monocyte-derived dendritic cells stimulate the progression of lung cancer cells, including the migration and invasion of cells. To the best of our knowledge, these secretions remain unknown, and require additional study. The present study identified that treatment with BaP-H1395-tumor-associated dendritic cell-conditioned medium had the most marked effect on cell migration and invasion. This result may be associated with the female gender, stage 2 adenocarcinoma or mutation of the proto-oncogene B-Raf (BRAF), according to the cell line background. Laricitrin, a dietary flavonoid derivative present in grapes and red wine, suppresses certain factors and decreases the progression of lung cancer cells that are promoted by BaP in the lung cancer tumor microenvironment. The results of the present study suggest that prolonged exposure to BaP exacerbates lung cancer, particularly in female lung cancer patients with the BRAF mutation, but that laricitrin may ameliorate this effect. PMID:26998077

  1. Rho Guanine Nucleotide Exchange Factor 5 Increases Lung Cancer Cell Tumorigenesis via MMP-2 and Cyclin D1 Upregulation.

    PubMed

    He, Ping; Wu, Wei; Yang, Kang; Tan, Deli; Tang, Meng; Liu, Hongxiang; Wu, Tao; Zhang, Shixin; Wang, Haidong

    2015-07-01

    We sought to elucidate the role of Rho guanine nucleotide exchange factor 5 (ARHGEF5) in tumorigenesis of lung adenocarcinoma cells. ARHGEF5 protein levels were assessed in 91 human lung adenocarcinoma specimens, and A549 and NCI-H1650 cells, by IHC and Western blotting. In addition, ARHGEF5 mRNA expression was evaluated by quantitative reverse transcriptase-PCR. Furthermore, ARHGEF5 long and short isoform coexpression was detected by immunofluorescence. Finally, flow cytometry; CCK8 and wound-healing assays; cell invasion, migration and adhesion; and xenografts were used to evaluate the biologic significance of ARHGEF5. ARHGEF5 was significantly increased in lung adenocarcinoma tissues and cell lines. Interestingly, ARHGEF5 levels were significantly associated with tumor grade and pathologic stage, but not age, gender, T stage, or lymph node metastasis status. ARHGEF5 knockdown by RNAi resulted in dramatically reduced proliferation, adhesion, invasion, and migratory capability of A549 and NCI-H1650 cells. Likewise, protein levels of p-Src, p-Akt, and NF-κB were significantly decreased after ARHGEF5 knockdown. In parallel, increased S-phase population and MMP-2/cyclin D1 expression were observed in the cancer cells, which were not apoptotic. In addition, ARHGEF5 knockdown A549 and NCI-H1650 cells injected s.c. and i.v. into nude mice exhibited decreased xenograft volume and overtly reduced metastasis. Conversely, ARHGEF5 overexpression in A549 and NCI-H1650 cells increased their tumorigenicity in vitro. ARHGEF5 acts as a proto-oncogene in human lung adenocarcinoma cell tumorigenesis. PMID:25777963

  2. Lung and Bronchus Cancer

    MedlinePlus

    ... at a Glance Show More At a Glance Estimated New Cases in 2016 224,390 % of All New Cancer Cases 13.3% Estimated Deaths in 2016 158,080 % of All Cancer ... of This Cancer : In 2013, there were an estimated 415,707 people living with lung and bronchus ...

  3. Functional imaging in lung cancer

    PubMed Central

    Harders, S W; Balyasnikowa, S; Fischer, B M

    2014-01-01

    Lung cancer represents an increasingly frequent cancer diagnosis worldwide. An increasing awareness on smoking cessation as an important mean to reduce lung cancer incidence and mortality, an increasing number of therapy options and a steady focus on early diagnosis and adequate staging have resulted in a modestly improved survival. For early diagnosis and precise staging, imaging, especially positron emission tomography combined with CT (PET/CT), plays an important role. Other functional imaging modalities such as dynamic contrast-enhanced CT (DCE-CT) and diffusion-weighted MR imaging (DW-MRI) have demonstrated promising results within this field. The purpose of this review is to provide the reader with a brief and balanced introduction to these three functional imaging modalities and their current or potential application in the care of patients with lung cancer. PMID:24289258

  4. Lung Cancer Screening Update.

    PubMed

    Ruchalski, Kathleen L; Brown, Kathleen

    2016-07-01

    Since the release of the US Preventive Services Task Force and Centers for Medicare and Medicaid Services recommendations for lung cancer screening, low-dose chest computed tomography screening has moved from the research arena to clinical practice. Lung cancer screening programs must reach beyond image acquisition and interpretation and engage in a multidisciplinary effort of clinical shared decision-making, standardization of imaging and nodule management, smoking cessation, and patient follow-up. Standardization of radiologic reports and nodule management will systematize patient care, provide quality assurance, further reduce harm, and contain health care costs. Although the National Lung Screening Trial results and eligibility criteria of a heavy smoking history are the foundation for the standard guidelines for low-dose chest computed tomography screening in the United States, currently only 27% of patients diagnosed with lung cancer would meet US lung cancer screening recommendations. Current and future efforts must be directed to better delineate those patients who would most benefit from screening and to ensure that the benefits of screening reach all socioeconomic strata and racial and ethnic minorities. Further optimization of lung cancer screening program design and patient eligibility will assure that lung cancer screening benefits will outweigh the potential risks to our patients. PMID:27306387

  5. Women and Lung Cancer

    MedlinePlus

    ... Horrigan Conners Center for Women’s Health and Gender Biology, Brigham and Women’s Hospital, Harvard Medical School, April, ... Lung Cancer in Women: The Differences in Epidemiology, Biology and Treatment Outcomes, Maria Patricia Rivera MD Expert ...

  6. Lycopene and Lung Cancer

    Technology Transfer Automated Retrieval System (TEKTRAN)

    Although epidemiological studies have shown dietary intake of lycopene is associated with decreased risk of lung cancer, the effect of lycopene on lung carcinogenesis has not been well studied. A better understanding of lycopene metabolism and the mechanistic basis of lycopene chemoprevention must ...

  7. Lung Cancer Rates by State

    MedlinePlus

    ... HPV-Associated Ovarian Prostate Skin Uterine Cancer Home Lung Cancer Rates by State Language: English Español (Spanish) ... incidence data are currently available. Rates of Getting Lung Cancer by State The number of people who ...

  8. Development of APE1 enzymatic DNA repair assays: low APE1 activity is associated with increase lung cancer risk.

    PubMed

    Sevilya, Ziv; Leitner-Dagan, Yael; Pinchev, Mila; Kremer, Ran; Elinger, Dalia; Lejbkowicz, Flavio; Rennert, Hedy S; Freedman, Laurence S; Rennert, Gad; Paz-Elizur, Tamar; Livneh, Zvi

    2015-09-01

    The key role of DNA repair in removing DNA damage and minimizing mutations makes it an attractive target for cancer risk assessment and prevention. Here we describe the development of a robust assay for apurinic/apyrimidinic (AP) endonuclease 1 (APE1; APEX1), an essential enzyme involved in the repair of oxidative DNA damage. APE1 DNA repair enzymatic activity was measured in peripheral blood mononuclear cell protein extracts using a radioactivity-based assay, and its association with lung cancer was determined using conditional logistic regression with specimens from a population-based case-control study with 96 lung cancer cases and 96 matched control subjects. The mean APE1 enzyme activity in case patients was 691 [95% confidence interval (CI) = 655-727] units/ng protein, significantly lower than in control subjects (mean = 793, 95% CI = 751-834 units/ng protein, P = 0.0006). The adjusted odds ratio for lung cancer associated with 1 SD (211 units) decrease in APE1 activity was 2.0 (95% CI = 1.3-3.1; P = 0.002). Comparison of radioactivity- and fluorescence-based assays showed that the two are equivalent, indicating no interference by the fluorescent tag. The APE1Asp148Glu SNP was associated neither with APE1 enzyme activity nor with lung cancer risk. Taken together, our results indicate that low APE1 activity is associated with lung cancer risk, consistent with the hypothesis that 'bad DNA repair', rather than 'bad luck', is involved in cancer etiology. Such assays may be useful, along with additional DNA repair biomarkers, for risk assessment of lung cancer and perhaps other cancers, and for selecting individuals to undergo early detection techniques such as low-dose CT. PMID:26045303

  9. The interaction of APEX1 variant with polycyclic aromatic hydrocarbons on increasing chromosome damage and lung cancer risk among male Chinese.

    PubMed

    Li, Xiaoliang; Wei, Jinyu; Xu, Ping; Yin, Xiangqian; Hu, Die; Zhang, Xiao; Liu, Li; Zhang, Kai; Zhou, Changchun; Wang, Tian; Zhang, Xiaomin; He, Meian; Wu, Tangchun; Yang, Ming; Guo, Huan

    2015-06-01

    Polycyclic aromatic hydrocarbons (PAHs) are the most significant contributors to tobacco-induced lung carcinogenesis. Apurinic/apyrimidinic endonuclease 1 (APE1) is a central enzyme in the removal of apurinic/apyrimidinic sites caused by DNA damaging agents. This study aimed to investigate the potential interaction of APEX1 polymorphisms and PAHs on genetic damage and lung cancer risk among male Chinese. We recruited an occupational cohort of 922 male coke oven workers and determined their DNA damage levels by calculating the lymphocytic micronucleus (MN) frequencies. Two well-studied APEX1 polymorphisms (-307A > C and Asp148Glu) and their associations with MN frequencies were examined. The impact of MN-related single nucleotide polymorphism (SNP) on lung cancer risk was further investigated in two case-control studies including 1634 male lung cancer patients and 1678 controls. It was shown that, the APEX1 148Glu allele was associated with significantly higher MN frequencies than 148Asp allele, with strongest associations among the highest PAH-exposure workers (P = 0.008). The APEX1 148Glu allele was also associated with increased lung cancer risk among male smokers, especially among heavy smokers in both case-control studies (odd ratio: 4.40, 95%CI: 3.29-5.72). In addition, APEX1 148Glu variant interacts with smoking in increasing male lung cancer risk, as measured by the attributable proportion due to interaction, which was 0.23 (95%CI: 0.06-0.39). This study showed evidence on interaction between APEX1 148Glu variant and cigarette smoking in increasing lung cancer susceptibility among male Chinese, which may be due to the synergistic effects of APEX1 148Glu and PAHs in increasing chromosome damage levels. The results provide a new insight into gene-interactions in lung carcinogenesis. PMID:25156607

  10. Immunotherapy in lung cancer.

    PubMed Central

    Al-Moundhri, M.; O'Brien, M.; Souberbielle, B. E.

    1998-01-01

    More research and new treatment options are needed in all stages of lung cancer. To this end immunotherapy needs a revival in view of recent improved technologies and greater understanding of the underlying biology. In this review we discuss mechanisms of tumour immunotherapy, non-specific, specific and adoptive, with particular reference to a direct therapeutic action on all subtypes of lung cancer. PMID:9703271

  11. Chemoprevention of lung cancer.

    PubMed

    Keith, Robert L

    2009-04-15

    Lung cancer is the leading cause of cancer death in the United States, and the majority of diagnoses are made in former smokers. While avoidance of tobacco abuse and smoking cessation clearly will have the greatest impact on lung cancer development, effective chemoprevention could prove to be more effective than treatment of established disease. Chemoprevention is the use of dietary or pharmaceutical agents to reverse or inhibit the carcinogenic process and has been successfully applied to common malignancies other than lung. Despite previous studies in lung cancer chemoprevention failing to identify effective agents, our ability to determine higher risk populations and the understanding of lung tumor and pre-malignant biology continues to advance. Additional biomarkers of risk continue to be investigated and validated. The World Health Organization/International Association for the Study of Lung Cancer classification for lung cancer now recognizes distinct histologic lesions that can be reproducibly graded as precursors of non-small cell lung cancer. For example, carcinogenesis in the bronchial epithelium starts with normal epithelium and progresses through hyperplasia, metaplasia, dysplasia, and carcinoma in situ to invasive squamous cell cancer. Similar precursor lesions exist for adenocarcinoma, and these pre-malignant lesions are targeted by chemopreventive agents in current and future trials. At this time, chemopreventive agents can only be recommended as part of well-designed clinical trials, and multiple trials are currently in progress and additional trials are in the planning stages. This review will discuss the principles of chemoprevention, summarize the completed trials, and discuss ongoing and potential future trials with a focus on targeted pathways. PMID:19349487

  12. [Pathology of lung cancer].

    PubMed

    Theegarten, D; Hager, T

    2016-09-01

    Lung cancer is the leading cause of cancer death in men and the second most frequent cause in women. The pathology of lung tumors is of special relevance concerning therapy and prognosis and current classification systems have to be taken into consideration. The results of molecular tissue subtyping allow further classification and therapeutic options. The histological entities are mainly associated with typical X‑ray morphological features. PMID:27495784

  13. Lung cancer screening: from imaging to biomarker.

    PubMed

    Xiang, Dong; Zhang, Bicheng; Doll, Donald; Shen, Kui; Kloecker, Goetz; Freter, Carl

    2013-01-01

    Despite several decades of intensive effort to improve the imaging techniques for lung cancer diagnosis and treatment, primary lung cancer is still the number one cause of cancer death in the United States and worldwide. The major causes of this high mortality rate are distant metastasis evident at diagnosis and ineffective treatment for locally advanced disease. Indeed, approximately forty percent of newly diagnosed lung cancer patients have distant metastasis. Currently, the only potential curative therapy is surgical resection of early stage lung cancer. Therefore, early detection of lung cancer could potentially increase the chance of cure by surgery and underlines the importance of screening and detection of lung cancer. In the past fifty years, screening of lung cancer by chest X-Ray (CXR), sputum cytology, computed tomography (CT), fluorescence endoscopy and low-dose spiral CT (LDCT) has not improved survival except for the recent report in 2010 by the National Lung Screening Trial (NLST), which showed a 20 percent mortality reduction in high risk participants screened with LDCT compared to those screened with CXRs. Furthermore, serum biomarkers for detection of lung cancer using free circulating DNA and RNA, exosomal microRNA, circulating tumor cells and various lung cancer specific antigens have been studied extensively and novel screening methods are being developed with encouraging results. The history of lung cancer screening trials using CXR, sputum cytology and LDCT, as well as results of trials involving various serum biomarkers, are reviewed herein. PMID:24252206

  14. Lung cancer screening: from imaging to biomarker

    PubMed Central

    2013-01-01

    Despite several decades of intensive effort to improve the imaging techniques for lung cancer diagnosis and treatment, primary lung cancer is still the number one cause of cancer death in the United States and worldwide. The major causes of this high mortality rate are distant metastasis evident at diagnosis and ineffective treatment for locally advanced disease. Indeed, approximately forty percent of newly diagnosed lung cancer patients have distant metastasis. Currently, the only potential curative therapy is surgical resection of early stage lung cancer. Therefore, early detection of lung cancer could potentially increase the chance of cure by surgery and underlines the importance of screening and detection of lung cancer. In the past fifty years, screening of lung cancer by chest X-Ray (CXR), sputum cytology, computed tomography (CT), fluorescence endoscopy and low-dose spiral CT (LDCT) has not improved survival except for the recent report in 2010 by the National Lung Screening Trial (NLST), which showed a 20 percent mortality reduction in high risk participants screened with LDCT compared to those screened with CXRs. Furthermore, serum biomarkers for detection of lung cancer using free circulating DNA and RNA, exosomal microRNA, circulating tumor cells and various lung cancer specific antigens have been studied extensively and novel screening methods are being developed with encouraging results. The history of lung cancer screening trials using CXR, sputum cytology and LDCT, as well as results of trials involving various serum biomarkers, are reviewed herein. PMID:24252206

  15. Increased polysomy of chromosome 7 in bronchial epithelium from patients at high risk for lung cancer

    SciTech Connect

    Belinsky, S.A.; Neft, R.E.; Lechner, J.F.

    1995-12-01

    Current models of carcinogenesis suggest that tissues progress through multiple genetic and epigenetic changes which ultimately lead to development of invasive cancer. Epidemiologic studies of Peto, R.R. and J.A. Doll indicate that the accumulation of these genetic changes over time, rather than any single unique genetic change, is probably responsible for development of the malignant phenotype. The bronchial epithelium of cigarette smokers is diffusely exposed to a broad spectrum of carcinogens, toxicants, and tumor promoters contained in tobacco smoke. This exposure increases the risk of developing multiple, independent premalignant foci throughout the lower respiratory tract that may contain independent gene aberrations. This {open_quotes}field cancerization{close_quotes} theory is supported by studies that have demonstrated progressive histologic changes distributed throughout the lower respiratory tract of smokers. A series of autopsy studies demonstrated that cigarette smokers exhibit premalignant histologic changes ranging from hyperplasia and metaplasia to severe dysplasia and carcinoma in situ diffusely throughout the bronchial mucosa. The proximal bronchi appear to exhibit the greatest number of changes, particularly at bifurcations. The results described are the first to quantitate the frequency for a chromosome aberration in {open_quotes}normal{close_quotes} bronchial epithelial cells.

  16. [Geographic spreading of lung cancer in Azerbaijan].

    PubMed

    Soltanov, A A

    2009-01-01

    Lung cancer is the second most common cancer and the leading cause of cancer death for both men and women. The impact of geographic as well as of exogenous factor and factors of risk, life style and environment play an important role in etiology of lung cancer. Geographic spread of lung cancer data in literature is fragmentary. The limited existing literature does not report a consistent story of geographic variation in Azerbaijan for the incidence associated with lung cancer. The aim of this study was to evaluate the impact of geographic variation on spread of lung cancer in Azerbaijan. Frequency of lung cancer in various regions of Azerbaijan; different histological types, sex, age and particular risk factors were investigated. It was revealed that epidermoid cancer was the most common histological type in all regions. The highest rate of epidermoid cancer 230 (55.56%) was revealed in industrial regions and industrial cities (Baku and Sumgait). The lowest rate of lung cancer was found in mountain region 12 (3.76%). Smoking and drinking alcohol increases risk of epidermoid cancer (41.2% of patients smoke and drink alcohol). The highest morbidity (13.55 per 100,000 population) and mortality (0.11) rates from lung cancer were observed in industrial regions. Analyses revealed that different endogenous and exogenous factors are associated with lung cancer. PMID:19202230

  17. Lung Cancer Cell Line Screen Links Fanconi Anemia/BRCA Pathway Defects to Increased Relative Biological Effectiveness of Proton Radiation

    SciTech Connect

    Liu, Qi; Ghosh, Priyanjali; Magpayo, Nicole; Testa, Mauro; Tang, Shikui; Gheorghiu, Liliana; Biggs, Peter; Paganetti, Harald; Efstathiou, Jason A.; Lu, Hsiao-Ming; Held, Kathryn D.; Willers, Henning

    2015-04-01

    Purpose: Growing knowledge of genomic heterogeneity in cancer, especially when it results in altered DNA damage responses, requires re-examination of the generic relative biological effectiveness (RBE) of 1.1 of protons. Methods and Materials: For determination of cellular radiosensitivity, we irradiated 17 lung cancer cell lines at the mid-spread-out Bragg peak of a clinical proton beam (linear energy transfer, 2.5 keV/μm). For comparison, 250-kVp X rays and {sup 137}Cs γ-rays were used. To estimate the RBE of protons relative to {sup 60}Co (Co60eq), we assigned an RBE(Co60Eq) of 1.1 to X rays to correct the physical dose measured. Standard DNA repair foci assays were used to monitor damage responses. FANCD2 was depleted using RNA interference. Results: Five lung cancer cell lines (29.4%) exhibited reduced clonogenic survival after proton irradiation compared with X-irradiation with the same physical doses. This was confirmed in a 3-dimensional sphere assay. Corresponding proton RBE(Co60Eq) estimates were statistically significantly different from 1.1 (P≤.05): 1.31 to 1.77 (for a survival fraction of 0.5). In 3 of these lines, increased RBE was correlated with alterations in the Fanconi anemia (FA)/BRCA pathway of DNA repair. In Calu-6 cells, the data pointed toward an FA pathway defect, leading to a previously unreported persistence of proton-induced RAD51 foci. The FA/BRCA-defective cells displayed a 25% increase in the size of subnuclear 53BP1 foci 18 hours after proton irradiation. Conclusions: Our cell line screen has revealed variations in proton RBE that are partly due to FA/BRCA pathway defects, suggesting that the use of a generic RBE for cancers should be revisited. We propose that functional biomarkers, such as size of residual 53BP1 foci, may be used to identify cancers with increased sensitivity to proton radiation.

  18. Interleukin-17 potently increases non-small cell lung cancer growth.

    PubMed

    Wei, Lei; Wang, Hui; Yang, Fen; Ding, Qi; Zhao, Jianhua

    2016-02-01

    The aim of the present study was to explore the effects of interleukin (IL)-17 on the growth and metastasis of tumors that were subcutaneously implanted into C57BL/6 mice. Lewis lung carcinoma (LLC) cells were subcutaneously injected into C57BL/6 mice followed by intraperitoneal injection of mouse recombinant IL-17 protein (IL-17 groups) or phosphate‑buffered saline (control groups). Tumor growth and metastasis were assessed by measuring the size and weight of tumors and cervical lymph nodes, respectively. Cytokine expression in tumor masses was quantified by reverse transcription‑quantitative polymerase chain reaction and western blotting, respectively. CCR2‑positive macrophage infiltration in tumor masses was detected by flow cytometric analysis. The proliferation and migration of LLC cells, stimulated by the IL-17 protein were detected by Cell Counting kit (CCK)‑8 and wound scratch assays in vitro. Tumors were grafted into the C57BL/6 mice. The mice that were intraperitoneally injected with IL-17 exhibited significantly larger tumors compared with the control mice. After day 7 of injection and beyond, the weight of cervical lymph nodes in IL-17 groups was higher than that in the control mice. It was also demonstrated that the number of CCR2-positive macrophages that infiltrated the tumor masses in the IL-17 groups was higher than that of the control mice. CD34 expression in vascular endothelial cells was also higher in tumors grafted in IL-17 mice than those grafted in control mice. Furthermore, the tumor tissue mRNA and protein expression levels of vascular endothelial growth factor, matrix metalloproteinase (MMP)-2, MMP-9 and tumor necrosis factor-α were greater in mice from the IL-17 group than the control mice, while levels of migration inhibitory factor and thrombospondin‑1 were lower in mice from the IL-17 group than in the control. IL-17 also increased the migration of LLC cells in vitro. In conclusion, IL-17 exhibited the ability to promote

  19. Lung cancer - non-small cell

    MedlinePlus

    Cancer - lung - non-small cell; Non-small cell lung cancer; NSCLC; Adenocarcinoma - lung; Squamous cell carcinoma - lung ... Smoking causes most cases (around 90%) of lung cancer. The risk depends on the number of cigarettes ...

  20. Lung cancer chemoprevention.

    PubMed

    Keith, Robert L

    2012-05-01

    Lung cancer is the leading cause of cancer death in the United States, and the majority of diagnoses are made in former smokers. Although avoidance of tobacco abuse and smoking cessation clearly will have the greatest impact on lung cancer development, effective chemoprevention could prove to be more effective than treatment of established, advanced-stage disease. Chemoprevention is the use of dietary or pharmaceutical agents to reverse or block the carcinogenic process and has been successfully applied to common malignancies other than lung (including recent reports on the prevention of breast cancer in high-risk individuals). Despite previous studies in lung cancer chemoprevention failing to identify effective agents, our ability to define the highest-risk populations and the understanding of lung tumor and premalignant biology continue to make advances. Squamous cell carcinogenesis in the bronchial epithelium starts with normal epithelium and progresses through hyperplasia, metaplasia, dysplasia, and carcinoma in situ to invasive cancer. Precursor lesions also have been identified for adenocarcinoma, and these premalignant lesions are targeted by chemopreventive agents in current and future trials. Chemopreventive agents can currently only be recommended as part of well-designed clinical trials, and multiple trials have recently been completed or are enrolling subjects. PMID:22550242

  1. Lung cancer stem cells—characteristics, phenotype

    PubMed Central

    George, Rachel; Sethi, Tariq

    2016-01-01

    Lung cancer remains a major cause of cancer-related deaths worldwide with unfavourable prognosis mainly due to the late stage of disease at presentation. High incidence and disease recurrence rates are a fact despite advances in treatment. Ongoing experimental and clinical observations suggest that the malignant phenotype in lung cancer is sustained by lung cancer stem cells (CSCs) which are putative stem cells situated throughout the airways that have the potential of initiating lung cancer formation. These cells share the common characteristic of increased proliferation and differentiation, long life span and resistance to chemotherapy and radiation therapy. This review summarises the current knowledge on their characteristics and phenotype. PMID:27413709

  2. Lung cancer screening

    PubMed Central

    Pastorino, U

    2010-01-01

    Lung cancer is the primary cause of cancer mortality in developed countries. First diagnosis only when disease has already reached the metastatic phase is the main reason for failure in treatment. To this regard, although low-dose spiral computed tomography (CT) has proven to be effective in the early detection of lung cancer (providing both higher resectability and higher long-term survival rates), the capacity of annual CT screening to reduce lung cancer mortality in heavy smokers has yet to be demonstrated. Numerous ongoing large-scale randomised trials are under way in high-risk individuals with different study designs. The initial results should be available within the next 2 years. PMID:20424610

  3. Lung cancer and air pollution.

    PubMed Central

    Cohen, A J; Pope, C A

    1995-01-01

    Epidemiologic studies over the last 40 years suggest rather consistently that general ambient air pollution, chiefly due to the incomplete combustion of fossil fuels, may be responsible for increased rates of lung cancer. This evidence derives from studies of lung cancer trends, studies of occupational groups, comparisons of urban and rural populations, and case-control and cohort studies using diverse exposure metrics. Recent prospective cohort studies observed 30 to 50% increases in lung cancer rates associated with exposure to respirable particles. While these data reflect the effects of exposures in past decades, and despite some progress in reducing air pollution, large numbers of people in the United States continue to be exposed to pollutant mixtures containing known or suspected carcinogens. It is not known how many people in the United States are exposed to levels of fine respirable particles that have been associated with lung cancer in recent epidemiologic studies. These observations suggest that the most widely cited estimates of the proportional contribution of air pollution to lung cancer occurrence in the United States based largely on the results of animal studies, may be too low. It is important that better epidemiologic research be conducted to allow improved estimates of lung cancer risk from air pollution among the general population. The development and application of new epidemiologic methods, particularly the improved characterization of population-wide exposure to mixtures of air pollutants and the improved design of ecologic studies, could improve our ability to measure accurately the magnitude of excess cancer associated with air pollution. PMID:8741787

  4. The ALCHEMIST Lung Cancer Trial

    Cancer.gov

    A collection of material about the ALCHEMIST lung cancer trial that will examine tumor tissue from patients with early-stage, completely resected lung cancer for gene mutations in the EGFR and ALK genes, and a

  5. Screening for lung cancer.

    PubMed Central

    Carter, D.

    1981-01-01

    The survival from bronchogenic carcinoma is highly dependent upon stage at the time of treatment. This is particularly true for squamous cell carcinoma, adenocarcinoma, and large cell carcinoma, but holds true for small cell carcinoma as well. The problem presented to the medical profession has been to find a practical means of detecting lung cancer while it is still at an early stage. Three studies in progress have indicated that a larger proportion of the patients may be found to have early stage lung cancer when screened with a combination of chest X-rays and sputum cytology. However, the detection of these early stage cases has not yet been translated into an improvement in the overall mortality rate from lung cancer. PMID:6278787

  6. Increased Expression of Eps15 Homology Domain 1 is Associated with Poor Prognosis in Resected Small Cell Lung Cancer

    PubMed Central

    Meng, Qingwei; Sun, Weiling; Li, Man; Zhao, Yanbin; Chen, Xuesong; Sun, Lichun; Cai, Li

    2015-01-01

    One of the great challenges of small cell lung cancer (SCLC) treatment is identifying patients at high risk for recurrence after surgical resection and chemotherapy. We examined Eps15 homology domain 1 (EHD1) protein expression in paraffin sections of 85 resected SCLC tissues, metastatic lymph nodes and normal bronchial epithelial tissues using immunohistochemistry to study the correlation between EHD1 expression and patient clinicopathological features. Within these variables, disease free survival (DFS) analyzed by the log-rank test was constructed using the multivariate Cox proportional hazards regression model and Kaplan-Meier analysis. Immunohistochemistry results showed that EHD1 protein was significantly increased in SCLC tissues compared with normal tissues (P < 0.001). Moreover, EHD1 expression was positively correlated with tumor size (P = 0.019). Multivariate Cox proportional hazards model analysis showed that EHD1 expression (P = 0.047; HR, 1.869; 95% CI, 1.008-3.466) and American Joint Committee on Cancer (AJCC) status (P < 0.001; HR, 1.412; 95% CI, 1.165-1.711) were independent prognostic indicators of DFS. In conclusion, these data demonstrated a remarkable correlation between the cytoplasmic expression of EHD1 protein and adverse prognosis in patients receiving early-stage cisplatin treatment for resected SCLC. PMID:26366212

  7. Small Cell Lung Cancer

    PubMed Central

    Kalemkerian, Gregory P.; Akerley, Wallace; Bogner, Paul; Borghaei, Hossein; Chow, Laura QM; Downey, Robert J.; Gandhi, Leena; Ganti, Apar Kishor P.; Govindan, Ramaswamy; Grecula, John C.; Hayman, James; Heist, Rebecca Suk; Horn, Leora; Jahan, Thierry; Koczywas, Marianna; Loo, Billy W.; Merritt, Robert E.; Moran, Cesar A.; Niell, Harvey B.; O’Malley, Janis; Patel, Jyoti D.; Ready, Neal; Rudin, Charles M.; Williams, Charles C.; Gregory, Kristina; Hughes, Miranda

    2013-01-01

    Neuroendocrine tumors account for approximately 20% of lung cancers; most (≈15%) are small cell lung cancer (SCLC). These NCCN Clinical Practice Guidelines in Oncology for SCLC focus on extensive-stage SCLC because it occurs more frequently than limited-stage disease. SCLC is highly sensitive to initial therapy; however, most patients eventually die of recurrent disease. In patients with extensive-stage disease, chemotherapy alone can palliate symptoms and prolong survival in most patients; however, long-term survival is rare. Most cases of SCLC are attributable to cigarette smoking; therefore, smoking cessation should be strongly promoted. PMID:23307984

  8. Radiotherapy for lung cancer

    SciTech Connect

    Bleehen, N.M.; Cox, J.D.

    1985-05-01

    The role of radiation therapy in the management of lung cancer was reviewed at a workshop held in Cambridge, England, in June 1984. It was concluded that there was a continuing role for radiation therapy in the primary management of small cell lung cancer, including the loco-regional treatment for patients with limited disease. Radical radiotherapy for patients with non-small cell carcinoma could be curative for a proportion of patients with limited disease. Careful planning and quality control was essential. Palliative radiotherapy provided useful treatment for many other patients. Other related aspects of treatment are also presented.

  9. Radiotherapy of inoperable lung cancer

    SciTech Connect

    Namer, M.; Lalanne, C.M.; Boublil, J.L.; Hery, M.; Chauvel, P.; Verschoore, J.; Aubanel, J.M.; Bruneton, J.N.

    1980-08-01

    Evaluation of loco-regional results obtained by radiotherapy for 31 patients with inoperable epidermoid lung cancer revealed objective remission (over 50%) in only 25% of patients. These results emphasize the limited effectiveness of radiotherapy in such cases and point out the need for increased research in radiotherapy techniques if survival rates are to be improved.

  10. Adenosine triphosphate infusion increases liver energy status in advanced lung cancer patients: an in vivo 31P magnetic resonance spectroscopy study.

    PubMed

    Leij-Halfwerk, Susanne; Agteresch, Hendrik J; Sijens, Paul E; Dagnelie, Pieter C

    2002-02-01

    We recently observed inhibition of weight loss in patients with advanced nonsmall-cell lung cancer after intravenous infusion of ATP. Because liver ATP levels were found to be decreased in lung cancer patients with weight loss, the present 31P magnetic resonance spectroscopy (MRS) study was aimed at investigating whether ATP infusion restores liver energy status in these patients. Nine patients with advanced nonsmall-cell lung cancer (stage IIIB/IV) were studied 1 week before (baseline) and at 22 to 24 hours of continuous ATP infusion (37-75 microg/kg/min). Localized hepatic 31P MR spectra (repetition time 15 seconds), obtained in the overnight-fasted state, were analyzed for ATP and P(i) content. Ten healthy subjects (without ATP infusion) served as control. Liver ATP levels in lung cancer patients increased from 8.8 +/- 0.7% (relative to total MR-detectable phosphate; mean +/- SE) at baseline to 12.2 +/- 0.9% during ATP infusion (P <.05), i.e., a level similar to that in healthy subjects (11.9 +/- 0.9%). The increase in ATP level during ATP infusion was most prominent in patients with > or = 5% weight loss (baseline: 7.9 +/- 0.7%, during ATP infusion: 12.8 +/- 1.0%, P < 0.01). In conclusion, ATP infusion restores hepatic energy levels in patients with advanced lung cancer, especially in weight-losing patients. These changes may contribute to the previously reported beneficial effects of ATP infusion on the nutritional status of lung cancer patients. PMID:11826418

  11. Lung Cancer – Vaccines

    PubMed Central

    Kelly, Ronan J.; Giaccone, Giuseppe

    2011-01-01

    In lung cancer, early attempts to modulate the immune system via vaccine based therapeutics have to date, been unsuccessful. An improved understanding of tumor immunology has facilitated the production of more sophisticated lung cancer vaccines. It is anticipated, that it will likely require multiple epitopes of a diverse set of genes restricted to multiple haplotypes to generate a truly effective vaccine that is able to overcome the various immunologic escape mechanisms that tumors employ. Other issues to overcome include optimal patient selection, which adjuvant agent to use and how to adequately monitor for an immunological response. This review discusses the most promising vaccination strategies for non small cell lung cancer including the allogeneic tumor cell vaccine belagenpumatucel-L, which is a mixture of 4 allogeneic non small cell lung cancer cell lines genetically modified to secrete an antisense oligonucleotide to TGF-β2 and three other target protein-specific vaccines designed to induce responses against melanoma-associated antigen A3 (MAGE-A3), mucin 1 (MUC1) and epidermal growth factor (EGF). PMID:21952280

  12. Nonsmall cell lung cancer.

    PubMed

    Sculier, Jean-Paul

    2013-03-01

    The objective of this review is to report the Clinical Year in Review proceedings in the field of nonsmall cell lung cancer that were presented at the 2012 European Respiratory Society Congress in Vienna, Austria. Various topics were reviewed, including epidemiology, screening, diagnosis, treatment, prognosis, and palliative and end of life care. PMID:23457162

  13. Update in Lung Cancer 2014.

    PubMed

    Spira, Avrum; Halmos, Balazs; Powell, Charles A

    2015-08-01

    In the past 2 years, lung cancer research and clinical care have advanced significantly. Advancements in the field have improved outcomes and promise to lead to further reductions in deaths from lung cancer, the leading cause of cancer death worldwide. These advances include identification of new molecular targets for personalized targeted therapy, validation of molecular signatures of lung cancer risk in smokers, progress in lung tumor immunotherapy, and implementation of population-based lung cancer screening with chest computed tomography in the United States. In this review, we highlight recent research in these areas and challenges for the future. PMID:26230235

  14. Lung cancer among Navajo uranium miners

    SciTech Connect

    Gottlieb, L.S.; Husen, L.A.

    1982-04-01

    Lung cancer has been a rare disease among the Indians of the southwestern United States. However, the advent of uranium mining in the area has been associated with an increased incidence of lung cancer among Navajo uranium miners. This study centers on Navajo men with lung cancer who were admitted to the hospital from February 1965 to May 1979. Of a total of 17 patients with lung cancer, 16 were uranium miners, and one was a nonminer. The mean value of cumulative radon exposure for this group was 1139.5 working level months (WLMs). The predominant cancer type was the small cell undifferentiated category (62.5 percent). The low frequency of cigarette smoking in this group supports the view that radiation is the primary cause of lung cancer among uranium miners and that cigarette smoking acts as a promoting agent.

  15. World conference on lung cancer.

    PubMed

    Felip, Enriqueta; Rosell, Rafael

    2003-12-01

    Lung cancer is the most frequent cause of cancer death. Improving this dismal outcome requires cooperation among several specialists. The 10th World Conference on Lung Cancer was held in Vancouver, Canada last month. The meeting was organised on behalf of the International Association for the Study of Lung Cancer (IASLC) and the British Columbia Cancer Agency. This Conference was chaired by Nevin Murray and the scientific sessions took place 10 - 14 August, with > 3000 participating lung cancer experts. The Vancouver programme included > 140 invited speakers throughout the 'meet the professor', plenary and interactive sessions, as well as 300 oral and 500 poster presentations. PMID:14640956

  16. Progression of Lung Cancer Is Associated with Increased Dysfunction of T Cells Defined by Coexpression of Multiple Inhibitory Receptors.

    PubMed

    Thommen, Daniela S; Schreiner, Jens; Müller, Philipp; Herzig, Petra; Roller, Andreas; Belousov, Anton; Umana, Pablo; Pisa, Pavel; Klein, Christian; Bacac, Marina; Fischer, Ozana S; Moersig, Wolfgang; Savic Prince, Spasenija; Levitsky, Victor; Karanikas, Vaios; Lardinois, Didier; Zippelius, Alfred

    2015-12-01

    Dysfunctional T cells present in malignant lesions are characterized by a sustained and highly diverse expression of inhibitory receptors, also referred to as immune checkpoints. Yet, their relative functional significance in different cancer types remains incompletely understood. In this study, we provide a comprehensive characterization of the diversity and expression patterns of inhibitory receptors on tumor-infiltrating T cells from patients with non-small cell lung cancer. In spite of the large heterogeneity observed in the amount of PD-1, Tim-3, CTLA-4, LAG-3, and BTLA expressed on intratumoral CD8(+) T cells from 32 patients, a clear correlation was established between increased expression of these inhibitory coreceptors and progression of the disease. Notably, the latter was accompanied by a progressively impaired capacity of T cells to respond to polyclonal activation. Coexpression of several inhibitory receptors was gradually acquired, with early PD-1 and late LAG-3/BTLA expression. PD-1 blockade was able to restore T-cell function only in a subset of patients. A high percentage of PD-1(hi) T cells was correlated with poor restoration of T-cell function upon PD-1 blockade. Of note, PD-1(hi) expression marked a particularly dysfunctional T-cell subset characterized by coexpression of multiple inhibitory receptors and thus may assist in identifying patients likely to respond to inhibitory receptor-specific antibodies. Overall, these data may provide a framework for future personalized T-cell-based therapies aiming at restoration of tumor-infiltrating lymphocyte effector functions. PMID:26253731

  17. Antisense bcl-2 treatment increases programmed cell death in non-small cell lung cancer cell lines.

    PubMed

    Koty, P P; Zhang, H; Levitt, M L

    1999-02-01

    Programmed cell death (PCD) is a genetically regulated pathway that is altered in many cancers. This process is, in part, regulated by the ratio of PCD inducers (Bax) or inhibitors (Bcl-2). An abnormally high ratio of Bcl-2 to Bax prevents PCD, thus contributing to resistance to chemotherapeutic agents, many of which are capable of inducing PCD. Non-small cell lung cancer (NSCLC) cells demonstrate resistance to these PCD-inducing agents. If Bcl-2 prevents NSCLC cells from entering the PCD pathway, then reducing the amount of endogenous Bcl-2 product may allow these cells to spontaneously enter the PCD pathway. Our purpose was to determine the effects of bcl-2 antisense treatment on the levels of programmed cell death in NSCLC cells. First, we determined whether bcl-2 and bax mRNA were expressed in three morphologically distinct NSCLC cell lines: NCI-H226 (squamous), NCI-H358 (adenocarcinoma), and NCI-H596 (adenosquamous). Cells were then exposed to synthetic antisense bcl-2 oligonucleotide treatment, after which programmed cell death was determined, as evidenced by DNA fragmentation. Bcl-2 protein expression was detected immunohistochemically. All three NSCLC cell lines expressed both bcl-2 and bax mRNA and had functional PCD pathways. Synthetic antisense bcl-2 oligonucleotide treatment resulted in decreased Bcl-2 levels, reduced cell proliferation, decreased cell viability, and increased levels of spontaneous PCD. This represents the first evidence that decreasing Bcl-2 in three morphologically distinct NSCLC cell lines allows the cells to spontaneously enter a PCD pathway. It also indicates the potential therapeutic use of antisense bcl-2 in the treatment of NSCLC. PMID:10217615

  18. Treatment Option Overview (Small Cell Lung Cancer)

    MedlinePlus

    ... Cancer Prevention Lung Cancer Screening Research Small Cell Lung Cancer Treatment (PDQ®)–Patient Version General Information About Small Cell Lung Cancer Go to Health Professional Version Key Points ...

  19. Stages of Small Cell Lung Cancer

    MedlinePlus

    ... Cancer Prevention Lung Cancer Screening Research Small Cell Lung Cancer Treatment (PDQ®)–Patient Version General Information About Small Cell Lung Cancer Go to Health Professional Version Key Points ...

  20. The Antitumor Peptide CIGB-552 Increases COMMD1 and Inhibits Growth of Human Lung Cancer Cells

    PubMed Central

    Fernández Massó, Julio R.; Oliva Argüelles, Brizaida; Tejeda, Yelaine; Astrada, Soledad; Garay, Hilda; Reyes, Osvaldo; Delgado-Roche, Livan; Bollati-Fogolín, Mariela; Vallespí, Maribel G.

    2013-01-01

    We have demonstrated that the peptide L-2 designed from an alanine scanning of the Limulus-derived LALF32-51 region is a potential candidate for the anticancer therapy and its cell-penetrating capacity is an associated useful property. By the modification in the primary structure of L-2, a second-generation peptide (CIGB-552) was developed. However, the molecular mechanism underlying its cytotoxic activity remains partially unknown. In this study, it was shown that CIGB-552 increases the levels of COMMD1, a protein involved in copper homeostasis, sodium transport, and the NF-κB signaling pathway. We found that CIGB-552 induces ubiquitination of RelA and inhibits the antiapoptotic activity regulated by NF-κB, whereas the knockdown of COMMD1 blocks this effect. We also found that CIGB-552 decreases the antioxidant capacity and induces the peroxidation of proteins and lipids in the tumor cells. Altogether, this study provides new insights into the mechanism of action of the peptide CIGB-552, which could be relevant in the design of future anticancer therapies. PMID:23401744

  1. [Advances in Lung Stem Cells and Lung Cancer Stem Cells].

    PubMed

    Yin, Huijing; Deng, Jiong

    2015-10-20

    Cancer stem cells (CSCs) are emerging as a hot topic for cancer research. Lung CSCs share many characteristics with normal lung stem cells (SCs), including self-renewal and multi-potency for differentiation. Many molecular markers expressed in various types of CSCs were also found in lung CSCs, such as CD133, CD44, aldehyde dehydrogenase (ALDH) and ATP-binding cassette sub-family G member 2 (ABCG2). Similarly, proliferation and expansion of lung CSCs are regulated not only by signal transduction pathways functioning in normal lung SCs, such as Notch, Hedgehog and Wnt pathways, but also by those acting in tumor cells, such as epidermal growth factor receptor (EGFR), signal transducer and activator of transcription 3 (STAT3) and phosphatidylinositol 3 kinase (PI3K) pathways. As CSC plays an critical role in tumor recurrence, metastasis and drug-resistance, understanding the difference between lung CSCs and normal lung SCs, identifying and targeting CSC markers or related signaling pathways may increase the efficacy of therapy on lung cancer and improved survival of lung cancer patients. PMID:26483336

  2. Screening for lung cancer.

    PubMed

    Miettinen, O S

    2000-05-01

    Screening for lung cancer serves to prevent deaths from this disease insofar as earlier resections are associated with higher rates of cure. There is good reason to believe that this is the case: in stage I, the 5-year survival rate with resection is 70%, whereas without resection the corresponding rate is only 10%. Before this evidence emerged, various authoritative organizations and agencies in North America advised against screening for lung cancer on the grounds of the results of several RCTs. As for CXR, I argue that the study results are consistent with up to 40% reduction in the fatality rate. Moreover, modern helical CT screening provides for detecting much smaller tumors than were detected in those studies. It is time to revoke the conclusion that screening for lung cancer does not serve to prevent deaths from this disease, and to quantify the usefulness of CT screening in particular. As for the requisite research, the prevailing orthodoxy has it that RCTs are to be used, but I argue that more meaningful results are obtainable, more rapidly and much less expensively, by the use of noncomparative (and hence unrandomized) studies. PMID:10855255

  3. Exposure to welding fumes increases lung cancer risk among light smokers but not among heavy smokers: evidence from two case-control studies in Montreal.

    PubMed

    Vallières, Eric; Pintos, Javier; Lavoué, Jérôme; Parent, Marie-Élise; Rachet, Bernard; Siemiatycki, Jack

    2012-08-01

    We investigated relationships between occupational exposure to gas and arc welding fumes and the risk of lung cancer among workers exposed to these agents throughout the spectrum of industries. Two population-based case-control studies were conducted in Montreal. Study I (1979-1986) included 857 cases and 1066 controls, and Study II (1996-2001) comprised 736 cases and 894 controls. Detailed job histories were obtained by interview and evaluated by an expert team of chemist-hygienists to estimate degree of exposure to approximately 300 substances for each job. Gas and arc welding fumes were among the agents evaluated. We estimated odds ratios (ORs) and 95% confidence intervals (CIs) of lung cancer using logistic regression, adjusting for smoking history and other covariates. The two studies provided similar results, so a pooled analysis was conducted. Among all subjects, no significant association was found between lung cancer and gas welding fumes (OR = 1.1; 95% CI = 0.9-1.4) or arc welding fumes (OR = 1.0; 95% CI = 0.8-1.2). However, when restricting attention to light smokers, there was an increased risk of lung cancer in relation to gas welding fumes (OR = 2.9; 95% CI = 1.7-4.8) and arc welding fumes (OR = 2.3; 95% CI = 1.3-3.8), with even higher OR estimates among workers with the highest cumulative exposures. In conclusion, there was no detectable excess risk of lung cancer due to welding fumes among moderate to heavy smokers; but among light smokers we found an excess risk related to both types of welding fumes. PMID:23342253

  4. Exposure to welding fumes increases lung cancer risk among light smokers but not among heavy smokers: evidence from two case–control studies in Montreal

    PubMed Central

    Vallières, Eric; Pintos, Javier; Lavoué, Jérôme; Parent, Marie-Élise; Rachet, Bernard; Siemiatycki, Jack

    2012-01-01

    We investigated relationships between occupational exposure to gas and arc welding fumes and the risk of lung cancer among workers exposed to these agents throughout the spectrum of industries. Two population-based case–control studies were conducted in Montreal. Study I (1979–1986) included 857 cases and 1066 controls, and Study II (1996–2001) comprised 736 cases and 894 controls. Detailed job histories were obtained by interview and evaluated by an expert team of chemist–hygienists to estimate degree of exposure to approximately 300 substances for each job. Gas and arc welding fumes were among the agents evaluated. We estimated odds ratios (ORs) and 95% confidence intervals (CIs) of lung cancer using logistic regression, adjusting for smoking history and other covariates. The two studies provided similar results, so a pooled analysis was conducted. Among all subjects, no significant association was found between lung cancer and gas welding fumes (OR = 1.1; 95% CI = 0.9–1.4) or arc welding fumes (OR = 1.0; 95% CI = 0.8–1.2). However, when restricting attention to light smokers, there was an increased risk of lung cancer in relation to gas welding fumes (OR = 2.9; 95% CI = 1.7–4.8) and arc welding fumes (OR = 2.3; 95% CI = 1.3–3.8), with even higher OR estimates among workers with the highest cumulative exposures. In conclusion, there was no detectable excess risk of lung cancer due to welding fumes among moderate to heavy smokers; but among light smokers we found an excess risk related to both types of welding fumes. PMID:23342253

  5. Betulinic acid decreases specificity protein 1 (Sp1) level via increasing the sumoylation of sp1 to inhibit lung cancer growth.

    PubMed

    Hsu, Tsung-I; Wang, Mei-Chun; Chen, Szu-Yu; Huang, Shih-Ting; Yeh, Yu-Min; Su, Wu-Chou; Chang, Wen-Chang; Hung, Jan-Jong

    2012-12-01

    Previous studies have shown that the inhibitory effect of betulinic acid (BA) on specificity protein 1 (Sp1) expression is involved in the prevention of cancer progression, but the mechanism of this effect remains to be delineated. In this study, we determined that BA treatment in HeLa cells increased the sumoylation of Sp1 by inhibiting sentrin-specific protease 1 expression. The subsequent recruitment of E3 ubiquitin-protein ligase RING finger protein 4 resulted in ubiquitin-mediated degradation in a 26S-proteosome-dependent pathway. In addition, both BA treatment and mithramycin A (MMA) treatment inhibited lung tumor growth and down-regulated Sp1 protein expression in Kras(G12D)-induced lung cancers of bitransgenic mice. In gene expression profiles of Kras(G12D)-induced lung cancers in bitransgenic mice with and without Sp1 inhibition, 542 genes were affected by MMA treatment. One of the gene products, cyclin A2, which was involved in the S and G(2)/M phase transition during cell cycle progression, was investigated in detail because its expression was regulated by Sp1. The down-regulation of cyclin A2 by BA treatment resulted in decreased retinoblastoma protein phosphorylation and cell cycle G(2)/M arrest. The BA-mediated cellular Sp1 degradation and antitumor effect were also confirmed in a xenograft mouse model by using H1299 cells. The knockdown of Sp1 in lung cancer cells attenuated the tumor-suppressive effect of BA. Taken together, the results of this study clarify the mechanism of BA-mediated Sp1 degradation and identify a pivotal role for Sp1 in the BA-induced repression of lung cancer growth. PMID:22956772

  6. Scientific Advances in Lung Cancer 2015.

    PubMed

    Tsao, Anne S; Scagliotti, Giorgio V; Bunn, Paul A; Carbone, David P; Warren, Graham W; Bai, Chunxue; de Koning, Harry J; Yousaf-Khan, A Uraujh; McWilliams, Annette; Tsao, Ming Sound; Adusumilli, Prasad S; Rami-Porta, Ramón; Asamura, Hisao; Van Schil, Paul E; Darling, Gail E; Ramalingam, Suresh S; Gomez, Daniel R; Rosenzweig, Kenneth E; Zimmermann, Stefan; Peters, Solange; Ignatius Ou, Sai-Hong; Reungwetwattana, Thanyanan; Jänne, Pasi A; Mok, Tony S; Wakelee, Heather A; Pirker, Robert; Mazières, Julien; Brahmer, Julie R; Zhou, Yang; Herbst, Roy S; Papadimitrakopoulou, Vassiliki A; Redman, Mary W; Wynes, Murry W; Gandara, David R; Kelly, Ronan J; Hirsch, Fred R; Pass, Harvey I

    2016-05-01

    Lung cancer continues to be a major global health problem; the disease is diagnosed in more than 1.6 million new patients each year. However, significant progress is underway in both the prevention and treatment of lung cancer. Lung cancer therapy has now emerged as a "role model" for precision cancer medicine, with several important therapeutic breakthroughs occurring during 2015. These advances have occurred primarily in the immunotherapy field and in treatments directed against tumors harboring specific oncogenic drivers. Our knowledge about molecular mechanisms for oncogene-driven tumors and about resistance to targeted therapies has increased quickly over the past year. As a result, several regulatory approvals of new agents that significantly improve survival and quality of life for patients with lung cancer who have advanced disease have occurred. The International Association for the Study of Lung Cancer has gathered experts in different areas of lung cancer research and management to summarize the most significant scientific advancements related to prevention and therapy of lung cancer during the past year. PMID:27013409

  7. Bronchoplastic procedures for lung cancer.

    PubMed

    Naruke, T; Yoneyama, T; Ogata, T; Suemasu, K

    1977-06-01

    Twenty patients with lung cancer have undergone bronchoplastic procedures September, 1965, to June, 1976 in our hospital. Bronchoplastic procedures are considered to be indicated for early cases of hilar lung cancer rather than for somewhat advanced cases. Endoscopic examination and roentgenograms of the bronchial arteries are needed to delineate resectional lines of bronchus, the former for deciding the mucosal extent and the latter the intrabronchial extent of the tumor. The bronchoplastic procedures we adopted were free from the risks and dangers generally accompanying the operation, and there were no postoperative deaths. For the prevention of postoperative complications, careful attention to suture technique is needed, and postoperative bronchoscopic suction of intrabronchial secretions is absolutely necessary. These procedures assure good quality of life postoperatively and improvement in the survival rate by preserving pulmonary function, enhancing curability, and increasing the operative indications. These advantages warrant high evaluation of the operation. PMID:870767

  8. Increased Plasma miRNA-30a as a Biomarker for Non-Small Cell Lung Cancer

    PubMed Central

    Sun, Ling; Chen, Yifan; Su, Qiaoli; Tang, Xiaoju; Liang, Yasha; Che, Guowei; Luo, Fengming

    2016-01-01

    Background MicroRNA (miRNA) is a small, non-coding RNA molecule which plays a role in the carcinogenesis and progression of cancers. Abnormal expression of miRNA in plasma has been found in some patients with malignant tumors. Material/Methods This study was conducted to investigate the expression of miRNA-30a in plasma of patients with non-small cell lung cancer (NSCLC). The plasma miRNA-30a in 87 patients with NSCLC, 20 patients with benign lung diseases, and 76 healthy subjects were measured by real-time PCR. The diagnostic value of miRNA-30a in NSCLC was evaluated via the ROC curve method. Results Plasma miRNA-30a level was significantly higher in the NSCLC group compared with benign control and healthy control groups (P<0.01). No statistically significant difference was found in the expression level of miRNA-30a among various clinical pathologic features in NSCLC. ROC curve analysis showed that the specificity and sensitivity cut-off points were at 61.0% and 84.3% for NSCLC. The specificity and sensitivity values were 54.9% and 94.4%, respectively, in the analysis based on in-patients only. Conclusions All these results suggest that plasma miRNA-30a measurement may be a novel and noninvasive method for NSCLC preliminary screening and differential diagnosis. PMID:26918265

  9. Increased levels of urinary PGE-M, a biomarker of inflammation, occur in association with obesity, aging, and lung metastases in patients with breast cancer.

    PubMed

    Morris, Patrick G; Zhou, Xi Kathy; Milne, Ginger L; Goldstein, Daniel; Hawks, Laura C; Dang, Chau T; Modi, Shanu; Fornier, Monica N; Hudis, Clifford A; Dannenberg, Andrew J

    2013-05-01

    Elevated levels of COX-derived prostaglandin E2 (PGE2) occur in inflamed tissues. To evaluate the potential links between inflammation and breast cancer, levels of urinary prostaglandin E metabolite (PGE-M), a stable end metabolite of PGE2, were quantified. We enrolled 400 patients with breast cancer: controls with early breast cancer (n = 200), lung metastases (n = 100), and metastases to other sites (n = 100). Patients completed a questionnaire, provided urine, and had measurements of height and weight. Urinary PGE-M was quantified by mass spectrometry. Ever smokers with lung metastasis who had not been exposed to nonsteroidal anti-inflammatory drugs (NSAIDs) had the highest PGE-M levels. PGE-M levels were increased in association with elevated body mass index (BMI; P < 0.001), aging (P < 0.001), pack-year smoking history (P = 0.02), lung metastases (P = 0.02), and recent cytotoxic chemotherapy (P = 0.03). Conversely, use of NSAIDs, prototypic inhibitors of COX activity, was associated with reduced PGE-M levels (P < 0.001). On the basis of the current findings, PGE-M is likely to be a useful biomarker for the selection of high-risk subgroups to determine the use of interventions that aim to reduce inflammation and possibly the development and progression of breast cancer, especially in overweight and obese women. PMID:23531446

  10. Drugs Approved for Lung Cancer

    Cancer.gov

    This page lists cancer drugs approved by the Food and Drug Administration (FDA) for lung cancer. The list includes generic names, brand names, and common drug combinations, which are shown in capital letters.

  11. Screening for Lung Cancer.

    PubMed

    Stiles, Brendon M; Pua, Bradley; Altorki, Nasser K

    2016-07-01

    Lung cancer is a global health burden and is among the most common and deadliest of all malignancies worldwide. The goal of screening programs is to detect tumors in earlier, curable stages, consequently reducing disease-specific mortality. The issue of screening has great relevance to thoracic surgeons, who should play a leading role in the debate over screening and its consequences. The burden is on thoracic surgeons to work in a multidisciplinary setting to guide and treat these patients safely and responsibly, ensuring low morbidity and mortality of potential diagnostic or therapeutic interventions. PMID:27261909

  12. Increased Potency of the PHSCN Dendrimer as an Inhibitor of Human Prostate Cancer Cell Invasion, Extravasation, and Lung Colony Formation

    PubMed Central

    Yao, Hongren; Zeng, Zhao-Zhu; Fay, Kevin S.; Staszewski, Evan D.; Veine, Donna M.; Livant, Donna L.

    2011-01-01

    Background Activated α5β1 integrin occurs specifically on tumor cells and on endothelial cells of tumor–associated vasculature, and plays a key role in invasion and metastasis. The PHSCN peptide (Ac-PHSCN-NH2) preferentially binds activated α5β1, to block invasion in vitro, and inhibit growth, metastasis and tumor recurrence in preclinical models of prostate cancer. In Phase I clinical trial, systemic Ac-PHSCN-NH2 monotherapy was well tolerated, and metastatic disease progression was prevented for 4–14 months in one third of treated patients. Results We have developed a significantly more potent derivative, the PHSCN-polylysine dendrimer (Ac-PHSCNGGK-MAP). Using in vitro invasion assays with naturally serum-free basement membranes, we observed that the PHSCN dendrimer was 130– to 1900–fold more potent than the PHSCN peptide at blocking α5β1–mediated invasion by DU 145 and PC-3 human prostate cancer cells, whether invasion was induced by serum, or by the Ac-PHSRN-NH2 peptide, under serum-free conditions. The PHSCN dendrimer was also approximately 800 times more effective than PHSCN peptide at preventing DU 145 and PC-3 extravasation in the lungs of athymic mice. Chou-Talalay analysis suggested that inhibition of both invasion in vitro and extravasation in vivo by the PHSCN dendrimer are highly synergistic. We found that many extravasated DU 145 and PC-3 cells go on to develop into metastatic colonies, and that a single pretreatment with the PHSCN dendrimer was 100–fold more affective than the PHSCN peptide at reducing lung colony formation. Conclusions Since many patients newly diagnosed with prostate cancer already have locally advanced or metastatic disease, the availability of a well-tolerated, nontoxic systemic therapy, like the PHSCN dendrimer, which prevents metastatic progression by inhibiting invasion, could be very beneficial. PMID:20339907

  13. Lung cancer during pregnancy: A narrative review.

    PubMed

    Mitrou, Sotirios; Petrakis, Dimitrios; Fotopoulos, George; Zarkavelis, George; Pavlidis, Nicholas

    2016-07-01

    Lung cancer, the leading cause of cancer deaths in males for decades, has recently become one of commonest causes for women too. As women delay the start of their family, the co-existence of cancer and pregnancy is increasingly observed. Nevertheless, lung cancer during pregnancy remains a rather uncommon condition with less than 70 cases published in recent years. Non-small cell lung carcinoma is the commonest type accounting for about 85% of all cases. Overall survival rates are low. Chemotherapy and/or targeted treatment have been used with poor outcomes. The disease has been also found to affect the products of conception with no short- or long-term consequences for the neonate. This article is referring to a narrative review of lung cancers diagnosed in pregnant women around the world. PMID:27408759

  14. UK partnership targets lung cancer.

    PubMed

    2014-07-01

    Cancer Research UK has joined with two major pharmaceutical companies to launch a large multiarm clinical trial, dubbed the National Lung Matrix trial, to test the effectiveness of promising experimental therapies in treating rare forms of advanced lung cancer. PMID:25002593

  15. LUNG CANCER AND PULMONARY THROMBOEMBOLISM

    PubMed Central

    Cukic, Vesna; Ustamujic, Aida

    2015-01-01

    Introduction: Malignant diseases including lung cancer are the risk for development of pulmonary thromboembolism (PTE). Objective: To show the number of PTE in patients with lung cancer treated in Clinic for pulmonary diseases and TB “Podhrastovi” in three-year period: from 2012-2014. Material and methods: This is the retrospective study in which we present the number of various types of lung cancer treated in three-year period, number and per cent of PTE in different types of lung carcinoma, number and per cent of PTE of all diagnosed PTE in lung carcinoma according to the type of carcinoma. Results: In three-year period (from 2012 to 2014) 1609 patients with lung cancer were treated in Clinic for pulmonary diseases and TB “Podhrastovi” Clinical Centre of Sarajevo University. 42 patients: 25 men middle –aged 64.4 years and 17 women middle- aged 66.7 or 2.61% of all patients with lung cancer had diagnosed PTE. That was the 16. 7% of all patients with PTE treated in Clinic “Podhrastovi “in that three-year period. Of all 42 patients with lung cancer and diagnosed PTE 3 patients (7.14%) had planocellular cancer, 4 patients (9.53%) had squamocellular cancer, 9 (21.43%) had adenocarcinoma, 1 (2.38%) had NSCLC, 3 (7.14 %) had microcellular cancer, 1 (2.38%) had neuroendocrine cancer, 2 (4.76%) had large cell-macrocellular and 19 (45.24%) had histological non-differentiated lung carcinoma. Conclusion: Malignant diseases, including lung cancer, are the risk factor for development of PTE. It is important to consider the including anticoagulant prophylaxis in these patients and so to slow down the course of diseases in these patients. PMID:26622205

  16. [Grading of lung cancer].

    PubMed

    Bohle, R M; Schnabel, P A

    2016-07-01

    In comparison with other tumor entities there is no common generally accepted grading system for lung cancer with clearly defined criteria and clinical relevance. In the recent fourth edition of the World Health Organization (WHO) classification from 2015 of tumors of the lungs, pleura, thymus and heart, there is no generally applicable grading for pulmonary adenocarcinomas, squamous cell carcinomas or rarer forms of carcinoma. Since the new IASLC/ATS/ERS classification of adenocarcinomas published in 2011, 5 different subtypes with significantly different prognosis are proposed. This results in an architectural (histologic) grading, which is usually applied to resection specimens. For squamous cell carcinoma the number of different histological subtypes in the new WHO classification was reduced compared to earlier versions but without a common grading system. In recent publications nesting and budding were proposed as the main (histologic) criteria for a grading of squamous cell carcinomas. The grading of neuroendocrine tumors (NET) of the lungs in comparison with NET in other organs is presented in a separate article in this issue. Certain rare tumor types are high grade per definition: small cell, large cell and pleomorphic carcinomas, carcinosarcomas and pulmonary blastomas. In the future it is to be expected that these developments will be further refined, e. g. by adding further subtypes for adenocarcinomas and cytologic and/or nuclear criteria for adenocarcinoma and/or squamous cell carcinomas. PMID:27356985

  17. Gingerol Reverses the Cancer-Promoting Effect of Capsaicin by Increased TRPV1 Level in a Urethane-Induced Lung Carcinogenic Model.

    PubMed

    Geng, Shengnan; Zheng, Yaqiu; Meng, Mingjing; Guo, Zhenzhen; Cao, Ning; Ma, Xiaofang; Du, Zhenhua; Li, Jiahuan; Duan, Yongjian; Du, Gangjun

    2016-08-10

    Both gingerol and capsaicin are agonists of TRPV1, which can negatively control tumor progression. This study observed the long-term effects of oral administration of 6-gingerol alone or in combination with capsaicin for 20 weeks in a urethane-induced lung carcinogenic model. We showed that lung carcinoma incidence and multiplicity were 70% and 21.2 ± 3.6, respectively, in the control versus 100% and 35.6 ± 5.2 in the capsaicin group (P < 0.01) and 50% and 10.8 ± 3.1 in the 6-gingerol group (P < 0.01). The combination of 6-gingerol and capsaicin reversed the cancer-promoting effect of capsaicin (carcinoma incidence of 100% versus 20% and multiplicity of 35.6 ± 5.2 versus 4.7 ± 2.3; P < 0.001). The cancer-promoting effect of capsaicin was due to increased epidermal growth-factor receptor (EGFR) level by decreased transient receptor potential vanilloid type-1 (TRPV1) level (P < 0.01) . The capsaicin-decreased EGFR level subsequently reduced levels of nuclear factor-κB (NF-κB) and cyclin D1 that favored enhanced lung epithelial proliferation and epithelial-mesenchymal transition (EMT) during lung carcinogenesis (P < 0.01). In contrast, 6-gingerol promoted TRPV1 level and drastically decreased the levels of EGFR, NF-κB, and cyclin D1 that favored reduced lung epithelial proliferation and EMT (P < 0.01). This study provides valuable information for the long-term consumption of chili-pepper-rich diets to decrease the risk of cancer development. PMID:27436516

  18. Bronchoscopy of Lung Cancer

    PubMed Central

    Emslander, H. P.

    1994-01-01

    Lung cancer is a leading cancer site in men and women with a high incidence and mortality rate. Most patients are diagnosed when the disease has already spread. An early, detection and immediate and accurate histological or cytological diagnosis are essential for a hopeful outcome. In most patients, bronchoscopy is the method of choice in establishing a suspected lung neoplasm. With the rigid and flexible method, two complementary techniques are available. The methods bear a very low mortality rate if sufficient monitoring and resuscitative instrumentation is available. Rigid bronchoscopy offers the possibility of obtaining large biopsy specimens from the tumorous tissue and provides an effective tool in the control of major haemorrhage. However, it cannot be used for the inspection of further peripherally located parts of the bronchial system and needs general anaesthesia. In contrast, the flexible method can be quickly and readily performed at practically any location using portable equipment. Bronchi can be inspected up to the 8th order and with bronchial washing, forceps biopsy, brush biopsy and fluorescence bronchoscopy techniques with a high diagnostic yield are available. This holds true, especially if these sampling techniques are used as complementary methods. PMID:18493335

  19. Polonium and Lung Cancer

    PubMed Central

    Zagà, Vincenzo; Lygidakis, Charilaos; Chaouachi, Kamal; Gattavecchia, Enrico

    2011-01-01

    The alpha-radioactive polonium 210 (Po-210) is one of the most powerful carcinogenic agents of tobacco smoke and is responsible for the histotype shift of lung cancer from squamous cell type to adenocarcinoma. According to several studies, the principal source of Po-210 is the fertilizers used in tobacco plants, which are rich in polyphosphates containing radio (Ra-226) and its decay products, lead 210 (Pb-210) and Po-210. Tobacco leaves accumulate Pb-210 and Po-210 through their trichomes, and Pb-210 decays into Po-210 over time. With the combustion of the cigarette smoke becomes radioactive and Pb-210 and Po-210 reach the bronchopulmonary apparatus, especially in bifurcations of segmental bronchi. In this place, combined with other agents, it will manifest its carcinogenic activity, especially in patients with compromised mucous-ciliary clearance. Various studies have confirmed that the radiological risk from Po-210 in a smoker of 20 cigarettes per day for a year is equivalent to the one deriving from 300 chest X-rays, with an autonomous oncogenic capability of 4 lung cancers per 10000 smokers. Po-210 can also be found in passive smoke, since part of Po-210 spreads in the surrounding environment during tobacco combustion. Tobacco manufacturers have been aware of the alpha-radioactivity presence in tobacco smoke since the sixties. PMID:21772848

  20. An Online Learning Module to Increase Self-Efficacy and Involvement in Care for Patients With Advanced Lung Cancer: Research Protocol

    PubMed Central

    Nagrial, Adnan; Pene, Christopher; Rabbets, Melanie; Carlino, Matteo; Zachulski, Clare; Phillips, Jane; Birnbaum, Robert; Gandhi, Tejal; Harnett, Paul

    2016-01-01

    Background Improving patient care for individuals with lung cancer is a priority due to the increasing burden of the disease globally. One way this can be done is by improving patient self-management capabilities through increasing their self-efficacy. This can improve positive outcomes for patients with chronic conditions and increase their ability to manage the challenges of such illnesses. Unfortunately, patients with chronic conditions often struggle to travel far from home to engage with patient education events, a common means of improving self-efficacy. The development of more accessible tools for improving patient self-efficacy is required to increase quality of life for patients with chronic conditions. Objective To evaluate the feasibility of delivering symptom identification and management information to patients with advanced lung cancer using an online program. Methods This article describes a pre-post test study to evaluate a Qstream online learning platform to improve patient self-efficacy for managing advanced lung cancer symptoms. Undertaking this program should increase participant knowledge about the side-effects they may experience as a result of their treatment and in turn increase help-seeking behavior and self-efficacy for the participant cohort. Quantitative data collected by the Qstream platform on the completion rates of participants will be used as a tool to evaluate the intervention. Additionally, validated scales will be used to collect data on patient self-efficacy. Qualitative data will also be collected via an exit survey and thematic content analysis of semi-structured interviews. Results The research is in the preliminary stages but thus far a protocol has been approved in support of the project. Additionally, advisory committee members have been identified and initial meetings have been undertaken. Conclusions Development of new approaches for increasing patient understanding of their care is important to ensure high quality care

  1. Increased level of exhaled nitric oxide and up-regulation of inducible nitric oxide synthase in patients with primary lung cancer.

    PubMed Central

    Liu, C. Y.; Wang, C. H.; Chen, T. C.; Lin, H. C.; Yu, C. T.; Kuo, H. P.

    1998-01-01

    Monocyte-macrophage series have an important role in host surveillance against cancer. The cytotoxic/cytostatic activity of macrophages is, to a great extent, attributed to the up-regulation of inducible nitric oxide synthase (iNOS) and production of nitric oxide (NO). Here, in 28 patients with primary lung cancer and 20 control subjects, we measured the concentration of exhaled NO and nitrite in epithelial lining fluid (ELF) using a chemiluminescence NO analyser, and studied NOS expression in alveolar macrophages (AM) and lung tissues by flow cytometry; immunohistochemical analysis was also undertaken. The mean fluorescence intensity (FI) of iNOS expression in AM was significantly increased in patients with lung cancer (tumour side 263.5 +/- 15.2 FI, normal side 232.4 +/- 18.6 FI; n = 28) compared with that in control subjects (27.3 +/- 3.2 FI; n = 20, P< 0.001). The level of exhaled NO from cancer patients (16.9 +/- 0.9 p.p.b.; n = 28) was significantly higher than that in the control group (6.0 +/- 0.5 p.p.b.; n = 20, P < 0.001). The level of nitrite was also significantly higher in ELF from cancer patients (tumour side 271.1 +/- 28.9 nM and normal side 257.4 +/- 19.6 nM vs control subjects 32.9 +/- 4.1 nM; P< 0.001). The intensity of iNOS expression in AM was correlated with the level of exhaled NO (rs = 0.73, n = 76, P< 0.001) and the nitrite released in ELF (rs = 0.56, n = 76, P< 0.001). The nitrite generation of cultured AM from patients with lung cancer was significantly enhanced compared with that of control subjects after culture for 24 h (tumour side 5.75 +/- 0.69 and normal side 5.68 +/- 0.58 microM per 106 cells vs control group 38.3 +/- 3.6 nM per 106 cells; P< 0.001). The distribution of iNOS was identified in AM, tumour-associated macrophages, endothelium, chondrocytes, airway epithelium of both lungs and malignant cells (adenocarcinoma and alveolar cell carcinoma) of cancer patients. cNOS was labelled in alveolar macrophages, endothelial cells and

  2. Smoking Cessation: An Integral Part of Lung Cancer Treatment

    PubMed Central

    Cataldo, Janine K.; Dubey, Sarita; Prochaska, Jodi J.

    2010-01-01

    Lung cancer is the leading cause of cancer death in the US. About 50% of lung cancer patients are current smokers at the time of diagnosis and up to 83% continue to smoke after diagnosis. A recent study suggests that people who continue to smoke after a diagnosis of early-stage lung cancer almost double their risk of dying. Despite a growing body of evidence that continued smoking by patients after a lung cancer diagnosis is linked with less effective treatment and a poorer prognosis, the belief prevails that treating tobacco dependence is useless. With improved cancer treatments and survival rates, smoking cessation among lung cancer patients has become increasingly important. There is a pressing need to clarify the role of smoking cessation in the care of lung cancer patients. Objective This paper will report on the benefits of smoking cessation for lung cancer patients and the elements of smoking cessation treatment, with consideration of tailoring to the needs of lung cancer patients. Results Given the significant benefits of smoking cessation and that tobacco dependence remains a challenge for many lung cancer patients, cancer care providers need to offer full support and intensive treatment with a smoking cessation program that is tailored to lung cancer patients’ specific needs. Conclusion A tobacco dependence treatment plan for lung cancer patients is provided. PMID:20699622

  3. Lung cancer - non-small cell

    MedlinePlus

    Cancer - lung - non-small cell; Non-small cell lung cancer; NSCLC; Adenocarcinoma - lung; Squamous cell carcinoma - lung ... Smoking causes most cases (around 90%) of lung cancer. The risk ... day and for how long you have smoked. Being around the smoke ...

  4. Transthyretin as a potential biomarker for the differential diagnosis between lung cancer and lung infection

    PubMed Central

    DING, HONGMEI; LIU, JIANHUA; XUE, RONG; ZHAO, PENG; QIN, YI; ZHENG, FANG; SUN, XUGUO

    2014-01-01

    Satisfactory biomarkers for screening and early diagnosis of lung cancer remain scarce and require further investigation. The aim of the present study was to examine the changes of the biochemical and protein composition in the serum and pleural effusion from lung cancer and lung infection (bacterial pneumonia) patients. A total of 92 patients with lung cancer, 38 with bacterial pneumonia and 42 healthy controls were enrolled in the study. The serum levels of cholesterol, apolipoprotein A and transthyretin (TTR) in the lung cancer patients were higher than that of the lung infection patients (P<0.05). The levels of TTR were higher, whereas the activity of adenosine deaminase (ADA) was lower in the pleural effusion from the lung cancer patients compared to the lung infection patients (P<0.05). Furthermore, the pleural effusion/serum TTR ratios in the lung cancer patients were higher, whereas the ratios of ADA were lower (P<0.05). By matrix-assisted laser desorption/ionization time-of-flight mass spectrometry analysis, four major peaks corresponding to native TTR, Sul-TTR, Cys-TTR and Cysgly-TTR were observed in the serum of the lung cancer and lung infection patients. A significant increase was found in the proportion of Cysgly-TTR in the pleural effusion from the patients with lung cancer. The data indicated that a combination of pleural effusion/serum TTR ratios and modified TTR may be beneficial for the differential diagnosis between lung cancer and lung infection. PMID:25054025

  5. Lung Cancer Surgery Worthwhile for Older Patients

    MedlinePlus

    ... nlm.nih.gov/medlineplus/news/fullstory_158689.html Lung Cancer Surgery Worthwhile for Older Patients Study found those ... 2016 THURSDAY, May 5, 2016 (HealthDay News) -- Older lung cancer patients are surviving longer when they have lung ...

  6. Lung Cancer Surgery Worthwhile for Older Patients

    MedlinePlus

    ... page: https://medlineplus.gov/news/fullstory_158689.html Lung Cancer Surgery Worthwhile for Older Patients Study found those ... 2016 THURSDAY, May 5, 2016 (HealthDay News) -- Older lung cancer patients are surviving longer when they have lung ...

  7. RRM1 *151A>T, RRM1 -756T>C, and RRM1 -585T>Gis associated with increased susceptibility of lung cancer in Chinese patients.

    PubMed

    Xu, Xiao-Ling; Zheng, Ji; Mao, Wei-Min; Ling, Zhi-Qiang

    2016-08-01

    Ribonucleotide reductase M1 (RRM1) is a crucial gene in DNA repair. Recent studies have shown that RRM1 expression can be a powerful predictor of survival or chemotherapy sensitivity in patients presenting with carcinomas who are treated with adjuvant gemcitabine-based chemotherapy including lung cancer. However, the relationship between the single nucleotide polymorphisms (SNP) of RRM1 and the susceptibility of lung cancer to chemotherapy has not been well addressed. We detected six tag SNPs of RRM1 genotypes in a cohort of 1007 patients with primary lung cancer and 1007 age- and sex-matched population controls using SNaPshot detection technology. Logistic regression, odds ratios (OR), and 95% confidence intervals were calculated to estimate lung cancer risk associated with SNP genotypes and haplotypes, after adjusting for case-control matching factors. Compared with the T/T and A/T genotype of RRM1 *151A>T, the A/A genotype had an increased risk for overall lung cancer (adjusted OR, 1.33). Additionally, the T/T+T/C genotypes of RRM1 -756T>C were risk factors that increased the susceptibility to lung cancer (adjusted OR 1.54, as compared with the C/C genotype). While the T/T+G/T genotypes of RRM1 -585T>G behaved as protective factors to increase the susceptibility to lung cancer (adjusted OR 0.44, as compared with the C/C genotype). In summary, this is the first study to systematically identify the relationship between the polymorphisms of RRM1 and individual susceptibility to lung cancer. It is anticipated that the RRM1 *151A>T, RRM1 -756T>C, and RRM1 -585T>G polymorphisms will improve the predictive prognosis of lung cancer sensitivity. PMID:27335251

  8. Occupational exposure and lung cancer

    PubMed Central

    Spyratos, Dionysios; Porpodis, Konstantinos; Tsakiridis, Kosmas; Machairiotis, Nikolaos; Katsikogiannis, Nikolaos; Kougioumtzi, Ioanna; Dryllis, Georgios; Kallianos, Anastasios; Rapti, Aggeliki; Li, Chen; Zarogoulidis, Konstantinos

    2013-01-01

    Lung cancer is the leading cause of cancer death for male and the second most usual cancer for women after breast cancer. Currently there are available several non-specific cytotoxic agents and several targeted agents for lung cancer therapy. However; early stage diagnosis is still unavailable and several efforts are being made towards this direction. Novel biomarkers are being investigated along with new biopsy techniques. The occupational and environmental exposure to carcinogenic agents is an everyday phenomenon. Therefore until efficient early diagnosis is available, avoidance of exposure to carcinogenic agents is necessary. In the current mini-review occupational and environmental carcinogenic agents will be presented. PMID:24102018

  9. H460 non-small cell lung cancer stem-like holoclones yield tumors with increased vascularity

    PubMed Central

    Manley, Eugene; Waxman, David J.

    2014-01-01

    Cancer stem-like cells were isolated from several human tumor cell lines by limiting dilution assays and holoclone morphology, followed by assessment of self-renewal capacity, tumor growth, vascularity, and blood perfusion. H460 holoclone-derived tumors grew slower than parental H460 tumors, but displayed significantly increased microvessel density and tumor blood perfusion. Microarray analysis identified 177 differentially regulated genes in the holoclone-derived tumors, of which 47 were associated with angiogenesis. The dysregulated genes include several small leucine-rich proteoglycans that may modulate angiogenesis and serve as novel therapeutic targets for inhibiting cancer stem cell-driven angiogenesis. PMID:24334139

  10. SULF2 Methylation is Prognostic for Lung Cancer Survival and Increases Sensitivity to Topoisomerase-I inhibitors via Induction of ISG15

    PubMed Central

    Tessema, Mathewos; Yingling, Christin M.; Thomas, Cynthia L.; Klinge, Donna M.; Bernauer, Amanda M.; Liu, Yushi; Dacic, Sanja; Siegfried, Jill M.; Dahlberg, Suzanne E.; Schiller, Joan H.; Belinsky, Steven A.

    2011-01-01

    The heparan sulfate 6-O-endosulfatase (SULF2) promotes growth and metastasis of solid tumors. We recently identified that cytosine methylation of the SULF2 promoter is associated with better survival of resected lung adenocarcinoma patients and now also demonstrate a marginal improvement in survival of advanced non-small cell lung cancer (NSCLC) patients receiving standard chemotherapy (HR = 0.63, p = 0.07). Subsequent studies focused on investigating the effect of methylation on SULF2 expression and its genome-wide impact. The genes and pathways modulated by epigenetic inactivation of SULF2 and the effects on sensitivity to chemotherapy were characterized in vitro and in vivo. Silencing SULF2 through siRNA or methylation primarily increased expression of interferon-inducible genes including ISG15, a marker for increased sensitivity to topoisomerase-1 inhibitors such as camptothecin. NSCLC cell lines with methylated SULF2 (SULF2M) express 60-fold higher ISG15 compared to SULF2 unmethylated (SULF2U) NSCLC cell lines and normal human bronchial epithelial cells. In vitro, SULF2M and high ISG15 (ISG15H) expressing NSCLC cell lines were 134-fold more sensitive to camptothecin than SULF2U and low ISG15 (ISG15L) expressing cell lines. Topotecan, a soluble analogue of camptothecin and FDA approved anti-cancer drug, dramatically arrested the growth of SULF2M-ISG15H, but not SULF2U-ISG15L lung tumors in nude mice (p < 0.002). Similarly, high ISG15 expression that is comparable to the topotecan sensitive NSCLC cell lines was found in tumors from 25% of NSCLC patients compared to normal lung indicating a potential to identify and target the most sensitive NSCLC subpopulation for personalized topotecan therapy. PMID:22158045

  11. Proteomic biomarkers in lung cancer.

    PubMed

    Pastor, M D; Nogal, A; Molina-Pinelo, S; Carnero, A; Paz-Ares, L

    2013-09-01

    The correct understanding of tumour development relies on the comprehensive study of proteins. They are the main orchestrators of vital processes, such as signalling pathways, which drive the carcinogenic process. Proteomic technologies can be applied to cancer research to detect differential protein expression and to assess different responses to treatment. Lung cancer is the number one cause of cancer-related death in the world. Mostly diagnosed at late stages of the disease, lung cancer has one of the lowest 5-year survival rates at 15 %. The use of different proteomic techniques such as two-dimensional gel electrophoresis (2D-PAGE), isotope labelling (ICAT, SILAC, iTRAQ) and mass spectrometry may yield new knowledge on the underlying biology of lung cancer and also allow the development of new early detection tests and the identification of changes in the cancer protein network that are associated with prognosis and drug resistance. PMID:23606351

  12. Deaths in Canada from lung cancer due to involuntary smoking.

    PubMed Central

    Wigle, D T; Collishaw, N E; Kirkbride, J; Mao, Y

    1987-01-01

    Recently published evidence indicates that involuntary smoking causes an increased risk of lung cancer among nonsmokers. Information was compiled on the proportion of people who had never smoked among victims of lung cancer, the risk of lung cancer for nonsmokers married to smokers and the prevalence of such exposure. On the basis of these data we estimate that 50 to 60 of the deaths from lung cancer in Canada in 1985 among people who had never smoked were caused by spousal smoking; about 90% occurred in women. The total number of deaths from lung cancer attributable to exposure to tobacco smoke from spouses and other sources (mainly the workplace) was derived by applying estimated age- and sex-specific rates of death from lung cancer attributable to such exposure to the population of Canadians who have never smoked; about 330 deaths from lung cancer annually are attributable to such exposure. PMID:3567810

  13. Screening for occult lung cancer.

    PubMed Central

    Barclay, T. H.; MacIntosh, J. H.

    1983-01-01

    A pilot screening program for the early detection of lung cancer was carried out in Saskatchewan in 1968 using chest roentgenography and cytologic examination of sputum samples. The yield from 23 000 men aged 40 years and over was only 10 cases. Nine of the men had advanced disease. One had occult lung cancer. A period of 31 months elapsed between the discovery of malignant cells in this patient's sputum and roentgenographic localization of the tumour. Following pneumonectomy he has survived with no discernible residual or metastatic tumour for 12 years. The morphologic changes in the resected lung provided a basis for discussing the preclinical phase of squamous cancer of the lung, the treatment of occult cancer and multicentric primary pulmonary tumours. The survey would have been more successful with a narrower target group and more frequent examination. Images FIG. 1 FIG. 2 FIG. 3 PMID:6299495

  14. [Photodynamic Therapy for Lung Cancer].

    PubMed

    Ohtani, Keishi; Ikeda, Norihiko

    2016-07-01

    In Japan, Photodynamic therapy (PDT) is recommended as a treatment option for centrally located early-stage lung cancers (CLELCs). It is a minimally invasive treatment with excellent anti-tumor effects. The 2nd generation photosensitizer, talaporfin sodium has strong anti-tumor effects with much less photosensitivity than porfimer sodium. Moreover, the laser equipment is compact and portable, and talaporfin sodium is now the current mainstay of PDT for lung cancer. For successful PDT, accurate evaluation of tumor extent and bronchial invasion is crucial. Detailed examination of the tumor using autofluorescence bronchoscopy and endobronchial ultrasonography or optical coherence tomography is extremely useful before PDT. At present, PDT has become the 1st choice of treatment for CLELC in institutions with the necessary equipment. It can also be effective for advanced lung cancer causing tracheobronchial obstruction. With such advances in PDT for CLELC, we are expanding the indications of PDT for not only CLELC, but also peripheral type lung cancer. PMID:27440036

  15. Lung Cancer Screening Recommendation Questioned.

    PubMed

    2016-06-01

    According to a retrospective analysis of data from the National Lung Screening Trial, participants with a history of heavy smoking who test negative for abnormalities suggestive of lung cancer on an initial low-dose CT screen may not need yearly CT scans. Instead, they could work with their doctors to devise an appropriate screening schedule based on individual risk factors. PMID:27076372

  16. Cisplatin treatment increases stemness through upregulation of hypoxia-inducible factors by interleukin-6 in non-small cell lung cancer.

    PubMed

    Zhang, Fuquan; Duan, Shanzhou; Tsai, Ying; Keng, Peter C; Chen, Yongbing; Lee, Soo Ok; Chen, Yuhchyau

    2016-06-01

    Cisplatin-resistant A549 and H157 (A549CisR and H157CisR) non-small cell lung cancer cells show increased stemness of cancer stem cells (CSCs) compared to their parental cells. We investigated whether interleukin-6 (IL-6) signaling contributes to this increased stemness in cisplatin-resistant cells. When A549CisR and H157CisR cells were treated with neutralizing IL-6 antibody, decreased cisplatin resistance was observed, whereas IL-6 treatment of parental cells resulted in increased cisplatin resistance. Expression of the CSC markers was significantly upregulated in IL-6-expressing scramble cells (in vitro) and scramble cell-derived tumor tissues (in vivo) after cisplatin treatment, but not in IL-6 knocked down (IL-6si) (in vitro) cells and in IL-6si cell-derived tumor tissues (in vivo), suggesting the importance of IL-6 signaling in triggering increased stemness during cisplatin resistance development. Hypoxia inducible factors (HIFs) were upregulated by IL-6 and responsible for the increased CSC stemness on cisplatin treatment. Mechanism dissection studies found that upregulation of HIFs by IL-6 was through transcriptional control and inhibition of HIF degradation. Treatment of HIF inhibitor (FM19G11) abolished the upregulation of CSC markers and increased sphere formations in IL-6 expressing cells on cisplatin treatment. In all, IL-6-mediated HIF upregulation is important in increasing stemness during cisplatin resistance development, and we suggest that the strategies of inhibiting IL-6 signaling or its downstream HIF molecules can be used as future therapeutic approaches to target CSCs after cisplatin treatment for lung cancer. PMID:27009878

  17. Lung Cancer and Hispanics: Know the Facts

    MedlinePlus

    ... other segments of the American population. However, lung cancer is still the leading cause of cancer death among Hispanic men and the second-leading cause among Hispanic women. November is Lung Cancer Awareness ...

  18. Cancer-Prone Mice Expressing the Ki-rasG12C Gene Show Increased Lung Carcinogenesis after CT Screening Exposures

    PubMed Central

    Munley, Michael T.; Moore, Joseph E.; Walb, Matthew C.; Isom, Scott P.; Olson, John D.; Zora, J. Gregory; Kock, Nancy D.; Wheeler, Kenneth T.; Miller, Mark Steven

    2011-01-01

    A >20-fold increase in X-ray computed tomography (CT) use during the last 30 years has caused considerable concern because of the potential carcinogenic risk from these CT exposures. Estimating the carcinogenic risk from high-energy, single high-dose exposures obtained from atomic bomb survivors and extrapolating these data to multiple low-energy, low-dose CT exposures using the Linear No-Threshold (LNT) model may not give an accurate assessment of actual cancer risk. Recently, the National Lung Cancer Screening Trial (NLST) reported that annual CT scans of current and former heavy smokers reduced lung cancer mortality by 20%, highlighting the need to better define the carcinogenic risk associated with these annual CT screening exposures. In this study, we used the bitransgenic CCSP-rtTA/Ki-ras mouse model that conditionally expresses the human mutant Ki-rasG12C gene in a doxycycline-inducible and lung-specific manner to measure the carcinogenic risk of exposure to multiple whole-body CT doses that approximate the annual NLST screening protocol. Irradiated mice expressing the Ki-rasG12C gene in their lungs had a significant (P = 0.01) 43% increase in the number of tumors/mouse (24.1 ± 1.9) compared to unirradiated mice (16.8 ± 1.3). Irradiated females had significantly (P < 0.005) more excess tumors than irradiated males. No tumor size difference or dose response was observed over the total dose range of 80–160 mGy for either sex. Irradiated bitransgenic mice that did not express the Ki-rasG12C gene had a low tumor incidence (≤0.1/mouse) that was not affected by exposure to CT radiation. These results suggest that (i) estimating the carcinogenic risk of multiple CT exposures from high-dose carcinogenesis data using the LNT model may be inappropriate for current and former smokers and (ii) any increased carcinogenic risk after exposure to fractionated low-dose CT-radiation may be restricted to only those individuals expressing cancer susceptibility genes in

  19. Silencing of tripartite motif (TRIM) 29 inhibits proliferation and invasion and increases chemosensitivity to cisplatin in human lung squamous cancer NCI-H520 cells

    PubMed Central

    Liu, Chunxiao; Huang, Xiaoxi; Hou, Shengcai; Hu, Bin; Li, Hui

    2015-01-01

    Background TRIM29 belongs to the tripartite motif (TRIM) protein family. It has been reported to be a tumor suppressor or have oncogenic function in many cancer types. The aim of this study was to investigate whether downregulation of TRIM29 by small interfering ribonucleic acid (siRNA) could inhibit cell proliferation and invasion and increase chemosensitivity to cisplatin in human lung squamous cancer NCI-H520 cells in vitro. Methods We transformed TRIM29 siRNA into NCI-H520 cells. Real time reverse transcriptase polymerase chain reaction and Western blotting assay were employed to determine TRIM29 messenger (m)RNA and protein expressions. MTT assay was used to determine the cell proliferation. Transwell invasion assay was used to determine the cell invasion. An Annexin V-propidium iodide (AnnV/PI) staining apoptosis test was used for detecting apoptosis. Results TRIM29 siRNA could specifically and efficiently suppress TRIM29 expression at both mRNA and protein levels. Silencing of the TRIM29 by siRNA in NCI-H520 cells inhibited cell proliferation and invasion in vitro. TRIM29 knockdown resulted in chemosensitivity enhancement in NCI-H520 cells. Conclusion Downregulation of TRIM29 can lead to potent antitumor activity and chemosensitizing effect in human lung squamous cancer NCI-H520 cells. PMID:26273332

  20. Mimulone-Induced Autophagy through p53-Mediated AMPK/mTOR Pathway Increases Caspase-Mediated Apoptotic Cell Death in A549 Human Lung Cancer Cells

    PubMed Central

    Lee, Ji-Won; Park, Mi-Hyun; Moon, Hyung-In; Park, Shin-Ji; Baik, Ji-Sue; Kim, Cheorl-Ho; Lee, Young-Choon

    2014-01-01

    Anticancer properties and mechanisms of mimulone (MML), C-geranylflavonoid isolated from the Paulownia tomentosa fruits, were firstly elucidated in this study. MML prevented cell proliferation in a dose- and time-dependent way and triggered apoptosis through the extrinsic pathway in A549 human lung adenocarcinoma cells. Furthermore, MML-treated cells displayed autophagic features, such as the formation of autophagic vacuoles, a primary morphological feature of autophagy, and the accumulation of microtubule-associated protein 1 light chain 3 (LC3) puncta, another typical maker of autophagy, as determined by FITC-conjugated immunostaining and monodansylcadaverine (MDC) staining, respectively. The expression levels of LC3-I and LC3-II, specific markers of autophagy, were also augmented by MML treatment. Autophagy inhibition by 3-methyladenine (3-MA), pharmacological autophagy inhibitor, and shRNA knockdown of Beclin-1 reduced apoptotic cell death induced by MML. Autophagic flux was not significantly affected by MML treatment and lysosomal inhibitor, chloroquine (CQ) suppressed MML-induced autophagy and apoptosis. MML-induced autophagy was promoted by decreases in p53 and p-mTOR levels and increase of p-AMPK. Moreover, inhibition of p53 transactivation by pifithrin-α (PFT-α) and knockdown of p53 enhanced induction of autophagy and finally promoted apoptotic cell death. Overall, the results demonstrate that autophagy contributes to the cytotoxicity of MML in cancer cells harboring wild-type p53. This study strongly suggests that MML is a potential candidate for an anticancer agent targeting both autophagy and apoptotic cell death in human lung cancer. Moreover, co-treatment of MML and p53 inhibitor would be more effective in human lung cancer therapy. PMID:25490748

  1. Mimulone-induced autophagy through p53-mediated AMPK/mTOR pathway increases caspase-mediated apoptotic cell death in A549 human lung cancer cells.

    PubMed

    An, Hyun-Kyu; Kim, Kyoung-Sook; Lee, Ji-Won; Park, Mi-Hyun; Moon, Hyung-In; Park, Shin-Ji; Baik, Ji-Sue; Kim, Cheorl-Ho; Lee, Young-Choon

    2014-01-01

    Anticancer properties and mechanisms of mimulone (MML), C-geranylflavonoid isolated from the Paulownia tomentosa fruits, were firstly elucidated in this study. MML prevented cell proliferation in a dose- and time-dependent way and triggered apoptosis through the extrinsic pathway in A549 human lung adenocarcinoma cells. Furthermore, MML-treated cells displayed autophagic features, such as the formation of autophagic vacuoles, a primary morphological feature of autophagy, and the accumulation of microtubule-associated protein 1 light chain 3 (LC3) puncta, another typical maker of autophagy, as determined by FITC-conjugated immunostaining and monodansylcadaverine (MDC) staining, respectively. The expression levels of LC3-I and LC3-II, specific markers of autophagy, were also augmented by MML treatment. Autophagy inhibition by 3-methyladenine (3-MA), pharmacological autophagy inhibitor, and shRNA knockdown of Beclin-1 reduced apoptotic cell death induced by MML. Autophagic flux was not significantly affected by MML treatment and lysosomal inhibitor, chloroquine (CQ) suppressed MML-induced autophagy and apoptosis. MML-induced autophagy was promoted by decreases in p53 and p-mTOR levels and increase of p-AMPK. Moreover, inhibition of p53 transactivation by pifithrin-α (PFT-α) and knockdown of p53 enhanced induction of autophagy and finally promoted apoptotic cell death. Overall, the results demonstrate that autophagy contributes to the cytotoxicity of MML in cancer cells harboring wild-type p53. This study strongly suggests that MML is a potential candidate for an anticancer agent targeting both autophagy and apoptotic cell death in human lung cancer. Moreover, co-treatment of MML and p53 inhibitor would be more effective in human lung cancer therapy. PMID:25490748

  2. Targeted Therapies in Lung Cancer

    PubMed Central

    Chirieac, Lucian R.; Dacic, Sanja

    2010-01-01

    An ongoing research and multiple clinical trials involve new targeted therapies and less aggressive treatment regimens that improve survival in patients with lung cancer. Targeted therapeutic agents are based on the concept of discovering genetic alterations and the signaling pathways altered in cancer and have added significantly to our armamentarium in order to prolong patient survival and minimizing drug toxicity. Among 34 molecularly targeted drugs approved by U.S. Food and Drug Administration (FDA) for treatment of various cancers since 1998 three targeted therapies have been approved for treatment of lung cancer (gefitinib in 2002, erlotinib in 2003, and bevacizumab in 2006). This review focuses on the targeted therapies in lung cancer, the molecular biomarkers that help identify patients that will benefit for these targeted therapies, describes the basic molecular biology principles and selected molecular diagnostic techniques and the pathological features correlated with molecular abnormalities in lung cancer. Lastly, new molecular abnormalities described in lung cancer that are predictive to novel promising targeted agents in various phases of clinical trials are discussed. PMID:20680095

  3. Non-small-cell lung cancer-induced immunosuppression by increased human regulatory T cells via Foxp3 promoter demethylation.

    PubMed

    Ke, Xing; Zhang, Shuping; Xu, Jian; Liu, Genyan; Zhang, Lixia; Xie, Erfu; Gao, Li; Li, Daqian; Sun, Ruihong; Wang, Fang; Pan, Shiyang

    2016-05-01

    Patients with non-small-cell lung cancer (NSCLC) have immune defects that are poorly understood. Forkhead box protein P3 (Foxp3) is crucial for immunosuppression by CD4(+) regulatory T cells (Tregs). It is not well known how NSCLC induces Foxp3 expression and causes immunosuppression in tumor-bearing patients. Our study found a higher percentage of CD4(+) Tregs in the peripheral blood of NSCLC compared with healthy donors. NSCLC patients showed demethylation of eight CpG sites within the Foxp3 promoter with methylation ratios negatively correlated with CD4(+)CD25(+)Foxp3(+) T levels. Foxp3 expression in CD4(+) Tregs was directly regulated by Foxp3 promoter demethylation and was involved in immunosuppression by NSCLC. To verify the effect of tumor cells on the phenotype and function of CD4(+) Tregs, we established a coculture system using NSCLC cell line and healthy CD4(+) T cells and showed that SPC-A1 induced IL-10 and TGF-β1 secretion by affecting the function of CD4(+) Tregs. The activity of DNA methyltransferases from CD4(+) T was decreased during this process. Furthermore, eight CpG sites within the Foxp3 promoter also appeared to have undergone demethylation. Foxp3 is highly expressed in CD4(+) T cells, and this may be caused by gene promoter demethylation. These induced Tregs are highly immunosuppressive and dramatically inhibit the proliferative activity of naïve CD4(+) T cells. Our study provides one possible mechanism describing Foxp3 promoter demethylation changes by which NSCLC down-regulates immune responses and contributes to tumor progression. Foxp3 represents an important target for NSCLC anti-tumor immunotherapy. PMID:27000869

  4. Lung cancer in pregnancy.

    PubMed

    Holzmann, Kornelia; Kropfmüller, Roland; Schinko, Herwig; Bogner, Stephan; Fellner, Franz; Arzt, Wolfgang; Lamprecht, Bernd

    2015-08-01

    In the 26th week of gestation, a 29-year-old pregnant office employee was referred to the pulmonary department of Linz General Hospital (AKH) under the suspicion of tuberculosis. She complained of a cough with intermittent hemoptysis and pain in the thoracic spine from which she had been suffering the past 9 weeks. A plain chest X-ray showed a dense infiltrate on the right side and multiple smaller shadows in both lungs. Laboratory testing revealed anemia, leukocytosis, and an increase of C-reactive protein. All tests for tuberculosis were negative.A bronchoscopy was performed and biopsies were taken from the right upper and middle lobe. The histopathological examination found cells of an adenocarcinoma. A magnetic resonance imaging (MRI) revealed a large tumor and surrounding atelectasis were seen in the right upper and middle lobe, as well as multiple intrapulmonary metastases in both lungs. In addition, not only metastases in the thoracic spine (level Th2/3) but also at other osseous locations and multiple cerebral metastases were detected. The patient received one cycle of chemotherapy consisting of docetaxel and carboplatin (AUC5) in the 27th week of gestation. Additional radiotherapy was applied to the involved thoracic spine. Due to positive epidermal growth factor receptor mutation, therapy with gefitinib 250 mg/day was started 2 days after a Caesarean section (preceded by treatment for fetal lung maturation). A healthy girl was delivered in the 30th week of pregnancy. Staging with computed tomography (CT) after delivery revealed an unstable fracture of Th2 with compression of the spinal cord. Neurosurgery was performed, consisting of a ventral corporectomy of Th1-2 followed by an anterior and posterior osteosynthesis for stabilization. The patient was discharged without neurological deficits within 1 week. Subsequent treatment with gefitinib improved the performance status of the patient, and CT scans of the chest and an MRI of the brain showed the size of

  5. Smoking Cessation Is Followed by Increases in Serum Bilirubin, an Endogenous Antioxidant Associated With Lower Risk of Lung Cancer and Cardiovascular Disease

    PubMed Central

    Wu, Ran; Mayne, Susan T.; Jatlow, Peter I.

    2014-01-01

    Introduction: Lower concentrations of serum bilirubin, an endogenous antioxidant, have been associated with risk of many smoking-related diseases, including lung cancer and cardiovascular disease, and current smokers are reported to have lower bilirubin levels than nonsmokers and past smokers. This study evaluates the effects of smoking cessation on bilirubin levels. Methods: In a secondary analysis of a 6-week placebo-controlled trial of naltrexone for smoking cessation, indirect and total bilirubin concentrations were evaluated at baseline and following smoking cessation. Individuals who were continuously abstinent for 6 weeks (n = 155) were compared to those who were not (n = 193). Participants reported smoking ≥20 cigarettes daily at baseline and received smoking cessation counseling, 21mg nicotine patch daily, and either placebo or 1 of 3 doses of naltrexone (25, 50, or 100mg) for 6 weeks. Change in indirect and total bilirubin following the quit date was measured at Weeks 1, 4, and 6 compared to baseline. Results: Individuals who were continuously abstinent from smoking, independent of naltrexone condition, showed a significantly greater mean increase in indirect (~unconjugated) bilirubin (0.06mg/dl, SD = 0.165) compared to those who did not (mean = 0.02, SD = 0.148, p = .015). Similar results were obtained for total bilirubin (p = .037). Conclusions: Smoking cessation is followed by increases in bilirubin concentration that have been associated with lower risk of lung cancer and cardiovascular disease. PMID:24812024

  6. Quality of Life in Patients Undergoing Radiation Therapy for Primary Lung Cancer, Head and Neck Cancer, or Gastrointestinal Cancer

    ClinicalTrials.gov

    2016-04-19

    Anal Cancer; Colorectal Cancer; Esophageal Cancer; Extrahepatic Bile Duct Cancer; Gallbladder Cancer; Gastric Cancer; Head and Neck Cancer; Liver Cancer; Lung Cancer; Pancreatic Cancer; Small Intestine Cancer

  7. Early detection of lung cancer

    PubMed Central

    Midthun, David E.

    2016-01-01

    Most patients with lung cancer are diagnosed when they present with symptoms, they have advanced stage disease, and curative treatment is no longer an option. An effective screening test has long been desired for early detection with the goal of reducing mortality from lung cancer. Sputum cytology, chest radiography, and computed tomography (CT) scan have been studied as potential screening tests. The National Lung Screening Trial (NLST) demonstrated a 20% reduction in mortality with low-dose CT (LDCT) screening, and guidelines now endorse annual LDCT for those at high risk. Implementation of screening is underway with the desire that the benefits be seen in clinical practice outside of a research study format. Concerns include management of false positives, cost, incidental findings, radiation exposure, and overdiagnosis. Studies continue to evaluate LDCT screening and use of biomarkers in risk assessment and diagnosis in attempt to further improve outcomes for patients with lung cancer. PMID:27158468

  8. Early detection of lung cancer.

    PubMed

    Midthun, David E

    2016-01-01

    Most patients with lung cancer are diagnosed when they present with symptoms, they have advanced stage disease, and curative treatment is no longer an option. An effective screening test has long been desired for early detection with the goal of reducing mortality from lung cancer. Sputum cytology, chest radiography, and computed tomography (CT) scan have been studied as potential screening tests. The National Lung Screening Trial (NLST) demonstrated a 20% reduction in mortality with low-dose CT (LDCT) screening, and guidelines now endorse annual LDCT for those at high risk. Implementation of screening is underway with the desire that the benefits be seen in clinical practice outside of a research study format. Concerns include management of false positives, cost, incidental findings, radiation exposure, and overdiagnosis. Studies continue to evaluate LDCT screening and use of biomarkers in risk assessment and diagnosis in attempt to further improve outcomes for patients with lung cancer. PMID:27158468

  9. Early diagnosis of lung cancer

    NASA Astrophysics Data System (ADS)

    Saccomanno, Geno; Bechtel, Joel J.

    1991-06-01

    Lung cancer remains the leading cause of death in the United States. Although the incidence of cigarette smoking is decreasing in the United States it appears to be increasing worldwide. The five-year survival rate has not improved in cases with advanced disease, but several articles have indicated that survival can be improved in cases diagnosed early by sputum cytology and chest x-ray. In cases diagnosed while the lesion is in the in-situ stage or measures less than 1 cm in diameter, surgical excision and/or radiation therapy improves survival; therefore, the early diagnosis of high-risk patients should be vigorously pursued. A recent study at a community hospital in Grand Junction, Colorado, presented 45 lung cancer cases diagnosed with positive sputum cytology and negative chest x-ray, and indicates that early diagnosis does improve survival. This study has been conducted during the past six years; 16 cases have survived three years and six cases show five-year survival.

  10. Carotenoids and lung cancer prevention

    Technology Transfer Automated Retrieval System (TEKTRAN)

    Understanding the molecular actions of carotenoids is critical for human studies involving carotenoids for prevention of lung cancer and cancers at other tissue sites. While the original hypothesis prompting the beta-carotene intervention trials was that beta-carotene exerts beneficial effects thro...

  11. CIGARETTE SMOKE AND LUNG CANCER

    EPA Science Inventory

    Cigarette smoke has been implicated in a causal relationship with carcinoma of the lung. An intriguing feature of the disease is the site-selectivity with which bronchogenic cancer manifests itself; most cancers are detected in the main, lobar and segmental bronchi, perhaps speci...

  12. Palliative Care in Lung Cancer.

    PubMed

    Shinde, Arvind M; Dashti, Azadeh

    2016-01-01

    Lung cancer is the most common cancer worldwide and is the leading cause of cancer death for both men and women in the USA. Symptom burden in patients with advanced lung cancer is very high and has a negative impact on their quality of life (QOL). Palliative care with its focus on the management of symptoms and addressing physical, psychosocial, spiritual, and existential suffering, as well as medically appropriate goal setting and open communication with patients and families, significantly adds to the quality of care received by advanced lung cancer patients. The Provisional Clinical Opinion (PCO) of American Society of Clinical Oncology (ASCO) as well as the National Cancer Care Network's (NCCN) clinical practice guidelines recommends early integration of palliative care into routine cancer care. In this chapter, we will provide an overview of palliative care in lung cancer and will examine the evidence and recommendations with regard to a comprehensive and interdisciplinary approach to symptom management, as well as discussions of goals of care, advance care planning, and care preferences. PMID:27535397

  13. Lung Cancer Risk Prediction Models

    Cancer.gov

    Developing statistical models that estimate the probability of developing lung cancer over a defined period of time will help clinicians identify individuals at higher risk of specific cancers, allowing for earlier or more frequent screening and counseling of behavioral changes to decrease risk.

  14. Epidemiology of Lung Cancer in Korea: Recent Trends

    PubMed Central

    Park, Ji Young

    2016-01-01

    Lung cancer causes the most cancer deaths in Korea. Although the smoking rate has begun to decrease, the prevalence of lung cancer is still increasing. We reviewed the national lung cancer registry data and the data published about lung cancer in Korea. In 2012, the crude incidence rate of lung cancer was 43.9 per 100,000. The age-standardized mortality rate of lung cancer was 19.8 per 100,000. The 5-year relative survival rate for lung cancer was 11.3% from 1993 to 1995 and increased to 21.9% in the period from 2008 to 2012. Lung cancer occurring in never-smokers was estimated to increase in Korea. Adenocarcinoma is steadily increasing in both women and men and has replaced squamous cell carcinoma as the most common type of lung cancer in Korea. In patients with adenocarcinoma, the frequency of EGFR mutations was 43% (range, 20%–56%), while that of the EMK4-ALK gene was less than 5%. PMID:27064578

  15. Impacts of Exercise on Prognostic Biomarkers in Lung Cancer Patients

    ClinicalTrials.gov

    2016-02-18

    Extensive Stage Small Cell Lung Cancer; Healthy, no Evidence of Disease; Limited Stage Small Cell Lung Cancer; Recurrent Non-small Cell Lung Cancer; Recurrent Small Cell Lung Cancer; Stage IA Non-small Cell Lung Cancer; Stage IB Non-small Cell Lung Cancer; Stage IIA Non-small Cell Lung Cancer; Stage IIB Non-small Cell Lung Cancer; Stage IIIA Non-small Cell Lung Cancer; Stage IIIB Non-small Cell Lung Cancer; Stage IV Non-small Cell Lung Cancer

  16. Molecular oncology of lung cancer.

    PubMed

    Toyooka, Shinichi; Mitsudomi, Tetsuya; Soh, Junichi; Aokage, Keiju; Yamane, Masaomi; Oto, Takahiro; Kiura, Katsuyuki; Miyoshi, Shinichiro

    2011-08-01

    Progress in genetic engineering has made it possible to elucidate the molecular biological abnormalities in lung cancer. Mutations in KRAS and P53 genes, loss of specific alleles, and DNA methylation of the tumor suppressor genes were the major abnormalities investigated between 1980 and the 2000s. In 2004, mutations in the epidermal growth factor receptor (EGFR) gene that cause oncogene addiction were discovered in non-small-cell lung cancers (NSCLCs), especially in adenocarcinomas. Because they are strongly associated with sensitivity to EGFR-tyrosine kinase inhibitors (EGFR-TKIs), a great deal of knowledge has been acquired in regard to both EGFR and other genes in the EGFR family and their downstream genes. Moreover, in 2007 the existence of the echinoderm microtubule-associated protein-like 4 (EML4)-anaplastic lymphoma kinase (ALK) fusion gene was discovered in NSCLC; and the same as EGFR-TKIs, ALK inhibitors are being found to be highly effective in lung cancers that have this translocation. These discoveries graphically illustrate that molecular biological findings are directly linked to the development of clinical oncology and to improving the survival rates of lung cancer patients. Here, we review the remarkable progress in molecular biological knowledge acquired thus far in regard to lung cancer, especially NSCLC, and the future possibilities. PMID:21850578

  17. Lung scintigraphy in differential diagnosis of peripheral lung cancer and community-acquired pneumonia

    NASA Astrophysics Data System (ADS)

    Krivonogov, Nikolay G.; Efimova, Nataliya Y.; Zavadovsky, Konstantin W.; Lishmanov, Yuri B.

    2016-08-01

    Ventilation/perfusion lung scintigraphy was performed in 39 patients with verified diagnosis of community-acquired pneumonia (CAP) and in 14 patients with peripheral lung cancer. Ventilation/perfusion ratio, apical-basal gradients of ventilation (U/L(V)) and lung perfusion (U/L(P)), and alveolar capillary permeability of radionuclide aerosol were determined based on scintigraphy data. The study demonstrated that main signs of CAP were increases in ventilation/perfusion ratio, perfusion and ventilation gradient on a side of the diseased lung, and two-side increase in alveolar capillary permeability rate for radionuclide aerosol. Unlike this, scintigraphic signs of peripheral lung cancer comprise an increase in ventilation/perfusion ratio over 1.0 on a side of the diseased lung with its simultaneous decrease on a contralateral side, normal values of perfusion and ventilation gradients of both lungs, and delayed alveolar capillary clearance in the diseased lung compared with the intact lung.

  18. Multidisciplinary lung cancer meetings: improving the practice of radiation oncology and facing future challenges.

    PubMed

    Campbell, Belinda A; Ball, David; Mornex, Françoise

    2015-02-01

    Clinical guidelines widely recognize the importance of multidisciplinary meetings (MDM) in the optimal care of lung cancer patients. The published literature suggest that dedicated Lung Cancer MDM lead to increased treatment utilization rates and improved survival outcomes for patients with lung cancer. For radiation oncologists, Lung Cancer MDM have been proven to support evidence-based practice and improve the utilization of radiotherapy. Lung Cancer MDM also allow for education and promotion of specialty radiotherapy services. The fast pace of modern medicine is also presenting new challenges for the multidisciplinary lung cancer team, and technological advances are likely to lead to new changes in the structure of traditional Lung Cancer MDM. PMID:25581058

  19. General Information about Small Cell Lung Cancer

    MedlinePlus

    ... Cell Lung Cancer Treatment (PDQ®)–Patient Version General Information About Small Cell Lung Cancer Go to Health ... the PDQ Adult Treatment Editorial Board . Clinical Trial Information A clinical trial is a study to answer ...

  20. Risk Profiling May Improve Lung Cancer Screening

    Cancer.gov

    A new modeling study suggests that individualized, risk-based selection of ever-smokers for lung cancer screening may prevent more lung cancer deaths and improve the effectiveness and efficiency of screening compared with current screening recommendations

  1. Increased MET Gene Copy Number but Not mRNA Level Predicts Postoperative Recurrence in Patients with Non–Small Cell Lung Cancer1

    PubMed Central

    Kowalczuk, Oksana; Kozlowski, Miroslaw; Niklinska, Wiesława; Kisluk, Joanna; Niklinska, Barbara Joanna; Niklinski, Jacek

    2014-01-01

    The aim of the present study was to investigate the relationship of MET copy number (CN) and MET mRNA expression to other molecular alterations, clinicopathologic characteristics, and survival of patients with resected non–small cell lung cancer. One hundred fifty-one paired surgical samples of tumor and tumor-distant normal lung tissues were analyzed by comparative quantitative polymerase chain reaction (PCR) methods with commercially available assays and the CopyCaller software v. 1.0 for post-PCR data processing (downloadable from www.appliedbiosystems.com). MET copy gain (set as more than 3.0 copies per cell) was found in 18.5% of the samples and occurred more frequently in the adenocarcinomas (ADCs) with an increased epidermal growth factor receptor (EGFR) or human epidermal growth factor receptor 2 (HER2) CN (P = .001 and .030 for EGFR and HER2, respectively) and in the ADCs with EGFR activating mutations (P = .051) but did not correlate with KRAS dosage or mutational status. MET mRNA level was 1.76-fold higher [95% confidence interval (CI), 1.29-2.40] in the tumor compared to unaffected lung tissue and associated significantly with MET CN (beta coefficient, 1.51; 95% CI, 1.22-1.87; P < .001). In the multivariable analysis, patients diagnosed with ADC with increased MET CN had a significantly higher risk of disease recurrence (hazard ratio, 1.76; 95% CI, 1.20-2.57; P = .004). An increased MET CN in combination with histologic type appears to be a prognostic factor in patients with ADC after a curative surgery. PMID:25389455

  2. Tobacco Smoking and Lung Cancer

    PubMed Central

    Furrukh, Muhammad

    2013-01-01

    Tobacco smoking remains the most established cause of lung carcinogenesis and other disease processes. Over the last 50 years, tobacco refinement and the introduction of filters have brought a change in histology, and now adenocarcinoma has become the most prevalent subtype. Over the last decade, smoking also has emerged as a strong prognostic and predictive patient characteristic along with other variables. This article briefly reviews scientific facts about tobacco, and the process and molecular pathways involved in lung carcinogenesis in smokers and never-smokers. The evidence from randomised trials about tobacco smoking’s impact on lung cancer outcomes is also reviewed. PMID:23984018

  3. Lung cancer among women in north-east China.

    PubMed Central

    Wu-Williams, A. H.; Dai, X. D.; Blot, W.; Xu, Z. Y.; Sun, X. W.; Xiao, H. P.; Stone, B. J.; Yu, S. F.; Feng, Y. P.; Ershow, A. G.

    1990-01-01

    A case-control study of lung cancer involving interviews with 965 female patients and 959 controls in Shenyang and Harbin, two industrial cities which have among the highest rates of lung cancer in China, revealed that cigarette smoking is the main causal factor and accounted for about 35% of the tumours among women. Although the amount smoked was low (the cases averaged eight cigarettes per day), the percentage of smokers among women over age 50 in these cities was nearly double the national average. Air pollution from coal burning stoves was implicated, as risks of lung cancer increased in proportion to years of exposure to 'Kang' and other heating devices indigenous to the region. In addition, the number of meals cooked by deep frying and the frequency of smokiness during cooking were associated with risk of lung cancer. More cases than controls reported workplace exposures to coal dust and to smoke from burning fuel. Elevated risks were observed for smelter workers and decreased risks for textile workers. Prior chronic bronchitis/emphysema, pneumonia, and recent tuberculosis contributed significantly to lung cancer risk, as did a history of tuberculosis and lung cancer in family members. Higher intake of carotene-rich vegetables was not protective against lung cancer in this population. The findings were qualitatively similar across the major cell types of lung cancer, except that the associations with smoking and previous lung diseases were stronger for squamous/oat cell cancers than for adenocarcinoma of the lung. PMID:2257230

  4. Mitochondrial DNA Content and Lung Cancer Risk

    PubMed Central

    Bonner, Matthew R.; Shen, Min; Liu, Chin-San; DiVita, Margaret; He, Xingzhou; Lan, Qing

    2010-01-01

    Smoky coal contains polycyclic aromatic hydrocarbons (PAHs) and has been strongly implicated in etiology of lung cancer in Xuan Wei, China. While PAHs have been demonstrated to form bulky adducts in nuclear DNA, they have a 90-fold greater affinity for mitochondrial DNA (mtDNA). To compensate for mitochondrial dysfunction or damage, mtDNA content is thought to increase. We conducted a population-based case-control study of lung cancer in Xuan Wei, China hypothesizing that mtDNA content is associated with lung cancer risk. Cases (n = 122) and controls (n = 121) were individually matched on age (±2yrs), sex, village of residence, and type of heating/cooking fuel currently used. Lifetime smoky coal use and potential confounders were determined with questionnaires. mtDNA was extracted from sputum and content was determined with quantitative RT-PCR. Odds ratios (OR) and 95% confidence intervals (95% CI) were calculated with unconditional logistic regression. mtDNA content was dichotomized at the median based on the distribution among the controls. mtDNA content > 157 was associated with a 2-fold increase in lung cancer risk (OR = 1.8; 95% CI = 1.0–3.2) compared with those with ≤157 copies. Risk was higher among those >57 years of age compared with those ≤ 57 years (p interaction = 0.01). In summary, mtDNA content was positively associated with lung cancer risk. Furthermore, there was some evidence that mtDNA content was more strongly associated with lung cancer risk among older individuals. However, due to the small sample size, additional studies are needed to evaluate these associations. PMID:18691788

  5. Increased Expression of TGFβR2 Is Associated with the Clinical Outcome of Non-Small Cell Lung Cancer Patients Treated with Chemotherapy

    PubMed Central

    Yu, Fei; Cai, Haidong; Fang, Suyun; Cai, Li; Yang, Huiqiong; Sun, Yu; Li, Dan; Liu, Jin; Xie, Ruting; Yuan, Xueyu; Zhong, Xiaoming; Li, Ming; Wei, Qing; Lv, Zhongwei; Fu, Da; Ma, Yushui

    2015-01-01

    To investigate the prognostic significance of TGFβR2 expression and chemotherapy in Chinese non-small cell lung cancer (NSCLC) patients, TGFβR2 expression NSCLC was analyzed in silico using the Oncomine database, and subsequently analyzed with quantitative RT-PCR in 308 NSCLC biopsies, 42 of which were paired with adjacent non-neoplastic tissues. Our results show that TGFβR2 expression was also increased in NSCLC biopsies relative to normal tissue samples and correlated with poor prognosis. TGFβR2 expression was also significantly correlated with other clinical parameters such as tumor differentiation, invasion of lung membrane, and chemotherapy. Moreover, overall survival (OS) and disease free survival (DFS) was increased in patients with low TGFβR2 expressing NSCLC and who had undergone chemotherapy. Thus, high expression of TGFβR2 is a significant risk factor for decreased OS and DFS in NSCLC patients. Thus, TGFβR2 is a potential prognostic tumor biomarker for chemotherapy. PMID:26252213

  6. Lung cancer molecular epidemiology in China: recent trends

    PubMed Central

    2014-01-01

    Lung cancer is both the most common diagnosed cancer and the leading cause of cancer related deaths in China. During the past three decades, the incidence and mortality of lung cancer in China are increasing rapidly. According to data from National Central Cancer Registry (NCCR) in 2010, the crude incidence of lung cancer in China was 46.08 per 100,000 population (61.86 per 100,000 men and 29.54 per 100,000 women), with an estimated over 600,000 new diagnosed lung cancer patients (416,333 males and 189,613 females). Meanwhile, the crude mortality of lung cancer in China was 37.00 per 100,000 population (50.04 per 100,000 men and 23.33 per 100,000 women). Consistent with the change in developed countries, adenocarcinoma has become the most predominant histological subtype of lung cancer in China. For the majority advanced non-small-cell lung cancer (NSCLC) patients, especially patients with adenocarcinoma, targeted therapy became increasing important in the treatment. Chinese researcher have done a lot work in terms of lung cancer molecular epidemiology, therefore, in this review, we further summarized the epidemiology of driver genes in NSCLC, hoping to help clinicians to better screen certain driver genes in China for treatment decisions. PMID:25806311

  7. Mouse models for lung cancer.

    PubMed

    Kwon, Min-chul; Berns, Anton

    2013-04-01

    Lung cancer is a devastating disease and a major therapeutic burden with poor survival rates. It is responsible for 30% of all cancer deaths. Lung cancer is strongly associated with smoking, although some subtypes are also seen in non-smokers. Tumors in the latter group are mostly adenocarcinomas with many carrying mutations in the epidermal growth factor receptor (EGFR). Survival statistics of lung cancer are grim because of its late detection and frequent local and distal metastases. Although DNA sequence information from tumors has revealed a number of frequently occurring mutations, affecting well-known tumor suppressor genes and proto-oncogenes, many of the driver mutations remain ill defined. This is likely due to the involvement of numerous rather infrequently occurring driver mutations that are difficult to distinguish from the very large number of passenger mutations detected in smoking-related lung cancers. Therefore, experimental model systems are indispensable to validate putative driver lesions and to gain insight into their mechanisms of action. Whereas a large fraction of these analyzes can be performed in cell cultures in vitro, in many cases the consequences of the mutations have to be assessed in the context of an intact organism, as this is the context in which the Mendelian selection process of the tumorigenic process took place and the advantages of particular mutations become apparent. Current mouse models for cancer are very suitable for this as they permit mimicking many of the salient features of human tumors. The capacity to swiftly re-engineer complex sets of lesions found in human tumors in mice enables us to assess the contribution of defined combinations of lesions to distinct tumor characteristics such as metastatic behavior and response to therapy. In this review we will describe mouse models of lung cancer and how they are used to better understand the disease and how they are exploited to develop better intervention strategies

  8. Blockade of Hedgehog Signaling Synergistically Increases Sensitivity to Epidermal Growth Factor Receptor Tyrosine Kinase Inhibitors in Non-Small-Cell Lung Cancer Cell Lines

    PubMed Central

    Bai, Xiao-Yan; Zhang, Xu-Chao; Yang, Su-Qing; An, She-Juan; Chen, Zhi-Hong; Su, Jian; Xie, Zhi; Gou, Lan-Ying; Wu, Yi-Long

    2016-01-01

    Aberrant activation of the hedgehog (Hh) signaling pathway has been implicated in the epithelial-to-mesenchymal transition (EMT) and cancer stem-like cell (CSC) maintenance; both processes can result in tumor progression and treatment resistance in several types of human cancer. Hh cooperates with the epidermal growth factor receptor (EGFR) signaling pathway in embryogenesis. We found that the Hh signaling pathway was silenced in EGFR-TKI-sensitive non-small-cell lung cancer (NSCLC) cells, while it was inappropriately activated in EGFR-TKI-resistant NSCLC cells, accompanied by EMT induction and ABCG2 overexpression. Upregulation of Hh signaling through extrinsic SHH exposure downregulated E-cadherin expression and elevated Snail and ABCG2 expression, resulting in gefitinib tolerance (P < 0.001) in EGFR-TKI-sensitive cells. Blockade of the Hh signaling pathway using the SMO antagonist SANT-1 restored E-cadherin expression and downregulate Snail and ABCG2 in EGFR-TKI-resistant cells. A combination of SANT-1 and gefitinib markedly inhibited tumorigenesis and proliferation in EGFR-TKI-resistant cells (P < 0.001). These findings indicate that hyperactivity of Hh signaling resulted in EGFR-TKI resistance, by EMT introduction and ABCG2 upregulation, and blockade of Hh signaling synergistically increased sensitivity to EGFR-TKIs in primary and secondary resistant NSCLC cells. E-cadherin expression may be a potential biomarker of the suitability of the combined application of an Hh inhibitor and EGFR-TKIs in EGFR-TKI-resistant NSCLCs. PMID:26943330

  9. Blockade of Hedgehog Signaling Synergistically Increases Sensitivity to Epidermal Growth Factor Receptor Tyrosine Kinase Inhibitors in Non-Small-Cell Lung Cancer Cell Lines.

    PubMed

    Bai, Xiao-Yan; Zhang, Xu-Chao; Yang, Su-Qing; An, She-Juan; Chen, Zhi-Hong; Su, Jian; Xie, Zhi; Gou, Lan-Ying; Wu, Yi-Long

    2016-01-01

    Aberrant activation of the hedgehog (Hh) signaling pathway has been implicated in the epithelial-to-mesenchymal transition (EMT) and cancer stem-like cell (CSC) maintenance; both processes can result in tumor progression and treatment resistance in several types of human cancer. Hh cooperates with the epidermal growth factor receptor (EGFR) signaling pathway in embryogenesis. We found that the Hh signaling pathway was silenced in EGFR-TKI-sensitive non-small-cell lung cancer (NSCLC) cells, while it was inappropriately activated in EGFR-TKI-resistant NSCLC cells, accompanied by EMT induction and ABCG2 overexpression. Upregulation of Hh signaling through extrinsic SHH exposure downregulated E-cadherin expression and elevated Snail and ABCG2 expression, resulting in gefitinib tolerance (P < 0.001) in EGFR-TKI-sensitive cells. Blockade of the Hh signaling pathway using the SMO antagonist SANT-1 restored E-cadherin expression and downregulate Snail and ABCG2 in EGFR-TKI-resistant cells. A combination of SANT-1 and gefitinib markedly inhibited tumorigenesis and proliferation in EGFR-TKI-resistant cells (P < 0.001). These findings indicate that hyperactivity of Hh signaling resulted in EGFR-TKI resistance, by EMT introduction and ABCG2 upregulation, and blockade of Hh signaling synergistically increased sensitivity to EGFR-TKIs in primary and secondary resistant NSCLC cells. E-cadherin expression may be a potential biomarker of the suitability of the combined application of an Hh inhibitor and EGFR-TKIs in EGFR-TKI-resistant NSCLCs. PMID:26943330

  10. The relationship between COPD and lung cancer

    PubMed Central

    Durham, A.L.; Adcock, I.M.

    2015-01-01

    Both COPD and lung cancer are major worldwide health concerns owing to cigarette smoking, and represent a huge, worldwide, preventable disease burden. Whilst the majority of smokers will not develop either COPD or lung cancer, they are closely related diseases, occurring as co-morbidities at a higher rate than if they were independently triggered by smoking. Lung cancer and COPD may be different aspects of the same disease, with the same underlying predispositions, whether this is an underlying genetic predisposition, telomere shortening, mitochondrial dysfunction or premature aging. In the majority of smokers, the burden of smoking may be dealt with by the body’s defense mechanisms: anti-oxidants such as superoxide dismutases, anti-proteases and DNA repair mechanisms. However, in the case of both diseases these fail, leading to cancer if mutations occur or COPD if damage to the cell and proteins becomes too great. Alternatively COPD could be a driving factor in lung cancer, by increasing oxidative stress and the resulting DNA damage, chronic exposure to pro-inflammatory cytokines, repression of the DNA repair mechanisms and increased cellular proliferation. Understanding the mechanisms that drive these processes in primary cells from patients with these diseases along with better disease models is essential for the development of new treatments. PMID:26363803

  11. Lung cancer screening in patients with chronic obstructive pulmonary disease.

    PubMed

    Gonzalez, Jessica; Marín, Marta; Sánchez-Salcedo, Pablo; Zulueta, Javier J

    2016-04-01

    Lung cancer and chronic obstructive pulmonary disease (COPD) are two intimately related diseases, with great impact on public health. Annual screening using low-dose computed tomography (LDCT) of the chest significantly reduces mortality due to lung cancer, and several scientific societies now recommend this technique. COPD, defined by the presence of airflow obstruction [forced expiratory volume and forced vital capacity (FVC) ratio less than 0.70], and their clinical phenotypes, namely emphysema and chronic bronchitis, have been associated with increased lung cancer risk. Several epidemiological studies, including lung cancer screening trials, have found a 2- to 4-fold increase in lung cancer risk in patients with COPD when compared to individuals without airflow obstruction. Part of the risk attributed to airflow obstruction appears to be derived from the presence of radiographic emphysema. The latter has proven to be an important lung cancer risk factor in smokers without airflow obstruction and even in never smokers. This evidence supports the idea of including patients with COPD and/or emphysema in lung cancer screening programs. There is evidence that lung cancer screening in this population is effective and can potentially reduce mortality. Specific lung cancer risk scores have been developed for patients with COPD [COPD lung cancer screening score (LUCSS) and COPD-LUCSS-diffusing capacity for carbon monoxide (DLCO)] to identify those at high risk. A multidisciplinary approach for an adequate patient selection, especially of patients with severe disease, is key to maximize benefits and reduce harms from lung cancer screening in this population. Patients with COPD included in lung cancer screening programs could also benefit from other interventions, such as smoking cessation and adequate treatment. PMID:27195278

  12. Lung cancer screening in patients with chronic obstructive pulmonary disease

    PubMed Central

    Gonzalez, Jessica; Marín, Marta; Sánchez-Salcedo, Pablo

    2016-01-01

    Lung cancer and chronic obstructive pulmonary disease (COPD) are two intimately related diseases, with great impact on public health. Annual screening using low-dose computed tomography (LDCT) of the chest significantly reduces mortality due to lung cancer, and several scientific societies now recommend this technique. COPD, defined by the presence of airflow obstruction [forced expiratory volume and forced vital capacity (FVC) ratio less than 0.70], and their clinical phenotypes, namely emphysema and chronic bronchitis, have been associated with increased lung cancer risk. Several epidemiological studies, including lung cancer screening trials, have found a 2- to 4-fold increase in lung cancer risk in patients with COPD when compared to individuals without airflow obstruction. Part of the risk attributed to airflow obstruction appears to be derived from the presence of radiographic emphysema. The latter has proven to be an important lung cancer risk factor in smokers without airflow obstruction and even in never smokers. This evidence supports the idea of including patients with COPD and/or emphysema in lung cancer screening programs. There is evidence that lung cancer screening in this population is effective and can potentially reduce mortality. Specific lung cancer risk scores have been developed for patients with COPD [COPD lung cancer screening score (LUCSS) and COPD-LUCSS-diffusing capacity for carbon monoxide (DLCO)] to identify those at high risk. A multidisciplinary approach for an adequate patient selection, especially of patients with severe disease, is key to maximize benefits and reduce harms from lung cancer screening in this population. Patients with COPD included in lung cancer screening programs could also benefit from other interventions, such as smoking cessation and adequate treatment. PMID:27195278

  13. Dichloroacetate alters Warburg metabolism, inhibits cell growth, and increases the X-ray sensitivity of human A549 and H1299 NSC lung cancer cells.

    PubMed

    Allen, Kah Tan; Chin-Sinex, Helen; DeLuca, Thomas; Pomerening, Joseph R; Sherer, Jeremy; Watkins, John B; Foley, John; Jesseph, Jerry M; Mendonca, Marc S

    2015-12-01

    We investigated whether altering Warburg metabolism (aerobic glycolysis) by treatment with the metabolic agent dichloroacetate (DCA) could increase the X-ray-induced cell killing of the radiation-resistant human non-small-cell lung cancer (NSCLC) cell lines A549 and H1299. Treatment with 50mM DCA decreased lactate production and glucose consumption in both A549 and H1299, clear indications of attenuated aerobic glycolysis. In addition, we found that DCA treatment also slowed cell growth, increased population-doubling time, and altered cell cycle distribution. Furthermore, we report that treatment with 50mM DCA significantly increased single and fractionated X-ray-induced cell killing of A549 and H1299 cells. Assay of DNA double-strand break repair by neutral comet assays demonstrated that DCA inhibited both the fast and the slow kinetics of X-ray-induced DSB repair in both A549 and H1299 NSCL cancer cells. Taken together the data suggest a correlation between an attenuated aerobic glycolysis and enhanced cytotoxicity and radiation-induced cell killing in radiation-resistant NSCLC cells. PMID:26393423

  14. Molecular pathways and therapeutic targets in lung cancer

    PubMed Central

    Shtivelman, Emma; Hensing, Thomas; Simon, George R.; Dennis, Phillip A.; Otterson, Gregory A.; Bueno, Raphael; Salgia, Ravi

    2014-01-01

    Lung cancer is still the leading cause of cancer death worldwide. Both histologically and molecularly lung cancer is heterogeneous. This review summarizes the current knowledge of the pathways involved in the various types of lung cancer with an emphasis on the clinical implications of the increasing number of actionable molecular targets. It describes the major pathways and molecular alterations implicated in the development and progression of non-small cell lung cancer (adenocarcinoma and squamous cancer), and of small cell carcinoma, emphasizing the molecular alterations comprising the specific blueprints in each group. The approved and investigational targeted therapies as well as the immune therapies, and clinical trials exploring the variety of targeted approaches to treatment of lung cancer are the main focus of this review. PMID:24722523

  15. Occupation, Gender, Race, and Lung Cancer

    PubMed Central

    Amr, Sania; Wolpert, Beverly; Loffredo, Christopher A.; Zheng, Yun-Ling; Shields, Peter G.; Jones, Raymond; Harris, Curtis C.

    2008-01-01

    Objective To examine associations between occupation and lung cancer by gender and race. Methods We used data from the Maryland Lung Cancer Study of nonsmall cell lung carcinoma (NSCLC), a multicenter case control study, to estimate odds ratios (ORs) of NSCLC in different occupations. Results After adjusting for smoking, environmental tobacco smoke, and other covariates, NSCLC ORs among women but not men were elevated in clerical-sales, service, and transportation-material handling occupations; ORs were significantly increased in all three categories (OR [95% confidence interval]: 4.07 [1.44 to 11.48]; 5.15 [1.62 to 16.34]; 7.82 [1.08 to 56.25], respectively), among black women, but only in transportation-material handling occupations (OR [95% confidence interval[: 3.43 [1.02 to 11.50]) among white women. Conclusions Women, especially black women, in certain occupations had increased NSCLC ORs. PMID:18849762

  16. Circulating tumor cells in lung cancer.

    PubMed

    Young, Rachel; Pailler, Emma; Billiot, Fanny; Drusch, Françoise; Barthelemy, Amélie; Oulhen, Marianne; Besse, Benjamin; Soria, Jean-Charles; Farace, Françoise; Vielh, Philippe

    2012-01-01

    Circulating tumor cells (CTCs) have emerged as potential biomarkers in several cancers such as colon, prostate, and breast carcinomas, with a correlation between CTC number and patient prognosis being established by independent research groups. The detection and enumeration of CTCs, however, is still a developing field, with no universal method of detection suitable for all types of cancer. CTC detection in lung cancer in particular has proven difficult to perform, as CTCs in this type of cancer often present with nonepithelial characteristics. Moreover, as many detection methods rely on the use of epithelial markers to identify CTCs, the loss of these markers during epithelial-to-mesenchymal transition in certain metastatic cancers can render these methods ineffective. The development of personalized medicine has led to an increase in the advancement of molecular characterization of CTCs. The application of techniques such as FISH and RT-PCR to detect EGFR, HER2, and KRAS abnormalities in lung, breast, and colon cancer, for example, could be used to characterize CTCs in real time. The use of CTCs as a 'liquid biopsy' is therefore an exciting possibility providing information on patient prognosis and treatment efficacy. This review summarizes the state of CTC detection today, with particular emphasis on lung cancer, and discusses the future applications of CTCs in helping the clinician to develop new strategies in patient treatment. PMID:23207444

  17. Atmospheric pollution and lung cancer.

    PubMed Central

    Doll, R

    1978-01-01

    Lung cancer is consistently more common in urban areas than in rural. The excess cannot be accounted for by specific occupational hazards but some of it might be due to the presence of carcinogens in urban air. The excess cannot be wholly due to such agents, because the excess in nonsmokers is small and variable. Cigarette consumption has also been greater in urban areas, but it is difficult to estimate how much of the excess it can account for. Occupational studies confirm that pollutants present in town air are capable of causing lung cancer in man and suggest that the pollutants and cigarette smoke act synergistically. The trends in the mortality from lung cancer in young and middle-aged men in England and Wales provide uncertain evidence but support the belief that atmospheric pollution has contributed to the production of the disease. In the absence of cigarette smoking, the combined effect of all atmospheric carcinogens is not responsible for more than about 5 cases of lung cancer per 100,000 persons per year in European populations. PMID:648488

  18. Lung Cancer Staging and Prognosis.

    PubMed

    Woodard, Gavitt A; Jones, Kirk D; Jablons, David M

    2016-01-01

    The seventh edition of the non-small cell lung cancer (NSCLC) TNM staging system was developed by the International Association for the Staging of Lung Cancer (IASLC) Lung Cancer Staging Project by a coordinated international effort to develop data-derived TNM classifications with significant survival differences. Based on these TNM groupings, current 5-year survival estimates in NSLCC range from 73 % in stage IA disease to 13 % in stage IV disease. TNM stage remains the most important prognostic factor in predicting recurrence rates and survival times, followed by tumor histologic grade, and patient sex, age, and performance status. Molecular prognostication in lung cancer is an exploding area of research where interest has moved beyond TNM stage and into individualized genetic tumor analysis with immunohistochemistry, microarray, and mutation profiles. However, despite intense research efforts and countless publications, no molecular prognostic marker has been adopted into clinical use since most fail in subsequent cross-validation with few exceptions. The recent interest in immunotherapy for NSCLC has identified new biomarkers with early evidence that suggests that PD-L1 is a predictive marker of a good response to new immunotherapy drugs but a poor prognostic indicator of overall survival. Future prognostication of outcomes in NSCLC will likely be based on a combination of TNM stage and molecular tumor profiling and yield more precise, individualized survival estimates and treatment algorithms. PMID:27535389

  19. Increased 18F-FDG uptake within the reticuloendothelial system in patients with active lung cancer on PET imaging may indicate activation of the systemic immune response.

    PubMed

    Bural, Gonca G; Torigian, Drew A; Chen, Wengen; Houseni, Mohamed; Basu, Sandip; Alavi, Abass

    2010-01-01

    The reticuloendothelial system (RES) cells are in the defense against certain pathogens, and in the removal of dying cells, cell debris, microorganisms, and malignant cells. Liver, spleen, and bone marrow represent the major organs with high RES activity. We hypothesized that in subjects with active lung cancer, the metabolic activity of these organs would be greater than that of the subjects with no active tumor. We have studied two groups of subjects who had undergone (18)F-FDG-PET imaging for clinical purposes. The first group consisted of 39 subjects (20 women, 19 men, mean age 64.8+/-10.2 years) with benign lung nodules as demonstrated by (18)F-FDG-PET imaging. The second group consisted of 30 subjects (18 women, 12 men; mean age 65.1+/-11 years) who were known to have active lung cancer with or without distant metastases as seen on (18)F-FDG-PET imaging. The subjects in the second group did not have any evidence of liver, spleen, bone marrow, or heart involvement on (18)F-FDG-PET images. We measured the mean SUV of the liver, spleen, bone marrow, heart, and of the contralateral unaffected lung, and compared the average SUV for these organs between the two groups. We found that the mean SUV of the liver, bone marrow, and spleen were significantly greater in subjects with evidence of active primary or metastatic lung cancer compared with those of subjects who had benign lung nodules and no evidence of active malignant disease. There was a statistically significant difference between mean SUV for organs noted above between the two groups (P<0.05). In contrast, mean SUV for the heart and contralateral normal lung did not show any significant difference between the two groups. In conclusion, the mean SUV for the major organs of RES, liver, spleen, and bone marrow were higher in subjects with active lung cancer with or without metastases than in those without active malignancy. We believe these differences in SUV may indicate a differential activation of the

  20. Guidance molecules in lung cancer

    PubMed Central

    Nasarre, Patrick; Potiron, Vincent; Drabkin, Harry

    2010-01-01

    Guidance molecules were first described in the nervous system to control axon outgrowth direction. They are also widely expressed outside the nervous system where they control cell migration, tissue development and establishment of the vascular network. In addition, they are involved in cancer development, tumor angiogenesis and metastasis. This review is primarily focused on their functions in lung cancer and their involvement in lung development is also presented. Five guidance molecule families and their corresponding receptors are described, including the semaphorins/neuropilins/plexins, ephrins and Eph receptors, netrin/DCC/UNC5, Slit/Robo and Notch/Delta. In addition, the possibility to target these molecules as a therapeutic approach in cancer is discussed. PMID:20139699

  1. A Novel Bioluminescence Orthotopic Mouse Model for Advanced Lung Cancer

    PubMed Central

    Li, Bo; Torossian, Artour; Li, Wenyan; Schleicher, Stephen; Niu, Kathy; Giacalone, Nicholas J.; Kim, Sung June; Chen, Heidi; Gonzalez, Adriana; Moretti, Luigi; Lu, Bo

    2011-01-01

    Lung cancer is the leading cause of cancer-related death in the United States despite recent advances in our understanding of this challenging disease. An animal model for high-throughput screening of therapeutic agents for advanced lung cancer could help promote the development of more successful treatment interventions. To develop our orthotopic lung cancer model, luciferase-expressing A549 cancer cells were injected into the mediastinum of athymic nude mice. To determine whether the model would allow easy monitoring of response to therapeutic interventions, tumors were treated with 30 mg/kg Paclitaxel or were irradiated with 5 fractions of 2 Gy, and tumor burden was monitored using bioluminescence imaging. Evidence of radiation-induced lung injury was assessed using immunohistochemical staining for phospho-Smad2/3 and cleaved caspase-3. We found that tumor implantation recapitulated advanced human lung cancer as evidenced by tumor establishment and proliferation within the mediastinum. The tumor responded to Paclitaxel or radiation as shown by decreased tumor bioluminescence and improved overall survival. Immunohistochemistry revealed increased phospho-Smad2/3 and cleaved caspase-3 in irradiated lungs, consistent with radiation-induced lung injury. This orthotopic lung cancer model may help provide a method to assess therapeutic interventions in a preclinical setting that recapitulates locally advanced lung cancer. PMID:21663394

  2. Lung cancer treatment outcomes in recipients of lung transplant

    PubMed Central

    Du, Lingling; Pennell, Nathan A.; Elson, Paul

    2015-01-01

    Background Lung transplant recipients develop lung cancer more commonly than the general population. The best treatment approach for these patients is unclear. The goal of this study is to evaluate treatment outcomes in this population. Methods We used the Cleveland Clinic lung transplant database to identify patients diagnosed with lung cancer at the time of or after lung transplant. Transplant and lung cancer-related data were retrospectively reviewed. Results Among 847 patients underwent lung transplant between 2005 and 2013, 17 (2%) were diagnosed with lung cancer and included. Median age was 61 (range, 48–70) years. Majority were stage I/II (n=11), one had stage IIIA, five had stage IV. Non-small cell lung cancer (NSCLC) were more common than small cell lung cancer (SCLC) (n=15 vs. 2). Curative treatment was performed as lobectomy in native lung (n=1), and radiation in transplanted lung (n=2). Chemotherapy was given in 10 patients, primarily carboplatin-based doublets with docetaxel, pemetrexed, or etoposide. Six of these received palliative chemotherapy for either metastases at diagnosis (n=3) or recurrence after early stage disease (n=3). Except for one patient with complete response, all others had progressive disease following palliative chemotherapy. Overall, patients who received chemotherapy had a median survival of 7.5 months from the initiation of chemotherapy, but 30% developed grade 5 sepsis. Median survival for stage I–IIIA and stage IV were 23.2 and 2.5 months respectively. Conclusions Lung cancer in lung transplant recipients carries various clinical courses. Patients with metastatic disease have substantial toxicities from chemotherapy and poor survival. Early stage patients should be offered treatment with modified dosages to decrease the risk of severe toxicities. PMID:26798588

  3. Treatment Options by Stage (Small Cell Lung Cancer)

    MedlinePlus

    ... Cancer Prevention Lung Cancer Screening Research Small Cell Lung Cancer Treatment (PDQ®)–Patient Version General Information About Small Cell Lung Cancer Go to Health Professional Version Key Points ...

  4. LKB1/KRAS mutant lung cancers constitute a genetic subset of NSCLC with increased sensitivity to MAPK and mTOR signalling inhibition

    PubMed Central

    Mahoney, C L; Choudhury, B; Davies, H; Edkins, S; Greenman, C; Haaften, G van; Mironenko, T; Santarius, T; Stevens, C; Stratton, M R; Futreal, P A

    2009-01-01

    LKB1/STK11 is a multitasking tumour suppressor kinase. Germline inactivating mutations of the gene are responsible for the Peutz-Jeghers hereditary cancer syndrome. It is also somatically inactivated in approximately 30% of non-small-cell lung cancer (NSCLC). Here, we report that LKB1/KRAS mutant NSCLC cell lines are sensitive to the MEK inhibitor CI-1040 shown by a dose-dependent reduction in proliferation rate, whereas LKB1 and KRAS mutations alone do not confer similar sensitivity. We show that this subset of NSCLC is also sensitised to the mTOR inhibitor rapamycin. Importantly, the data suggest that LKB1/KRAS mutant NSCLCs are a genetically and functionally distinct subset and further suggest that this subset of lung cancers might afford an opportunity for exploitation of anti-MAPK/mTOR-targeted therapies. PMID:19165201

  5. Lung cancer screening and management.

    PubMed

    Jones, G S; Baldwin, D R

    2015-12-01

    Deaths from lung cancer are greater than for any other type of malignancy. Many people present with advanced stage cancer at diagnosis and survival is limited. Low radiation dose CT (LDCT) screening appears to offer part of the solution to this. The US National Lung Screening Trial (NLST) showed a 20% reduction in cancer related mortality and a 6.7% reduction in all cause mortality in patients who had LDCT compared to chest X-ray. Lung Cancer screening is now being implemented in the US using the NLST screening criteria but many questions remain about the details of the methodology of screening and its cost effectiveness. Many of these questions are being answered by ongoing European trials that are reporting their findings. In this review we objectively analyse current research evidence and explore the issues that need to be resolved before implementation, including technical considerations, selection criteria and effective nodule management protocols. We discuss the potential barriers that will be faced when beginning a national screening programme and possible solutions to them. PMID:26605556

  6. Phosphoproteomics and Lung Cancer Research

    PubMed Central

    López, Elena; Cho, William C. S.

    2012-01-01

    Massive evidence suggests that genetic abnormalities contribute to the development of lung cancer. These molecular abnormalities may serve as diagnostic, prognostic and predictive biomarkers for this deadly disease. It is imperative to search these biomarkers in different tumorigenesis pathways so as to provide the most appropriate therapy for each individual patient with lung malignancy. Phosphoproteomics is a promising technology for the identification of biomarkers and novel therapeutic targets for cancer. Thousands of proteins interact via physical and chemical association. Moreover, some proteins can covalently modify other proteins post-translationally. These post-translational modifications ultimately give rise to the emergent functions of cells in sequence, space and time. Phosphoproteomics clinical researches imply the comprehensive analysis of the proteins that are expressed in cells or tissues and can be employed at different stages. In addition, understanding the functions of phosphorylated proteins requires the study of proteomes as linked systems rather than collections of individual protein molecules. In fact, proteomics approaches coupled with affinity chromatography strategies followed by mass spectrometry have been used to elucidate relevant biological questions. This article will discuss the relevant clues of post-translational modifications, phosphorylated proteins, and useful proteomics approaches to identify molecular cancer signatures. The recent progress in phosphoproteomics research in lung cancer will be also discussed. PMID:23202899

  7. Biological considerations in lung cancer.

    PubMed

    Almand, B; Carbone, D P

    2001-01-01

    Our understanding of lung cancer biology has rapidly expanded in recent years. Lung cancer, unlike most human cancers, can be traced to an environmental risk factor in the majority of cases, and this fact is reflected in the vast number of genetic alterations discovered in lung tumors whose pathogenesis is believed to be mediated by carcinogen exposure. The discovery of these alterations has led to a greater understanding of tumor development. The dramatic progress in the understanding of the genetic and molecular basis of oncogenesis and the induction of immunity has led to a rejuvenation of efforts to apply this new knowledge to this common and refractory disease. Further, the resurgent interest in cancer immunology and tumor-host interactions holds promise for the development of new approaches to treatment based on harvesting the immune systems ability to recognize these alterations. Hopefully, this understanding will lead to novel approaches with real and convincing clinical efficacy once some of these strategies are tested in carefully performed randomized clinical trials with appropriate power to detect meaningful differences. PMID:11224984

  8. Cannabis smoking and lung cancer risk: Pooled analysis in the International Lung Cancer Consortium.

    PubMed

    Zhang, Li Rita; Morgenstern, Hal; Greenland, Sander; Chang, Shen-Chih; Lazarus, Philip; Teare, M Dawn; Woll, Penella J; Orlow, Irene; Cox, Brian; Brhane, Yonathan; Liu, Geoffrey; Hung, Rayjean J

    2015-02-15

    To investigate the association between cannabis smoking and lung cancer risk, data on 2,159 lung cancer cases and 2,985 controls were pooled from 6 case-control studies in the US, Canada, UK, and New Zealand within the International Lung Cancer Consortium. Study-specific associations between cannabis smoking and lung cancer were estimated using unconditional logistic regression adjusting for sociodemographic factors, tobacco smoking status and pack-years; odds-ratio estimates were pooled using random effects models. Subgroup analyses were done for sex, histology and tobacco smoking status. The shapes of dose-response associations were examined using restricted cubic spline regression. The overall pooled OR for habitual versus nonhabitual or never users was 0.96 (95% CI: 0.66-1.38). Compared to nonhabitual or never users, the summary OR was 0.88 (95%CI: 0.63-1.24) for individuals who smoked 1 or more joint-equivalents of cannabis per day and 0.94 (95%CI: 0.67-1.32) for those consumed at least 10 joint-years. For adenocarcinoma cases the ORs were 1.73 (95%CI: 0.75-4.00) and 1.74 (95%CI: 0.85-3.55), respectively. However, no association was found for the squamous cell carcinoma based on small numbers. Weak associations between cannabis smoking and lung cancer were observed in never tobacco smokers. Spline modeling indicated a weak positive monotonic association between cumulative cannabis use and lung cancer, but precision was low at high exposure levels. Results from our pooled analyses provide little evidence for an increased risk of lung cancer among habitual or long-term cannabis smokers, although the possibility of potential adverse effect for heavy consumption cannot be excluded. PMID:24947688

  9. Vaccine Therapy and Sargramostim With or Without Docetaxel in Treating Patients With Metastatic Lung Cancer or Metastatic Colorectal Cancer

    ClinicalTrials.gov

    2014-03-28

    Extensive Stage Small Cell Lung Cancer; Recurrent Colon Cancer; Recurrent Non-small Cell Lung Cancer; Recurrent Rectal Cancer; Recurrent Small Cell Lung Cancer; Stage IV Colon Cancer; Stage IV Non-small Cell Lung Cancer; Stage IV Rectal Cancer

  10. Bortezomib in Treating Patients With Stage IIIB or Stage IV Lung Cancer

    ClinicalTrials.gov

    2014-08-04

    Adenocarcinoma of the Lung; Bronchoalveolar Cell Lung Cancer; Non-small Cell Lung Cancer; Recurrent Non-small Cell Lung Cancer; Stage IIIB Non-small Cell Lung Cancer; Stage IV Non-small Cell Lung Cancer

  11. Lung cancer: Biology and treatment options.

    PubMed

    Lemjabbar-Alaoui, Hassan; Hassan, Omer Ui; Yang, Yi-Wei; Buchanan, Petra

    2015-12-01

    Lung cancer remains the leading cause of cancer mortality in men and women in the U.S. and worldwide. About 90% of lung cancer cases are caused by smoking and the use of tobacco products. However, other factors such as radon gas, asbestos, air pollution exposures, and chronic infections can contribute to lung carcinogenesis. In addition, multiple inherited and acquired mechanisms of susceptibility to lung cancer have been proposed. Lung cancer is divided into two broad histologic classes, which grow and spread differently: small-cell lung carcinomas (SCLCs) and non-small cell lung carcinomas (NSCLCs). Treatment options for lung cancer include surgery, radiation therapy, chemotherapy, and targeted therapy. Therapeutic-modalities recommendations depend on several factors, including the type and stage of cancer. Despite the improvements in diagnosis and therapy made during the past 25 years, the prognosis for patients with lung cancer is still unsatisfactory. The responses to current standard therapies are poor except for the most localized cancers. However, a better understanding of the biology pertinent to these challenging malignancies, might lead to the development of more efficacious and perhaps more specific drugs. The purpose of this review is to summarize the recent developments in lung cancer biology and its therapeutic strategies, and discuss the latest treatment advances including therapies currently under clinical investigation. PMID:26297204

  12. Lung Cancer Awareness Week

    ERIC Educational Resources Information Center

    Glennon, Catherine; Laczko, Lori

    2003-01-01

    Smoking is the most preventable cause of death in our society. Tobacco use is responsible for nearly one in five deaths in the United States and the cause of premature death of approximately 2 million individuals in developed countries. Smoking accounts for at least 30% of all cancer deaths and is a major cause of heart disease, cerebrovascular…

  13. Cryotherapy in Treating Patients With Lung Cancer That Has Spread to the Other Lung or Parts of the Body

    ClinicalTrials.gov

    2012-03-16

    Advanced Malignant Mesothelioma; Extensive Stage Small Cell Lung Cancer; Lung Metastases; Recurrent Malignant Mesothelioma; Recurrent Non-small Cell Lung Cancer; Recurrent Small Cell Lung Cancer; Stage IV Non-small Cell Lung Cancer

  14. [Cannabis smoking and lung cancer].

    PubMed

    Underner, M; Urban, T; Perriot, J; de Chazeron, I; Meurice, J-C

    2014-06-01

    Cannabis is the most commonly smoked illicit substance in the world. It can be smoked alone in plant form (marijuana) but it is mainly smoked mixed with tobacco. The combined smoking of cannabis and tobacco is a common-place phenomenon in our society. However, its use is responsible for severe pulmonary consequences. The specific impact of smoking cannabis is difficult to assess precisely and to distinguish from the effect of tobacco. Marijuana smoke contains polycyclic aromatic hydrocarbons and carcinogens at higher concentration than tobacco smoke. Cellular, tissue, animal and human studies, and also epidemiological studies, show that marijuana smoke is a risk factor for lung cancer. Cannabis exposure doubles the risk of developing lung cancer. This should encourage clinicians to identify cannabis use and to offer patients support in quitting. PMID:25012035

  15. [Graphic Evolution Witness the Development of Lung Cancer Translational Research].

    PubMed

    Zhang, Chao; Zhong, Wenzhao

    2016-06-20

    Lung cancer treatment has altered from conventional chemotherapy to targeted treatment, which now has been turned to the immunotherapy. Translational research has played an irreplaceable role during this progression which graphic evolution has witnessed. The evolution has gone through forest plot, KM-curve, waterfall plot, spider plot and timeline-area, showing us the refining concept and gradual process of lung cancer treatment undergoing from community towards individual. Even though the latest immunotherapy is getting increasingly hot, the result isn't quite expected. Meanwhile, the limitations of conventional treatment still exist which require further research. This article will primarily illustrate the development of translational research of lung cancer via the aspect of curve evolution and analysis some abortive clinical trials in lung cancer surgery for inspiring the next graphic style and lung cancer treatment. PMID:27335306

  16. Association Between NAT2 Polymorphisms and Lung Cancer Susceptibility.

    PubMed

    Liu, Chang; Cui, Wei; Cong, Lin; Wang, Li; Ruan, Xinjian; Jia, Jia; Liu, Yanfang; Jia, Xiaoyan; Zhang, Xia

    2015-12-01

    To further investigate the association between NAT2 polymorphisms and lung cancer susceptibility.In terms of phenotypes, we investigated the acetylator status of NAT2 polymorphisms associated with lung cancer risk. Additionally, in view of genotypes, we mainly analyzed 5 single nucleotide polymorphisms (SNPs) in NAT2 gene, namely C282T, A803G, C481T, G590A, and G857A. Twenty-six eligible studies were included in our meta-analysis by searching PubMed, Embase, and CNKI databases. We used odds ratios (ORs) with corresponding 95% confidence intervals (CIs) to evaluate the susceptibility to lung cancer associated with NAT2 polymorphisms.Overall, based on phenotypes, the pooled ORs showed no significant association between NAT2 polymorphisms and lung cancer susceptibility. In the subgroup analyses by ethnicity and source of control, there was still no significant association. In terms of genotypes, overall, no obvious relationship was observed between NAT2 polymorphisms and lung cancer risk. But increased risk of lung cancer was found in association with NAT2 C282T polymorphism (TT vs. CC + TC: OR = 1.58, 95% CI = 1.11-2.25).Our meta-analysis demonstrates that TT genotype in NAT2 C282T polymorphism may be a risk factor for lung cancer susceptibility. Additionally, the acetylator status of 5 SNPs in NAT2 gene may not be associated with lung cancer risk. PMID:26656326

  17. Effect of Resection of Lung Tumours on the Steroid Abnormalities in Patients with Lung Cancer

    PubMed Central

    Rao, L. G. S.

    1971-01-01

    The urinary excretion of androsterone, aetiocholanolone, total 17-oxosteroids, and 17-hydroxycorticosteroids (17-OHCS) was measured in 40 patients with lung cancer three days before resection and again 10-15 days after resection of their lung tumours. There was a significant postoperative increase in the excretion of 17-OHCS but a significant decrease in the excretion of androsterone and aetiocholanolone, resulting in an increase of the preoperative abnormalities in steroid excretion in these patients. Since there was no change in steroid excretion towards normal after resection of the lung tumours, it seems that the steroid abnormalities found in lung cancer are not the effect of the presence of the lung tumours. As the excretions of 17-OHCS and 11-deoxy-17-oxosteroids change in opposite directions after resection, it is suggested that a dissociation of factors that control the excretion of these two groups of steroids takes place as a response to surgical stress in patients with lung cancer. PMID:5130212

  18. Unmasking the lung cancer epigenome.

    PubMed

    Belinsky, Steven A

    2015-01-01

    The reprogramming of the epigenome through silencing of genes and microRNAs by cytosine DNA methylation and chromatin remodeling is critical for the initiation and progression of lung cancer through affecting all major cell regulatory pathways. Importantly, the fact that epigenetic reprogramming is reversible by pharmacological agents has opened new avenues for clinical intervention. This review focuses on the tremendous progress made in elucidating genes and microRNAs that are epigenetically silenced in lung cancer and highlights how loss of function impacts cell phenotype and major signaling pathways. The article describes the utility of (a) an in vitro model using hTERT/Cdk4 immortalized human bronchial epithelial cell lines to identify genes and microRNAs silenced during premalignancy and (b) an in vivo orthotopic nude rat lung cancer model to evaluate response to epigenetic therapy. New insights regarding the advantage of aerosol delivery of demethylating agents and the concept of priming tumors for subsequent therapy are presented and discussed. PMID:25668024

  19. Attitudes and Stereotypes in Lung Cancer versus Breast Cancer

    PubMed Central

    Sriram, N.

    2015-01-01

    Societal perceptions may factor into the high rates of nontreatment in patients with lung cancer. To determine whether bias exists toward lung cancer, a study using the Implicit Association Test method of inferring subconscious attitudes and stereotypes from participant reaction times to visual cues was initiated. Participants were primarily recruited from an online survey panel based on US census data. Explicit attitudes regarding lung and breast cancer were derived from participants’ ratings (n = 1778) regarding what they thought patients experienced in terms of guilt, shame, and hope (descriptive statements) and from participants’ opinions regarding whether patients ought to experience such feelings (normative statements). Participants’ responses to descriptive and normative statements about lung cancer were compared with responses to statements about breast cancer. Analyses of responses revealed that the participants were more likely to agree with negative descriptive and normative statements about lung cancer than breast cancer (P<0.001). Furthermore, participants had significantly stronger implicit negative associations with lung cancer compared with breast cancer; mean response times in the lung cancer/negative conditions were significantly shorter than in the lung cancer/positive conditions (P<0.001). Patients, caregivers, healthcare providers, and members of the general public had comparable levels of negative implicit attitudes toward lung cancer. These results show that lung cancer was stigmatized by patients, caregivers, healthcare professionals, and the general public. Further research is needed to investigate whether implicit and explicit attitudes and stereotypes affect patient care. PMID:26698307

  20. Attitudes and Stereotypes in Lung Cancer versus Breast Cancer.

    PubMed

    Sriram, N; Mills, Jennifer; Lang, Edward; Dickson, Holli K; Hamann, Heidi A; Nosek, Brian A; Schiller, Joan H

    2015-01-01

    Societal perceptions may factor into the high rates of nontreatment in patients with lung cancer. To determine whether bias exists toward lung cancer, a study using the Implicit Association Test method of inferring subconscious attitudes and stereotypes from participant reaction times to visual cues was initiated. Participants were primarily recruited from an online survey panel based on US census data. Explicit attitudes regarding lung and breast cancer were derived from participants' ratings (n = 1778) regarding what they thought patients experienced in terms of guilt, shame, and hope (descriptive statements) and from participants' opinions regarding whether patients ought to experience such feelings (normative statements). Participants' responses to descriptive and normative statements about lung cancer were compared with responses to statements about breast cancer. Analyses of responses revealed that the participants were more likely to agree with negative descriptive and normative statements about lung cancer than breast cancer (P<0.001). Furthermore, participants had significantly stronger implicit negative associations with lung cancer compared with breast cancer; mean response times in the lung cancer/negative conditions were significantly shorter than in the lung cancer/positive conditions (P<0.001). Patients, caregivers, healthcare providers, and members of the general public had comparable levels of negative implicit attitudes toward lung cancer. These results show that lung cancer was stigmatized by patients, caregivers, healthcare professionals, and the general public. Further research is needed to investigate whether implicit and explicit attitudes and stereotypes affect patient care. PMID:26698307

  1. [Minimally Invasive Open Surgery for Lung Cancer].

    PubMed

    Nakagawa, Kazuo; Watanabe, Shunichi

    2016-07-01

    Significant efforts have been made to reduce the invasiveness of surgical procedures by surgeons for a long time. Surgeons always keep it in mind that the basic principle performing less invasive surgical procedures for malignant tumors is to decrease the invasiveness for patients without compromising oncological curability and surgical safety. Video-assisted thoracic surgery (VATS) has been used increasingly as a minimally invasive approach to lung cancer surgery. Whereas, whether VATS lobectomy is a less invasive procedure and has equivalent or better clinical effect compared with open lobectomy for patients with lung cancer remains controversial because of the absence of randomized prospective studies. The degree of difficulty for anatomical lung resection depends on the degree of the fissure development, mobility of hilar lymph nodes, and the degree of pleural adhesions. During pulmonary surgery, thoracic surgeons always have to deal with not only these difficulties but other unexpected events such as intraoperative bleeding. Recently, we perform pulmonary resection for lung cancer with minimally invasive open surgery (MIOS) approach. In this article, we introduce the surgical procedure of MIOS and demonstrate short-term results. Off course, the efficacy of MIOS needs to be further evaluated with long-term results. PMID:27440030

  2. [Innovation in Surgery for Advanced Lung Cancer].

    PubMed

    Nakano, Tomoyuki; Yasunori, Sohara; Endo, Shunsuke

    2016-07-01

    Thoracoscopic surgery can be one of less invasive surgical interventions for early stage lung cancer. Locally advanced lung cancer, however, cannot avoid aggressive procedures including pneumonectomy and/or extended combined resection of chest wall, aorta, esophagus, etc. for complete resection. Surgical approach even for advanced lung cancer can be less invasive by benefit from new anti-cancer treatment, innovated manipulations of bronchoplasty and angioplasty, and bench surgery( lung autotransplantation technique). We herein reviewed the strategy to minimize invasive interventions for locally advanced lung cancer, introducing 2 successful cases with advanced lung cancer. The 1st patient is a 62-year old man with centrally advanced lung cancer invading to mediastinum. Right upper sleeve lobectomy with one-stoma carinoplasty following induction chemoradiation therapy was successful. The operation time was 241 minutes. The performance status is good with no recurrence for 60 months after surgery. The 2nd is a 79-year old man with advanced lung cancer invading to the distal aortic arch. Left upper segmentectomy following thoracic endovascular aortic repair with stentgraft was successful with no extracorporeal circulation. The operation time was 170 minutes. The performance status is good with no recurrence for 30 months after surgery. The invasiveness of surgical interventions for local advanced lung cancer can be minimized by innovated device and new anti-cancer drugs. PMID:27440037

  3. Study of occupational lung cancer in asbestos factories in China.

    PubMed

    Zhu, H; Wang, Z

    1993-11-01

    A retrospective cohort study (1972-81) of occupational cancers in asbestos (chrysotile) factories has been previously published. In this paper the results of continued tracing and interviewing of members of this cohort from 1982 to 1986 is reported. The cohort included 5893 persons (45,974 person-years for men and 39,445 person-years for women). Malignant tumours played a large part in causes of death (36.9%). There were 183 cancers and 67 lung cancers among 496 deaths. The mortality due to lung cancer had a tendency to increase. By comparison with a control group, the RR of lung cancer was 5.32 (p < 0.01), and the SRR of lung cancer was 4.2 (p < 0.01), significantly higher than those of a control group. Among 148 cases of death from asbestosis there were 33 cases complicated with lung cancer (22.3%). The dose-response relations between exposure to asbestos and incidence of asbestosis and lung cancer were also studied in one asbestos factory. There was a positive correlation. A synergistic effect was found between cigarette smoking and lung cancer. Preventive and control measures and exposure limits for asbestos dust in the air of workplaces were recommended. PMID:8280629

  4. Lung Cancer and Interstitial Lung Diseases: A Systematic Review

    PubMed Central

    Archontogeorgis, Kostas; Steiropoulos, Paschalis; Tzouvelekis, Argyris; Nena, Evangelia; Bouros, Demosthenes

    2012-01-01

    Interstitial lung diseases (ILDs) represent a heterogeneous group of more than two hundred diseases of either known or unknown etiology with different pathogenesis and prognosis. Lung cancer, which is the major cause of cancer death in the developed countries, is mainly attributed to cigarette smoking and exposure to inhaled carcinogens. Different studies suggest a link between ILDs and lung cancer, through different pathogenetic mechanisms, such as inflammation, coagulation, dysregulated apoptosis, focal hypoxia, activation, and accumulation of myofibroblasts as well as extracellular matrix accumulation. This paper reviews current evidence on the association between lung cancer and interstitial lung diseases such as idiopathic pulmonary fibrosis, sarcoidosis, systemic sclerosis, dermatomyositis/polymyositis, rheumatoid arthritis, systemic lupus erythematosus, and pneumoconiosis. PMID:22900168

  5. Year-in-Review of Lung Cancer

    PubMed Central

    2012-01-01

    In the last several years, we have made slow but steady progress in understanding molecular biology of lung cancer. This review is focused on advances in understanding the biology of lung cancer that have led to proof of concept studies on new therapeutic approaches. The three selected topics include genetics, epigenetics and non-coding RNA. This new information represents progress in the integration of molecular mechanisms that to identify more effective ways to target lung cancer. PMID:23166546

  6. In vivo selection for spine-derived highly metastatic lung cancer cells is associated with increased migration, inflammation and decreased adhesion

    PubMed Central

    Deng, Huayun; Zhang, Jishen; Li, Shichang; Wei, Haifeng; Yang, Cheng; Xu, Leqin; Jin, Rongrong; Li, Zhenxi; Zhou, Wang; Ding, JianDong; Chu, Jianjun; Jia, Lianshun; Jia, Qi; Tan, Chengjun; Liu, Mingyao; Xiao, Jianru

    2015-01-01

    We developed a murine spine metastasis model by screening five metastatic non-small cell lung cancer cell lines (PC-9, A549, NCI-H1299, NCI-H460, H2030). A549 cells displayed the highest tendency towards spine metastases. After three rounds of selection in vivo, we isolated a clone named A549L6, which induced spine metastasis in 80% of injected mice. The parameters of the A549L6 cell spinal metastatic mouse models were consistent with clinical spine metastasis features. All the spinal metastatic mice developed symptoms of nerve compression after 40 days. A549L6 cells had increased migration, invasiveness and decreased adhesion compared to the original A549L0 cells. In contrast, there was no significant differences in cell proliferation, apoptosis and sensitivity to chemotherapeutic agents such as cisplatin. Comparative transcriptomic analysis and Real-time PCR analysis showed that expression of signaling molecules regulating several tumor properties including migration (MYL9), metastasis (CEACAM6, VEGFC, CX3CL1, CST1, CCL5, S100A9, IGF1, NOTCH3), adhesion (FN1, CEACAM1) and inflammation (TRAF2, NFκB2 and RelB) were altered in A549L6 cells. We suggest that migration, adhesion and inflammation related genes contribute to spine metastatic capacity. PMID:26090868

  7. Curbing the burden of lung cancer.

    PubMed

    Urman, Alexandra; Hosgood, H Dean

    2016-06-01

    Lung cancer contributes substantially to the global burden of disease and healthcare costs. New screening modalities using low-dose computerized tomography are promising tools for early detection leading to curative surgery. However, the screening and follow-up diagnostic procedures of these techniques may be costly. Focusing on prevention is an important factor to reduce the burden of screening, treatment, and lung cancer deaths. The International Agency for Research on Cancer has identified several lung carcinogens, which we believe can be considered actionable when developing prevention strategies. To curb the societal burden of lung cancer, healthcare resources need to be focused on early detection and screening and on mitigating exposure(s) of a person to known lung carcinogens, such as active tobacco smoking, household air pollution (HAP), and outdoor air pollution. Evidence has also suggested that these known lung carcinogens may be associated with genetic predispositions, supporting the hypothesis that lung cancers attributed to differing exposures may have developed from unique underlying genetic mechanisms attributed to the exposure of interest. For instance, smokingattributed lung cancer involves novel genetic markers of risk compared with HAP-attributed lung cancer. Therefore, genetic risk markers may be used in risk stratification to identify subpopulations that are at a higher risk for developing lung cancer attributed to a given exposure. Such targeted prevention strategies suggest that precision prevention strategies may be possible in the future; however, much work is needed to determine whether these strategies will be viable. PMID:27178304

  8. Adaptive Radiotherapy for Locally Advanced Non-Small-Cell Lung Cancer Does Not Underdose the Microscopic Disease and has the Potential to Increase Tumor Control

    SciTech Connect

    Guckenberger, Matthias; Richter, Anne; Wilbert, Juergen; Flentje, Michael; Partridge, Mike

    2011-11-15

    Purpose: To evaluate doses to the microscopic disease (MD) in adaptive radiotherapy (ART) for locally advanced non-small-cell lung cancer (NSCLC) and to model tumor control probability (TCP). Methods and Materials: In a retrospective planning study, three-dimensional conformal treatment plans for 13 patients with locally advanced NSCLC were adapted to shape and volume changes of the gross tumor volume (GTV) once or twice during conventionally fractionated radiotherapy with total doses of 66 Gy; doses in the ART plans were escalated using an iso-mean lung dose (MLD) approach compared to non-adapted treatment. Dose distributions to the volumes of suspect MD were simulated for a scenario with synchronous shrinkage of the MD and GTV and for a scenario of a stationary MD despite GTV shrinkage; simulations were performed using deformable image registration. TCP calculations considering doses to the GTV and MD were performed using three different models. Results: Coverage of the MD at 50 Gy was not compromised by ART. Coverage at 60 Gy in the scenario of a stationary MD was significantly reduced from 92% {+-} 10% to 73% {+-} 19% using ART; however, the coverage was restored by iso-MLD dose escalation. Dose distributions in the MD were sufficient to achieve a TCP >80% on average in all simulation experiments, with the clonogenic cell density the major factor influencing TCP. The combined TCP for the GTV and MD was 19.9% averaged over all patients and TCP models in non-adaptive treatment with 66 Gy. Iso-MLD dose escalation achieved by ART increased the overall TCP by absolute 6% (adapting plan once) and by 8.7% (adapting plan twice) on average. Absolute TCP values were significantly different between the TCP models; however, all TCP models suggested very similar TCP increase by using ART. Conclusions: Adaptation of radiotherapy to the shrinking GTV did not compromise dose coverage of volumes of suspect microscopic disease and has the potential to increase TCP by >40

  9. E1AF/PEA3 activates the Rho/Rho-associated kinase pathway to increase the malignancy potential of non-small-cell lung cancer cells.

    PubMed

    Hakuma, Nobuyuki; Kinoshita, Ichiro; Shimizu, Yasushi; Yamazaki, Koichi; Yoshida, Koichi; Nishimura, Masaharu; Dosaka-Akita, Hirotoshi

    2005-12-01

    E1AF/PEA3, an Ets family transcription factor, is frequently overexpressed in non-small-cell lung cancers (NSCLCs). Overexpression of E1AF increases motility and invasion of VMRC-LCD and NCI-H226 NSCLC cells, which lack endogenous E1AF expression, and the effect is synergistically increased by hepatocyte growth factor (HGF). The small GTPase Rho/Rho-associated kinase (ROCK) pathway is also involved in motility and invasion. To determine the role of the Rho/ROCK pathway in malignant phenotypes induced by E1AF, we analyzed VMRC-LCD cells transfected with an E1AF expression vector (LCD-E1AF cells) or with empty vector (LCD-vector cells). LCD-E1AF cells had more GTP-bound (active) Rho than LCD-vector cells and Rho activation was synergistically increased by HGF. The Rho activation by E1AF and HGF was also shown in NCI-H226 cells. Phosphorylation of myosin light chain (MLC), a downstream effector of ROCK signaling, was higher in LCD-E1AF cells than in LCD-vector cells, especially under HGF treatment. A specific ROCK inhibitor, Y27632, strongly suppressed MLC phosphorylation, cell motility, and invasion. In nude mice implanted s.c. and intrapulmonarily, LCD-E1AF cells made more local tumors than LCD-vector cells (six of six versus one of seven mice and four of seven versus one of seven mice, respectively). Three of the four mice with lung tumors from LCD-E1AF cells had lymph node metastases whereas the mouse with LCD-vector tumors did not. LCD-E1AF tumors showed higher MLC phosphorylation than LCD-vector tumors. These results suggest that E1AF activates the Rho/ROCK pathway in an HGF-enhanced manner and its activation is important in E1AF-induced motility and invasion as well as tumorigenesis and metastasis in NSCLC cells. PMID:16322223

  10. Chemotherapy for lung cancers: here to stay.

    PubMed

    Kris, Mark G; Hellmann, Matthew D; Chaft, Jamie E

    2014-01-01

    Four decades of clinical research document the effectiveness of chemotherapy in patients with lung cancers. Chemotherapeutic agents can improve lung cancer symptoms, lengthen life in most patients with lung cancers, and enhance curability in individuals with locoregional disease when combined with surgery or irradiation. Chemotherapy's effectiveness is enhanced in patients with EGFR-mutant and ALK-positive lung cancers and can "rescue" individuals whose oncogene-driven cancers have become resistant to targeted agents. As immunotherapies become part of the therapeutic armamentarium for lung cancers, chemotherapeutic drugs have the potential to modulate the immune system to enhance the effectiveness of immune check point inhibitors. Even in this era of personalized medicine and targeted therapies, chemotherapeutic agents remain essential components in cancer care. PMID:24857127

  11. Combination Chemotherapy, Radiation Therapy, and Gefitinib in Treating Patients With Stage III Non-Small Cell Lung Cancer

    ClinicalTrials.gov

    2013-06-04

    Adenocarcinoma of the Lung; Adenosquamous Cell Lung Cancer; Bronchoalveolar Cell Lung Cancer; Large Cell Lung Cancer; Squamous Cell Lung Cancer; Stage IIIA Non-small Cell Lung Cancer; Stage IIIB Non-small Cell Lung Cancer

  12. Lung Cancer in the Era of Precision Medicine

    PubMed Central

    Politi, Katerina; Herbst, Roy S.

    2015-01-01

    The past decade has been transformative for lung cancer patients, physicians and scientists. The discovery of EGFR mutations that confer sensitivity to tyrosine kinase inhibitors in lung adenocarcinomas in 2004 heralded the beginning of the era of precision medicine for lung cancer. It also precipitated concerted efforts by many investigators to define molecular subgroups of lung cancer, characterize the genomic landscape of lung cancer subtypes, identify novel therapeutic targets and define mechanisms of sensitivity and resistance to targeted therapies. The fruits of these efforts are visible every day now in lung cancer clinics: patients receive molecular testing to determine whether their tumor harbors an actionable mutation, new and improved targeted therapies that can overcome resistance to first-generation drugs are in clinical trials and drugs targeting the immune system are showing activity in patients. This extraordinary promise is tempered by the sobering fact that even the newest treatments for metastatic disease are rarely curative and are effective only in a small fraction of patients. Ongoing and future efforts to find new vulnerabilities of lung cancers, unravel the complexity of drug resistance, increase the efficacy of immunotherapies and perform biomarker-driven clinical trials are necessary to improve outcomes for lung cancer patients. PMID:25979927

  13. TP53 Mutations in Nonsmall Cell Lung Cancer

    PubMed Central

    Mogi, Akira; Kuwano, Hiroyuki

    2011-01-01

    The tumor suppressor gene TP53 is frequently mutated in human cancers. Abnormality of the TP53 gene is one of the most significant events in lung cancers and plays an important role in the tumorigenesis of lung epithelial cells. Human lung cancers are classified into two major types, small cell lung cancer (SCLC) and nonsmall cell lung cancer (NSCLC). The latter accounts for approximately 80% of all primary lung cancers, and the incidence of NSCLC is increasing yearly. Most clinical studies suggest that NSCLC with TP53 alterations carries a worse prognosis and may be relatively more resistant to chemotherapy and radiation. A deep understanding of the role of TP53 in lung carcinogenesis may lead to a more reasonably targeted clinical approach, which should be exploited to enhance the survival rates of patients with lung cancer. This paper will focus on the role of TP53 in the molecular pathogenesis, epidemiology, and therapeutic strategies of TP53 mutation in NSCLC. PMID:21331359

  14. TNM classification for lung cancer.

    PubMed

    Watanabe, Yoh

    2003-12-01

    The international tumor-node-metastasis (TNM) staging system is the "international language" in cancer diagnosis and treatment. Six revisions of the TNM staging system for lung cancer have been repeated over the past 35 years after the beginning of UICC-TNM classification in 1968. The 1997 revision for lung cancer has undergone an extensive correction for many deficiencies of the old staging system. As a result, the new staging system appears to be a great improvement over previous editions. There are, however, still some controversies and proposals for revising, even when the new staging system is applied in daily diagnoses and treatment for lung cancer. In the present paper, these problems are presented and discussed. Main subjects for discussions are as follows: (1). Since the 2nd revision, T1 and T2 lesions were divided at the border of a 3 cm tumor size. Is 3 cm diameter an appropriate cut-off point for dividing T1 and T2 lesions? (2). Is it valid to subdivide T1 and T2 lesions into each A and B? (3). Is it appropriate to down-stage all of T3N0M0 to stage IIB, because there exists heterogeneity of T3? (4). Definitions of T4 lesion. (5). Controversies in three kinds of lymph node maps. Especially, where there is a boundary between N1 and N2 station in each map? (6) How to classify separate tumor nodules (STN) in the same lobe, and in the non-primary lobe. (7) Controversy exists concerning the validity of present stage grouping, because there are no significant difference of survivals between IB and IIA, IIA and IIB in most reports and also between T3N0M0 and T3N1M0 in some reports. PMID:15003094

  15. NK Cell Phenotypic Modulation in Lung Cancer Environment

    PubMed Central

    Hao, Jun-Wei; Li, Yang; Liu, Bin; Yu, Yan; Shi, Fu-Dong; Zhou, Qing-Hua

    2014-01-01

    Background Nature killer (NK) cells play an important role in anti-tumor immunotherapy. But it indicated that tumor cells impacted possibly on NK cell normal functions through some molecules mechanisms in tumor microenvironment. Materials and methods Our study analyzed the change about NK cells surface markers (NK cells receptors) through immunofluorescence, flow cytometry and real-time PCR, the killed function from mouse spleen NK cell and human high/low lung cancer cell line by co-culture. Furthermore we certificated the above result on the lung cancer model of SCID mouse. Results We showed that the infiltration of NK cells in tumor periphery was related with lung cancer patients' prognosis. And the number of NK cell infiltrating in lung cancer tissue is closely related to the pathological types, size of the primary cancer, smoking history and prognosis of the patients with lung cancer. The expression of NK cells inhibitor receptors increased remarkably in tumor micro-environment, in opposite, the expression of NK cells activated receptors decrease magnificently. Conclusions The survival time of lung cancer patient was positively related to NK cell infiltration degree in lung cancer. Thus, the down-regulation of NKG2D, Ly49I and the up-regulation of NKG2A may indicate immune tolerance mechanism and facilitate metastasis in tumor environment. Our research will offer more theory for clinical strategy about tumor immunotherapy. PMID:25299645

  16. Lung Cancer in Never Smokers

    PubMed Central

    Yang, Ping

    2012-01-01

    Lung cancer in never smokers (LCINS) has lately been recognized as a unique disease based on rapidly gained knowledge from genomic changes to treatment responses. The focus of this article is on current knowledge and challenges with regard to LCINS expanded from recent reviews highlighting five areas: (1) distribution of LCINS by temporal trends, geographic regions, and populations; (2) three well-recognized environmental risk factors; (3) other plausible environmental risk factors; (4) prior chronic lung diseases and infectious diseases as risk factors; and (5) lifestyles as risk or protective factors. This article will also bring attention to recently published literature in two pioneering areas: (1) histological characteristics, clinical features with emerging new effective therapies, and social and psychological stigma; and (2) searching for susceptibility genes using integrated genomic approaches. PMID:21500120

  17. Dietary factors in lung cancer prognosis.

    PubMed

    Goodman, M T; Kolonel, L N; Wilkens, L R; Yoshizawa, C N; Le Marchand, L; Hankin, J H

    1992-01-01

    A hypothesis-generating analysis of the role of diet on survival was conducted among a sample of 463 men and 212 women with histologically-confirmed lung cancer. Interview information was obtained from two population-based case-control studies of lung cancer conducted on the Island of Oahu, Hawaii, between 1979 and 1985. The interview consisted of a quantitative dietary history to assess the usual intake of foods 1 year prior to diagnosis, a complete tobacco history, and other demographic and lifestyle information. Records from the Hawaii Tumor Registry were reviewed for data on stage, histology, and follow-up status of these patients. A food group analysis showed a significant reduction in the risk of death with increasing consumption of all vegetables combined among women (P for trend = 0.03), but not among men. The covariate-adjusted median survival times for women from the highest to the lowest quartiles of vegetable intake were 33, 21, 15, and 18 months, respectively. The results also suggested an association of fruit intake and survival among women (P for trend = 0.02), although a similar effect was not found among men. Increased consumption of certain foods, such as tomatoes and oranges among men, and broccoli and, perhaps, tomatoes among women, appeared to improve survival. This exploratory analysis provides mixed indications that certain components of vegetables and fruits may prolong survival in lung cancer patients. PMID:1591072

  18. Reprocessed uranium exposure and lung cancer risk.

    PubMed

    Canu, Irina Guseva; Jacob, Sophie; Cardis, Elisabeth; Wild, Pascal; Caër-Lorho, Sylvaine; Auriol, Bernard; Laurier, Dominique; Tirmarche, Margot

    2010-09-01

    This study investigated the risk of lung cancer in regards to protracted occupational exposure to reprocessed uranium compounds. Two thousand seven hundred and nine male workers employed at the AREVA NC uranium processing plant between 1960 and 2005 in France were included in the cohort. Historical exposure to reprocessed uranium compounds classified by their solubility type was assessed on the basis of the plant's specific job-exposure matrix. Cox proportional hazard models adjusted for attained age, calendar period, and socioeconomic status were used to estimate relative risks in regards of each type of uranium compound. The relative risk of lung cancer tended to increase with decreasing solubility of reprocessed uranium compounds. The highest-though not statistically significant-relative risk was observed among workers exposed to slowly soluble reprocessed uranium dioxide. This study is the first suggesting an increasing risk of lung cancer associated with exposure to reprocessed uranium. Our results are consistent with data from experimental studies of biokinetics and the action mechanism of slowly soluble uranium compounds, but need to be confirmed in larger studies with more detailed dose-response analyses. PMID:20699691

  19. Enhanced Quitline Intervention in Smoking Cessation for Patients With Non-Metastatic Lung Cancer

    ClinicalTrials.gov

    2015-09-28

    Limited Stage Small Cell Lung Cancer; Recurrent Small Cell Lung Cancer; Stage IA Non-small Cell Lung Cancer; Stage IB Non-small Cell Lung Cancer; Stage IIA Non-small Cell Lung Cancer; Stage IIB Non-small Cell Lung Cancer; Stage IIIA Non-small Cell Lung Cancer; Stage IIIB Non-small Cell Lung Cancer; Tobacco Use Disorder

  20. What You Need to Know about Lung Cancer

    MedlinePlus

    ... Publications Reports What You Need To Know About™ Lung Cancer This booklet is about lung cancer. Learning about medical care for your cancer ... ePub This booklet covers: The anatomy of the lungs and basics about lung cancer Treatment for lung ...

  1. MET inhibition in lung cancer

    PubMed Central

    Giaj Levra, Matteo; Novello, Silvia

    2013-01-01

    Targeted agents have completely changed cancer treatment strategy, leading it from a “one size fits all” approach to a customized therapy. In this scenario Met, a heterodimere receptor tyrosine kinase deeply involved into embryogenesis and organogenesis, has been introduced many years ago as a potential target for biological agents, becoming “druggable” only in this last period of time. Met can be altered through receptor overexpression, genomic amplification, mutations or alternative splicing, autocrine or paracrine secretion of hepatic growth factor (HGF): these dysregulations stimulate tumorigenesis (in terms of cell-cell detachment, proliferation, invasion, angiogenesis and survival) and metastatization. Met is overexpressed in lung cancer and Met gene amplification can drive the dependency of cell survival and proliferation upon the Met signaling. Both Met overexpression and amplification seem to correlate with poor prognosis. Met amplification is also described to be linked to EGFR acquired resistance. Several Met inhibitors have been tested both in preclinical and human trials, demonstrating activity in lung cancer treatment. This paper aims to summarize data on Met biological function, on its interaction with cell signaling and other pathways and to present data on those Met inhibitors currently under evaluation. PMID:25806202

  2. Lineage factors and differentiation states in lung cancer progression.

    PubMed

    Cheung, W K C; Nguyen, D X

    2015-11-19

    Lung cancer encompasses a heterogeneous group of malignancies. Here we discuss how the remarkable diversity of major lung cancer subtypes is manifested in their transforming cell of origin, oncogenic dependencies, phenotypic plasticity, metastatic competence and response to therapy. More specifically, we review the increasing evidence that links this biological heterogeneity to the deregulation of cell lineage-specific pathways and the transcription factors that ultimately control them. As determinants of pulmonary epithelial differentiation, these poorly characterized transcriptional networks may underlie the etiology and biological progression of distinct lung cancers, while providing insight into innovative therapeutic strategies. PMID:25823023

  3. Differentiation of normal and cancerous lung tissues by multiphoton imaging

    NASA Astrophysics Data System (ADS)

    Wang, Chun-Chin; Li, Feng-Chieh; Wu, Ruei-Jr; Hovhannisyan, Vladimir A.; Lin, Wei-Chou; Lin, Sung-Jan; So, Peter T. C.; Dong, Chen-Yuan

    2010-02-01

    In this work, we utilized multiphoton microscopy for the label-free diagnosis of non-cancerous, lung adenocarcinoma (LAC), and lung squamous cell carcinoma (SCC) tissues from human. Our results show that the combination of second harmonic generation (SHG) and multiphoton excited autofluorescence (MAF) signals may be used to acquire morphological and quantitative information in discriminating cancerous from non-cancerous lung tissues. Specifically, non-cancerous lung tissues are largely fibrotic in structure while cancerous specimens are composed primarily of tumor masses. Quantitative ratiometric analysis using MAF to SHG index (MAFSI or SAAID) shows that the average MAFSI for noncancerous and LAC lung tissue pairs are 0.55 +/-0.23 and 0.87+/-0.15 respectively. In comparison, the MAFSIs for the noncancerous and SCC tissue pairs are 0.50+/-0.12 and 0.72+/-0.13 respectively. Intrinsic fluorescence ratio (FAD/NADH) of SCC and non-cancerous tissues are 0.40+/-0.05 and 0.53+/-0.05 respectively, the redox ratio of SCC diminishes significantly, indicating that increased cellular metabolic activity. Our study shows that nonlinear optical microscopy can assist in differentiating and diagnosing pulmonary cancer from non-cancerous tissues. With additional development, multiphoton microscopy may be used for the clinical diagnosis of lung cancers.

  4. COPD in primary lung cancer patients: prevalence and mortality

    PubMed Central

    Ytterstad, Elinor; Moe, Per C; Hjalmarsen, Audhild

    2016-01-01

    Background Previous studies have relied on international spirometry criteria to diagnose COPD in patients with lung cancer without considering the effect lung cancer might have on spirometric results. The aim of this study was to examine the prevalence of COPD and emphysema at the time of primary lung cancer diagnosis and to examine factors associated with survival. Materials and methods Medical records, pulmonary function tests, and computed tomography scans were used to determine the presence of COPD and emphysema in patients diagnosed with primary lung cancer at the University Hospital of North Norway in 2008–2010. Results Among the 174 lung cancer patients, 69% had COPD or emphysema (39% with COPD, 59% with emphysema; male:female ratio 101:73). Neither COPD nor emphysema were significantly associated with lung cancer mortality, whereas patients with non-small-cell lung cancer other than adenocarcinoma and squamous cell carcinoma had a risk of lung cancer mortality that was more than four times higher than that of patients with small-cell lung cancer (hazard ratio [HR] 4.19, 95% confidence interval [CI] 1.56–11.25). Females had a lower risk of lung cancer mortality than males (HR 0.63, 95% CI 0.42–0.94), and patients aged ≥75 years had a risk that was twice that of patients aged <75 years (HR 2.48, 95% CI 1.59–3.87). Low partial arterial oxygen pressure (4.0–8.4 kPa) increased the risk of lung cancer mortality (HR 2.26, 95% CI 1.29–3.96). So did low partial arterial carbon dioxide pressure (3.0–4.9 kPa) among stage IV lung cancer patients (HR 2.23, 95% CI 1.29–3.85). Several patients with respiratory failure had previously been diagnosed with COPD. Conclusion The observed prevalence of COPD was lower than that in previous studies. Neither COPD nor emphysema were significantly associated with lung cancer mortality. PMID:27042050

  5. Chemoprevention studies within lung cancer screening programmes.

    PubMed

    Veronesi, G; Guerrieri-Gonzaga, A; Infante, M; Bonanni, B

    2015-01-01

    While aggressive tobacco control and help to stop smoking are essential weapons in the fight against lung cancer, screening with low-dose computed tomography (LDCT) in high-risk populations and chemoprevention may also contribute to reducing lung cancer deaths. Persons undergoing LDCT screening are an ideal population to be tested for agents potentially able to prevent the development of lung cancer by the regression of precancerous lesions, which are routinely monitored as part of the screening process. Peripheral subsolid nodules appear as particularly suitable targets, since many are adenocarcinoma precursors. A study on inhaled budesonide (a potential chemopreventive drug) for 1 year found that the mean size of non-solid lung nodules was significantly reduced over 5 years of follow-up, compared to inhaled placebo, in a population of high-risk individuals with indeterminate lung nodules not requiring immediate specific investigation for lung cancer and detected as part of a lung cancer screening program with LDCT. A new randomised placebo-controlled phase-II trial to test the ability of aspirin to induce the regression of non-solid and partially solid nodules detected by LDCT screening has been started. The effect of aspirin on a miRNA signature able to predict the presence of both cancer and precancerous lesions in high-risk asymptomatic individuals is also being monitored in the trial. This signature was previously shown to predict the presence of both lung cancer and non-solid lung nodules in asymptomatic individuals. PMID:26635901

  6. [Developing surgical options for lung cancer].

    PubMed

    Sihvo, Eero

    2016-01-01

    The selection of correct treatment for lung cancer is multidisciplinary collaboration and requires careful assessment of the extent of the tumor and the condition of the patient. In localized non-small cell lung cancer, mere surgery or surgery in combination with adjuvant therapies are the best options for curing the disease. The trend in modern surgery is mini-invasiveness and preservation of lung tissue. Accordingly, any unit conducting lung cancer operations should have access to all modern techniques in order to provide each patient with optimal, patient-tailored surgical therapy. PMID:27132298

  7. Classification and Pathology of Lung Cancer.

    PubMed

    Zheng, Min

    2016-07-01

    Advancement in the understanding of lung tumor biology enables continued refinement of lung cancer classification, reflected in the recently introduced 2015 World Health Organization classification of lung cancer. In small biopsy or cytology specimens, special emphasis is placed on separating adenocarcinomas from the other lung cancers to effectively select tumors for targeted molecular testing. In resection specimens, adenocarcinomas are further classified based on architectural pattern to delineate tissue types of prognostic significance. Neuroendocrine tumors are divided into typical carcinoid, atypical carcinoid, small cell carcinoma, and large cell neuroendocrine carcinoma based on a combination of features, especially tumor cell proliferation rate. PMID:27261908

  8. Lung cancer epidemiology: contemporary and future challenges worldwide

    PubMed Central

    Wojciechowska, Urszula; Mańczuk, Marta; Łobaszewski, Jakub

    2016-01-01

    Over the last century, lung cancer from the rarest of diseases became the biggest cancer killer of men worldwide and in some parts of the world also of women (North America, East Asia, Northern Europe, Australia and New Zealand). In 2012 over 1.6 million of people died due to lung cancer. The cause-effect relationship between tobacco smoking and lung cancer occurrence has been proven in many studies, both ecological and clinical. In global perspective one can see the increasing tobacco consumption trend followed by ascending trends of lung cancer mortality, especially in developing countries. In some more developed countries, where the tobacco epidemics was on the rise since the beginning of the 20th century and peaked in its mid, in male population lung cancer incidence trend reversed or leveled off. Despite predicted further decline of incidence rates, the absolute number of deaths will continue to grow in these countries. In the remaining parts of the world the tobacco epidemics is still evolving what brings rapid increase of the number of new lung cancer cases and deaths. Number of lung cancer deaths worldwide is expected to grow up to 3 million until 2035. The figures will double both in men (from 1.1 million in 2012 to 2.1 million in 2035) and women (from 0.5 million in 2012 to 0.9 million in 2035) and the two-fold difference between sexes will persist. The most rapid increase is expected in Africa region (AFRO) and East Mediterranean region (EMRO). The increase of the absolute number of lung cancer deaths in more developed countries is caused mostly by population aging and in less developed countries predominantly by the evolving tobacco epidemic. PMID:27195268

  9. The impact of the Cancer Genome Atlas on lung cancer.

    PubMed

    Chang, Jeremy T-H; Lee, Yee Ming; Huang, R Stephanie

    2015-12-01

    The Cancer Genome Atlas (TCGA) has profiled more than 10,000 samples derived from 33 types of cancer to date, with the goal of improving our understanding of the molecular basis of cancer and advancing our ability to diagnose, treat, and prevent cancer. This review focuses on lung cancer as it is the leading cause of cancer-related mortality worldwide in both men and women. Particularly, non-small cell lung cancers (including lung adenocarcinoma and lung squamous cell carcinoma) were evaluated. Our goal was to demonstrate the impact of TCGA on lung cancer research under 4 themes: diagnostic markers, disease progression markers, novel therapeutic targets, and novel tools. Examples are given related to DNA mutation, copy number variation, messenger RNA, and microRNA expression along with methylation profiling. PMID:26318634

  10. Lung Cancer - Multiple Languages: MedlinePlus

    MedlinePlus

    ... Arabic) سرطان الرئة - العربية Bilingual PDF Health Information Translations Bosnian (Bosanski) Lung Cancer Karcinom pluća - Bosanski (Bosnian) Bilingual PDF Health Information Translations Chinese - Simplified (简体中文) Lung Cancer 肺癌 - 简体中文 (Chinese - ...

  11. Lung Cancer - Multiple Languages: MedlinePlus

    MedlinePlus

    ... Are Here: Home → Multiple Languages → All Health Topics → Lung Cancer URL of this page: https://medlineplus.gov/languages/lungcancer.html Other topics ... V W XYZ List of All Topics All Lung Cancer - Multiple Languages ... To use the sharing features on this page, please enable JavaScript. Arabic (العربية) Bosnian (Bosanski) Chinese - ...

  12. Recent advances in lung cancer biology

    SciTech Connect

    Lechner, J.

    1995-12-31

    This paper provides an overview of carcinogenesis, especially as related to lung cancers. Various growth factors and their mutated forms as oncogenes are discussed with respect to gene location and their role in the oncogenic process. Finally the data is related to lung cancer induction in uranium miners and exposure to radon.

  13. Gene Therapy for Lung Cancer.

    PubMed

    Lara-Guerra, Humberto; Roth, Jack A

    2016-01-01

    Gene therapy was originally conceived to treat monogenic diseases. The replacement of a defective gene with a functional gene can theoretically cure the disease. In cancer, multiple genetic defects are present and the molecular profile changes during the course of the disease, making the replacement of all defective genes impossible. To overcome these difficulties, various gene therapy strategies have been adopted, including immune stimulation, transfer of suicide genes, inhibition of driver oncogenes, replacement of tumor-suppressor genes that could mediate apoptosis or anti-angiogenesis, and transfer of genes that enhance conventional treatments such as radiotherapy and chemotherapy. Some of these strategies have been tested successfully in non-small-cell lung cancer patients and the results of laboratory studies and clinical trials are reviewed herein. PMID:27481008

  14. Human Leukocyte Antigen G Polymorphism and Expression Are Associated with an Increased Risk of Non-Small-Cell Lung Cancer and Advanced Disease Stage.

    PubMed

    Ben Amor, Amira; Beauchemin, Karine; Faucher, Marie-Claude; Hamzaoui, Agnes; Hamzaoui, Kamel; Roger, Michel

    2016-01-01

    Human leukocyte antigen (HLA)-G acts as negative regulator of the immune responses and its expression may enable tumor cells to escape immunosurveillance. The purpose of this study was to investigate the influence of HLA-G allelic variants and serum soluble HLA-G (sHLA-G) levels on risk of non-small-cell lung cancer (NSCLC). We analyzed 191 Caucasian adults with NSCLC and 191 healthy subjects recruited between January 2009 and March 2014 in Ariana (Tunisia). Serum sHLA-G levels were measured by immunoassay and HLA-G alleles were determined using a direct DNA sequencing procedures. The heterozygous genotypes of HLA-G 010101 and -G 010401 were associated with increased risks of both NSCLC and advanced disease stages. In contrast, the heterozygous genotypes of HLA-G 0105N and -G 0106 were associated with decreased risks of NSCC and clinical disease stage IV, respectively. Serum sHLA-G levels were significantly higher in patients with NSCLC and particularly in those with advanced disease stages compared to healthy subjects. The area under the receiver-operating characteristic (ROC) curves was 0.82 for controls vs patients. Given 100% specificity, the highest sensitivity achieved to detect NSCLC was 52.8% at a cutoff value of 24.9 U/ml. Patients with the sHLA-G above median level (≥ 50 U/ml) had a significantly shorter survival time. This study demonstrates that HLA-G allelic variants are independent risk factors for NSCLC. Serum sHLA-G levels in NSCLC patients could be useful biomarkers for the diagnostic and prognosis of NSCLC. PMID:27517300

  15. [Idiopathic pulmonary fibrosis and lung cancer].

    PubMed

    Yoshimura, Akinobu; Kudoh, Syoji

    2003-02-01

    It is widely known that patients with idiopathic pulmonary fibrosis (IPF) are frequently associated with lung cancer. Although a complication with lung cancer is an important prognostic factor for IPF, standard treatments for lung cancer cannot be given because of IPF. Especially, the administration of many anticancer agents is limited by a complication with IPF, which is recognized as a risk factor for the development of fatal lung injury in cancer chemotherapy. Epidemiological studies reveal that cigarette smoking and occupational and environmental exposure to toxic substances are common risk factors for both IPF and lung cancer. It has been assumed that metaplasia in fibrous lesions is pathologically a precancerous lesion, but it is necessary to prove several genetic abnormalities in the process of carcinogenesis in order to clarify that. Currently, several genetic abnormalities in IPF, including in p53, K-ras, FHIT and transforming growth factor (TGF)-beta 1 type II receptor, have been reported. PMID:12610869

  16. Functions and mechanisms of long noncoding RNAs in lung cancer

    PubMed Central

    Peng, Zhenzi; Zhang, Chunfang; Duan, Chaojun

    2016-01-01

    Lung cancer is a heterogeneous disease, and there is a lack of adequate biomarkers for diagnosis. Long noncoding RNAs (lncRNAs) are emerging as an important set of molecules because of their roles in various key pathophysiological pathways, including cell growth, apoptosis, and metastasis. We review the current knowledge of the lncRNAs in lung cancer. In-depth analyses of lncRNAs in lung cancer have increased the number of potential effective biomarkers, thus providing options to increase the therapeutic benefit. In this review, we summarize the functions, mechanisms, and regulatory networks of lncRNAs in lung cancer, providing a basis for further research in this field. PMID:27499635

  17. Pulmonary Rehabilitation in Improving Lung Function in Patients With Locally Advanced Non-Small Cell Lung Cancer Undergoing Chemoradiation

    ClinicalTrials.gov

    2015-03-17

    Cachexia; Fatigue; Pulmonary Complications; Radiation Toxicity; Recurrent Non-small Cell Lung Cancer; Stage IIIA Non-small Cell Lung Cancer; Stage IIIB Non-small Cell Lung Cancer; Stage IV Non-small Cell Lung Cancer

  18. Asbestos, Lung Cancers, and Mesotheliomas

    PubMed Central

    Heintz, Nicholas H.; Janssen-Heininger, Yvonne M. W.; Mossman, Brooke T.

    2010-01-01

    Fifteen years have passed since we published findings in the AJRCMB demonstrating that induction of early response fos/jun proto-oncogenes in rodent tracheal and mesothelial cells correlates with fibrous geometry and pathogenicity of asbestos. Our study was the first to suggest that the aberrant induction of signaling responses by crocidolite asbestos and erionite, a fibrous zeolite mineral associated with the development of malignant mesotheliomas (MMs) in areas of Turkey, led to altered gene expression. New data questioned the widely held belief at that time that the carcinogenic effects of asbestos in the development of lung cancer and MM were due to genotoxic or mutagenic effects. Later studies by our group revealed that proto-oncogene expression and several of the signaling pathways activated by asbestos were redox dependent, explaining why antioxidants and antioxidant enzymes were elevated in lung and pleura after exposure to asbestos and how they alleviated many of the phenotypic and functional effects of asbestos in vitro or after inhalation. Since these original studies, our efforts have expanded to understand the interface between asbestos-induced redox-dependent signal transduction cascades, the relationship between these pathways and cell fate, and the role of asbestos and cell interactions in development of asbestos-associated diseases. Of considerable significance is the fact that the signal transduction pathways activated by asbestos are also important in survival and chemoresistance of MMs and lung cancers. An understanding of the pathogenic features of asbestos fibers and dysregulation of signaling pathways allows strategies for the prevention and therapy of asbestos-related diseases. PMID:20068227

  19. Study of Ponatinib in Patients With Lung Cancer Preselected Using Different Candidate Predictive Biomarkers

    ClinicalTrials.gov

    2016-06-07

    Adenocarcinoma of the Lung; Extensive Stage Small Cell Lung Cancer; Limited Stage Small Cell Lung Cancer; Recurrent Non-small Cell Lung Cancer; Recurrent Small Cell Lung Cancer; Stage IIIA Non-small Cell Lung Cancer; Stage IIIB Non-small Cell Lung Cancer; Stage IV Non-small Cell Lung Cancer

  20. The association between human papillomavirus infection and female lung cancer

    PubMed Central

    Lin, Frank Cheau-Feng; Huang, Jing-Yang; Tsai, Stella Ching-Shao; Nfor, Oswald Ndi; Chou, Ming-Chih; Wu, Ming-Fang; Lee, Chun-Te; Jan, Cheng-Feng; Liaw, Yung-Po

    2016-01-01

    Abstract Lung cancer is the leading cause of cancer deaths among Taiwanese women. Human papillomavirus (HPV) has been detected in lung cancer tissues. The aim of this study was to investigate the association between HPV infection and lung cancer among the Taiwanese women. The analytical data were collected from the longitudinal health insurance databases (LHID 2005 and 2010) of the National Health Insurance Research Database (NHIRD). The study participants were 30 years and older and included 24,162 individuals who were identified with HPV infection from 2001 to 2004 and 1,026,986 uninfected individuals. Lung cancer incidence among infected and uninfected individuals was compared using the univariate and multivariate regression models. Among the total participants, 24,162 individuals were diagnosed with HPV. After adjusting for age, gender, low income, residential area, and comorbidity, the risk of lung cancer was higher in women (hazard ratio [HR] 1.263, 95% CI 1.015–1.571), while all cancer risks were high in both men and women with corresponding hazard ratios (HR) of 1.161 (95% CI 1.083–1.245) and HR 1.240 (95% CI 1.154–1.331), respectively. This study showed a significant increase in lung cancer risk among Taiwanese women who were exposed to HPV infection. PMID:27281096

  1. Tuberculosis and subsequent risk of lung cancer in Xuanwei, China

    PubMed Central

    Engels, Eric A.; Shen, Min; Chapman, Robert S.; Pfeiffer, Ruth M.; Yu, Ying-Ying; He, Xingzhou; Lan, Qing

    2008-01-01

    Tobacco and indoor air pollution from smoky coal are major causes of lung cancer in rural Xuanwei County, China. Tuberculosis has been suggested to increase lung cancer risk, but data from prior studies are limited. We conducted an analysis of data from a retrospective cohort study of 42,422 farmers in Xuanwei. In 1992, interviewers administered a standardized questionnaire that included lifetime medical history, including tuberculosis. Subjects were followed from 1976, with deaths from lung cancer ascertained through 1996. We used proportional hazards regression to assess the association between tuberculosis and subsequent lung cancer mortality. Tuberculosis was reported by 246 subjects (0.6%), and 2459 (5.8%) died from lung cancer during follow-up. Lung cancer mortality was substantially higher in subjects with tuberculosis than in those without (25 vs. 3.1 per 1000 person-years). The association was especially pronounced in the first five years after tuberculosis diagnosis (hazard ratios [HRs] ranging 6.7–13) but remained strong 5–9.9 years (HR 3.4, 95%CI 1.3–9.1) and 10+ years (HR 3.0, 95%CI 1.3–7.3) after tuberculosis. These associations were similar among men and women, and among smoky coal users (70.5% of subjects). Adjustment for demographic characteristics, lung disease, and tobacco use did not affect results. In Xuanwei, China, tuberculosis is an important risk factor for lung cancer. The increased lung cancer risk, persisting years after a tuberculosis diagnosis, could reflect the effects of chronic pulmonary inflammation and scarring arising from tuberculosis. PMID:19058197

  2. Tuberculosis and subsequent risk of lung cancer in Xuanwei, China

    SciTech Connect

    Engels, E.A.; Shen, M.; Chapman, R.S.; Pfeiffer, R.M.; Yu, Y.Y.; He, X.Z.; Lan, Q.

    2009-03-15

    Tobacco and indoor air pollution from smoky coal are major causes of lung cancer in rural Xuanwei County, China. Tuberculosis has been suggested to increase lung cancer risk, but data from prior studies are limited. We conducted an analysis of data from a retrospective cohort study of 42,422 farmers in Xuanwei. In 1992, interviewers administered a standardized questionnaire that included lifetime medical history, including tuberculosis. Subjects were followed from 1976, with deaths from lung cancer ascertained through 1996. We used proportional hazards regression to assess the association between tuberculosis and subsequent lung cancer mortality. Tuberculosis was reported by 246 subjects (0.6%), and 2,459 (5.8%) died from lung cancer during follow-up. Lung cancer mortality was substantially higher in subjects with tuberculosis than in those without (25 vs. 3.1 per 1,000 person-years). The association was especially pronounced in the first 5 years after tuberculosis diagnosis (hazard ratios (HRs) ranging 6.7-13) but remained strong 5-9.9 years (HR 3.4, 95% CI 1.3-9.1) and 10+ years (HR 3.0, 95% CI 1.3-7.3) after tuberculosis. These associations were similar among men and women and among smoky coal users (70.5% of subjects). Adjustment for demographic characteristics, lung disease and tobacco use did not affect results. In Xuanwei, China, tuberculosis is an important risk factor for lung cancer. The increased lung cancer risk, persisting years after a tuberculosis diagnosis, could reflect the effects of chronic pulmonary inflammation and scarring arising from tuberculosis.

  3. Early Lung Cancer Diagnosis by Biosensors

    PubMed Central

    Zhang, Yuqian; Yang, Dongliang; Weng, Lixing; Wang, Lianhui

    2013-01-01

    Lung cancer causes an extreme threat to human health, and the mortality rate due to lung cancer has not decreased during the last decade. Prognosis or early diagnosis could help reduce the mortality rate. If microRNA and tumor-associated antigens (TAAs), as well as the corresponding autoantibodies, can be detected prior to clinical diagnosis, such high sensitivity of biosensors makes the early diagnosis and prognosis of cancer realizable. This review provides an overview of tumor-associated biomarker identifying methods and the biosensor technology available today. Laboratorial researches utilizing biosensors for early lung cancer diagnosis will be highlighted. PMID:23892596

  4. PKM2 Thr454 phosphorylation increases its nuclear translocation and promotes xenograft tumor growth in A549 human lung cancer cells.

    PubMed

    Yu, Zhenhai; Huang, Liangqian; Qiao, Pengyun; Jiang, Aifang; Wang, Li; Yang, Tingting; Tang, Shengjian; Zhang, Wei; Ren, Chune

    2016-05-13

    Pyruvate kinase M2 (PKM2) is a key enzyme of glycolysis which is highly expressed in many tumor cells, and plays an important role in the Warburg effect. In previous study, we found PIM2 phosphorylates PKM2 at Thr454 residue (Yu, etl 2013). However, the functions of PKM2 Thr454 modification in cancer cells still remain unclear. Here we find PKM2 translocates into the nucleus after Thr454 phosphorylation. Replacement of wild type PKM2 with a mutant (T454A) enhances mitochondrial respiration, decreases pentose phosphate pathway, and enhances chemosensitivity in A549 cells. In addition, the mutant (T454A) PKM2 reduces xenograft tumor growth in nude mice. These findings demonstrate that PKM2 T454 phosphorylation is a potential therapeutic target in lung cancer. PMID:27045080

  5. A clinically relevant canine lung cancer model

    SciTech Connect

    Benfield, J.R.; Shors, E.C.; Hammond, W.G.; Paladugu, R.R.; Cohen, A.H.; Jensen, T.; Fu, P.C.; Pak, H.Y.; Teplitz, R.L.

    1981-12-01

    Research on early human lung cancer is difficult; we have sought a canine correlate. Regimens included endobronchial submucosal injections and topical focal applications of benzo(a)pyrene, nitrosomethylurea, dimethylbenzanthracene, and methylcholanthrene, singly or in combinations. Sustained-release discs were placed into lung parenchyma or sutured into major bronchi. Tracheal segments were isolated as cervical pedicle grafts. Gross and histological evolution was reproducible. Columnar and basal hyperplasia and squamous metaplasia were early changes. Atypia occurred within 6 weeks and was found in all dogs within 16 to 18 weeks. Invasive cancers occurred within 8 to 65 months. No tracheal graft developed cancer. Of 15 dogs with parenchymal sustained-release implants, 1 to date has developed cancer in 8 months. Four endobronchial regimens have produced 16 cancers in 56 lungs at risk for 18 to 65 months. No cancers developed in 23 lungs at risk from eight other regimens. Of 10 dogs at risk for unilateral endobronchial cancer, 5 have had cancer. Of 23 dogs with both lungs at risk, 9 developed cancer. We have shown focal carcinogenesis with well-defined pathogenesis and an extended preneoplastic period at predictable sites in a lung cancer model.

  6. Lung cancer tissue diagnosis in poor lung function: addressing the ongoing percutaneous lung biopsy FEV1 paradox using Heimlich valve.

    PubMed

    Abdullah, R; Tavare, A N; Creamer, A; Creer, D; Vancheeswaran, R; Hare, S S

    2016-08-01

    Many centres continue to decline percutaneous lung biopsy (PLB) in patients with poor lung function (particularly FEV1 <1 L) due to the theoretically increased risk of pneumothorax. This practice limits access to novel lung cancer therapies and minimally invasive surgical techniques. Our retrospective single-centre analysis of 212 patients undergoing PLB, all performed prospectively and blinded to lung function, demonstrates that using ambulatory Heimlich valve chest drain (HVCD) to treat significant postbiopsy pneumothorax facilitates safe, diagnostic, early discharge lung biopsy irrespective of lung function with neither FEV1 <1 L nor transfer coefficient for carbon monoxide (TLCO) <40% predicted shown to be independent predictors of HVCD insertion or pneumothorax outcomes. Incorporating ambulatory HVCD into standard PLB practice thereby elegantly bridges the gap that currently exists between tissue diagnosis in patients with poor lung function and the advanced therapeutic options available for this cohort. PMID:26980011

  7. Smoking and lung cancer: current trends in Austria

    PubMed Central

    Thompson, Caroline A.; Waldhör, Thomas; Schernhammer, Eva S.; Hackl, Monika; Vutuc, Christian; Haidinger, Gerald

    2013-01-01

    Summary Background Despite a recent decline in smoking behavior in many European countries, lung cancer rates remain high, especially in Central and Eastern Europe. This paper aims to describe trends in smoking behavior and lung cancer incidence and mortality, including histopathological classification of lung cancer, in a Central European country: Austria. Methods Using data from the Austrian Central Cancer Registry, we calculated age-standardized incidence, histopathology-specific incidence, and age-standardized and birth cohort-specific mortality rates for all lung cancer cases in Austria. Using national survey data, we estimated prevalence of smoking in the Austrian population. Our analysis covers the time period from 1970 to 2009. Results In 2009, lung cancer incidence rates were 41.3/100,000 and 18.5/100,000 and mortality rates were 36.3/100,000 and14.5/100,000, for males and females, respectively. Male lung cancer rates declined but increased steadily in females over the past three decades. In 2009, the most common histological type is adenocarcinoma, which reflects a shift from predominantly squamous cell carcinoma and large cell carcinoma in the mid 1980s. In 2009, 27 % of men and 19 % of women were smokers, which represent a rise of smoking rates in women, especially in younger women, and a decline in the men. Conclusions While in Austrian men the lung cancer rates, in accordance with their decreasing prevalence of smoking, declined over the past 30 years, the increasing smoking prevalence and lung cancer rates in women remain a public health concern. Antismoking laws and public health initiatives to curtail smoking habits are needed in Austria, especially targeting younger women. PMID:22815002

  8. Imaging Primary Lung Cancers in Mice to Study Radiation Biology

    PubMed Central

    Kirsch, David G.; Grimm, Jan; Guimaraes, Alexander R.; Wojtkiewicz, Gregory R.; Perez, Bradford A.; Santiago, Philip M.; Anthony, Nikolas K.; Forbes, Thomas; Doppke, Karen; Weissleder, Ralph; Jacks, Tyler

    2010-01-01

    Purpose To image a genetically engineered mouse model of non-small cell lung cancer with micro-CT to measure tumor response to radiation therapy. Methods and Materials The Cre-loxP system was utilized to generate primary lung cancers in mice with mutation in K-ras alone or in combination with p53 mutation. Mice were serially imaged by micro-CT and tumor volumes were determined. A comparison of tumor volume by micro-CT and tumor histology was performed. Tumor response to radiation therapy (15.5 Gy) was assessed with micro-CT. Results The tumor volume measured with free-breathing micro-CT scans was greater than the volume calculated by histology. Nevertheless, this imaging approach demonstrated that lung cancers with mutant p53 grew more rapidly than lung tumors with wild-type p53 and also showed that radiation therapy increased the doubling time of p53 mutant lung cancers five-fold. Conclusions Micro-CT is an effective tool to noninvasively measure the growth of primary lung cancers in genetically engineered mice and assess tumor response to radiation therapy. This imaging approach will be useful to study the radiation biology of lung cancer. PMID:20206017

  9. Imaging Primary Lung Cancers in Mice to Study Radiation Biology

    SciTech Connect

    Kirsch, David G.; Grimm, Jan; Guimaraes, Alexander R.; Wojtkiewicz, Gregory R.; Perez, Bradford A.; Santiago, Philip M.; Anthony, Nikolas K.; Forbes, Thomas; Doppke, Karen

    2010-03-15

    Purpose: To image a genetically engineered mouse model of non-small-cell lung cancer with micro-computed tomography (micro-CT) to measure tumor response to radiation therapy. Methods and Materials: The Cre-loxP system was used to generate primary lung cancers in mice with mutation in K-ras alone or in combination with p53 mutation. Mice were serially imaged by micro-CT, and tumor volumes were determined. A comparison of tumor volume by micro-CT and tumor histology was performed. Tumor response to radiation therapy (15.5 Gy) was assessed with micro-CT. Results: The tumor volume measured with free-breathing micro-CT scans was greater than the volume calculated by histology. Nevertheless, this imaging approach demonstrated that lung cancers with mutant p53 grew more rapidly than lung tumors with wild-type p53 and also showed that radiation therapy increased the doubling time of p53 mutant lung cancers fivefold. Conclusions: Micro-CT is an effective tool to noninvasively measure the growth of primary lung cancers in genetically engineered mice and assess tumor response to radiation therapy. This imaging approach will be useful to study the radiation biology of lung cancer.

  10. Inhibition of rhotekin exhibits antitumor effects in lung cancer cells

    PubMed Central

    ZHANG, WEIZHEN; LIANG, ZHENYU; LI, JING

    2016-01-01

    Lung cancer is the leading cause for cancer-related death, however, the pathogenesis mechanism is poorly understood. Although the rhotekin (RTKN) gene has been reported to encode an effector for the Rho protein that has critical roles in regulating cell growth, the role of RTKN in lung cancer has not been investigated. In clinical lung cancer patient tumor samples, we identified that the RTKN gene expression level was significantly higher in tumor tissues compared to that of the adjacent normal tissues. To investigate the molecular mechanisms of RTKN in lung cancer, we established RTKN stable knock-down A549 and SPC-A-1 lung adenocarcinoma cell lines using lentiviral transfection of RTKN shRNA and evaluated the antitumor effects. The results showed that RTKN knock-down inhibited lung adenocarcinoma cell viability, induced S phase arrest and increased cell apoptosis. In addition, RTKN knock-down inhibited lung cancer cell invasion and adhesion. Further analysis showed that the S phase promoting factors cyclindependent kinase (CDK)1 and CDK2 levels were decreased in RTKN knock-down cells, and that the DNA replication initiation complex proteins Minichromosome maintenance protein complex (MCM)2 and MCM6 were decreased as well in RTKN knock-down cells. These results indicated that the RTKN protein was associated with lung cancer in clinic samples and exerted anticancer activity in lung adenocarcinoma cells through inhibiting cell cycle progression and the DNA replication machinery. These findings suggest that RTKN inhibition may be a novel therapeutic strategy for lung adenocarcinoma. PMID:26935528

  11. Increasing Radiation Therapy Dose Is Associated With Improved Survival in Patients Undergoing Stereotactic Body Radiation Therapy for Stage I Non–Small-Cell Lung Cancer

    SciTech Connect

    Koshy, Matthew; Malik, Renuka; Weichselbaum, Ralph R.; Sher, David J.

    2015-02-01

    Purpose: To determine the comparative effectiveness of different stereotactic body radiation therapy (SBRT) dosing regimens for early-stage non–small-cell lung cancer, using a large national database, focusing on the relative impact of dose as a function of tumor stage. Methods and Materials: The study included patients in the National Cancer Database from 2003 to 2006 with T1-T2N0M0 inoperable lung cancer (n=498). The biologically effective dose (BED) was calculated according to the linear quadratic formula using an α/β ratio of 10. High versus lower-dose (HD vs LD) SBRT was defined as a calculated BED above or below 150 Gy. Overall survival was estimated using Kaplan-Meier methods and Cox proportional hazard regression. Results: The 5 most common dose fractionation schemes (percentage of cohort) used were 20 Gy × 3 (34%), 12 Gy × 4 (16%), 18 Gy × 3 (10%), 15 Gy × 3 (10%), and 16 Gy × 3 (4%). The median calculated BED was 150 Gy (interquartile range 106-166 Gy). The 3-year overall survival (OS) for patients who received HD versus LD was 55% versus 46% (log–rank P=.03). On subset analysis of the T1 cohort there was no association between calculated BED and 3-year OS (61% vs 60% with HD vs LD, P=.9). Among the T2 cohort, patients receiving HD experienced superior 3-year OS (37% vs 24%, P=.01). On multivariable analysis, factors independently prognostic for mortality were female gender (hazard ratio [HR] 0.76, P=.01), T2 tumor (HR 1.99, P=.0001), and HD (HR 0.68, P=.001). Conclusions: This comparative effectiveness analysis of SBRT dose for patients with stage I non–small-cell lung cancer suggests that higher doses (>150 Gy BED) are associated with a significant survival benefit in patients with T2 tumors.

  12. Development of lung cancer CT screening operating support system

    NASA Astrophysics Data System (ADS)

    Ishigaki, Rikuta; Hanai, Kozou; Suzuki, Masahiro; Kawata, Yoshiki; Niki, Noboru; Eguchi, Kenji; Kakinuma, Ryutaro; Moriyama, Noriyuki

    2009-02-01

    In Japan, lung cancer death ranks first among men and third among women. Lung cancer death is increasing yearly, thus early detection and treatment are needed. For this reason, CT screening for lung cancer has been introduced. The CT screening services are roughly divided into three sections: office, radiology and diagnosis sections. These operations have been performed through paper-based or a combination of paper-based and an existing electronic health recording system. This paper describes an operating support system for lung cancer CT screening in order to make the screening services efficient. This operating support system is developed on the basis of 1) analysis of operating processes, 2) digitalization of operating information, and 3) visualization of operating information. The utilization of the system is evaluated through an actual application and users' survey questionnaire obtained from CT screening centers.

  13. Increased Biological Effective Dose of Radiation Correlates with Prolonged Survival of Patients with Limited-Stage Small Cell Lung Cancer: A Systematic Review

    PubMed Central

    Xu, Xiao; Wang, Bing; Wu, Kan; Deng, Qinghua; Xia, Bing; Ma, Shenglin

    2016-01-01

    Objective Thoracic radiotherapy (TRT) is a critical component of the treatment of limited-stage small cell lung cancer (LS-SCLC). However, the optimal radiation dose/fractionation remains elusive. This study reviewed current evidence and explored the dose-response relationship in patients with LS-SCLC who were treated with radiochemotherapy. Materials and Methods A quantitative analysis was performed through a systematic search of PubMed, Web of Science, and the Cochrane Library. The correlations between the biological effective dose (BED) and median overall survival (mOS), median progression-free survival (mPFS), 1-, 3-, and 5-year overall survival (OS) as well as local relapse (LR) were evaluated. Results In all, 2389 patients in 19 trials were included in this study. Among these 19 trials, seven were conducted in Europe, eight were conducted in Asia and four were conducted in the United States. The 19 trials that were included consisted of 29 arms with 24 concurrent and 5 sequential TRT arms. For all included studies, the results showed that a higher BED prolonged the mOS (R2 = 0.198, p<0.001) and the mPFS (R2 = 0.045, p<0.001). The results also showed that increased BED improved the 1-, 3-, and 5-year OS. A 10-Gy increment added a 6.3%, a 5.1% and a 3.7% benefit for the 1-, 3-, and 5-year OS, respectively. Additionally, BED was negatively correlated with LR (R2 = 0.09, p<0.001). A subgroup analysis of concurrent TRT showed that a high BED prolonged the mOS (p<0.001) and the mPFS (p<0.001), improved the 1-, 3-, and 5-year OS (p<0.001) and decreased the rate of LR (p<0.001). Conclusion This study showed that an increased BED was associated with improved OS, PFS and decreased LR in patients with LS-SCLC who were treated with combined chemoradiotherapy, which indicates that the strategy of radiation dose escalation over a limited time frame is worth exploring in a prospective clinical trial. PMID:27227819

  14. Taste thresholds in patients with small-cell lung cancer.

    PubMed

    Ovesen, L; Hannibal, J; Sørensen, M

    1991-01-01

    Recognition thresholds for the four basic tastes (salt, sour, sweet and bitter) were tested by the forced-choice technique in 27 patients with small-cell lung cancer, and 22 weight-matched control patients with non-malignant diseases. No significant differences in threshold concentrations could be demonstrated. When patients who were losing weight were compared with weight-stable patients, significantly lower taste thresholds for bitter substances were found in weight losing groups in both cancer and control patients. Small-cell lung cancer patients who responded to therapy had obtained an increased threshold for bitter taste at the time of reevaluation than at the time of diagnosis, an effect that may be explained by the chemotherapeutic regimen. The results suggest that in patients with small-cell lung cancer it is not the cancer disease per se but the weight loss that often accompanies it that causes an increased taste sensitivity for bitter substances. PMID:1847701

  15. Early diagnosis of lung cancer.

    PubMed

    Yasufuku, Kazuhiro

    2010-03-01

    Early detection and surgical resection is essential for the treatment of lung cancer. Although the introduction of low-dose spiral computed tomography (CT) is considered to be one of the most promising clinical research developments, CT screening is used for detecting small peripheral lesions. Tumors arising in the central airways require other techniques for early detection. Centrally arising squamous cell carcinoma of the airway, especially in heavy smokers, is thought to develop through multiple stages from squamous metaplasia to dysplasia, followed by carcinoma in situ (CIS), progressing to invasive cancer. It would be ideal to be able to detect and treat preinvasive bronchial lesions defined as dysplasia and CIS before progressing to invasive cancer. Great efforts have been made to develop new mucosal imaging techniques. Bronchoscopic imaging techniques capable of detecting preinvasive lesions and currently available in clinical practice include autofluorescence bronchoscopy (AFB), high magnification ronchovideoscope, and narrow band imaging (NBI). For a more precise evaluation of newly detected preinvasive lesions, endobronchial ultrasound (EBUS) and optical coherence tomography (OCT) can be used. PMID:20172431

  16. Anthropometry and the Risk of Lung Cancer in EPIC.

    PubMed

    Dewi, Nikmah Utami; Boshuizen, Hendriek C; Johansson, Mattias; Vineis, Paolo; Kampman, Ellen; Steffen, Annika; Tjønneland, Anne; Halkjær, Jytte; Overvad, Kim; Severi, Gianluca; Fagherazzi, Guy; Boutron-Ruault, Marie-Christine; Kaaks, Rudolf; Li, Kuanrong; Boeing, Heiner; Trichopoulou, Antonia; Bamia, Christina; Klinaki, Eleni; Tumino, Rosario; Palli, Domenico; Mattiello, Amalia; Tagliabue, Giovanna; Peeters, Petra H; Vermeulen, Roel; Weiderpass, Elisabete; Torhild Gram, Inger; Huerta, José María; Agudo, Antonio; Sánchez, María-José; Ardanaz, Eva; Dorronsoro, Miren; Quirós, José Ramón; Sonestedt, Emily; Johansson, Mikael; Grankvist, Kjell; Key, Tim; Khaw, Kay-Tee; Wareham, Nick; Cross, Amanda J; Norat, Teresa; Riboli, Elio; Fanidi, Anouar; Muller, David; Bueno-de-Mesquita, H Bas

    2016-07-15

    The associations of body mass index (BMI) and other anthropometric measurements with lung cancer were examined in 348,108 participants in the European Investigation Into Cancer and Nutrition (EPIC) between 1992 and 2010. The study population included 2,400 case patients with incident lung cancer, and the average length of follow-up was 11 years. Hazard ratios were calculated using Cox proportional hazard models in which we modeled smoking variables with cubic splines. Overall, there was a significant inverse association between BMI (weight (kg)/height (m)(2)) and the risk of lung cancer after adjustment for smoking and other confounders (for BMI of 30.0-34.9 versus 18.5-25.0, hazard ratio = 0.72, 95% confidence interval: 0.62, 0.84). The strength of the association declined with increasing follow-up time. Conversely, after adjustment for BMI, waist circumference and waist-to-height ratio were significantly positively associated with lung cancer risk (for the highest category of waist circumference vs. the lowest, hazard ratio = 1.25, 95% confidence interval: 1.05, 1.50). Given the decline of the inverse association between BMI and lung cancer over time, the association is likely at least partly due to weight loss resulting from preclinical lung cancer that was present at baseline. Residual confounding by smoking could also have influenced our findings. PMID:27370791

  17. Genetic susceptibility to lung cancer--light at the end of the tunnel?

    PubMed

    Marshall, Ariela L; Christiani, David C

    2013-03-01

    Lung cancer is one of the most common and deadliest cancers in the world. The major socio-environmental risk factor involved in the development of lung cancer is cigarette smoking. Additionally, there are multiple genetic factors, which may also play a role in lung cancer risk. Early work focused on the presence of relatively prevalent but low-penetrance alterations in candidate genes leading to increased risk of lung cancer. Development of new technologies such as genomic profiling and genome-wide association studies has been helpful in the detection of new genetic variants likely involved in lung cancer risk. In this review, we discuss the role of multiple genetic variants and review their putative role in the risk of lung cancer. Identifying genetic biomarkers and patterns of genetic risk may be useful in the earlier detection and treatment of lung cancer patients. PMID:23349013

  18. Sequencing study on familial lung squamous cancer

    PubMed Central

    LI, SHAOMIN; WANG, LINA; MA, ZHENCHUAN; MA, YUEFENG; ZHAO, JIANGMAN; PENG, BO; QIAO, ZHE

    2015-01-01

    Lung cancer is the leading cause of cancer-related mortality worldwide. The majority of lung cancers are sporadic, and familial cases are extremely rare. Previous studies have mainly focused on sporadic lung cancer and identified a large quantity of driver genes. However, familial lung cancers are rarer and studied less. The present study recruited a Chinese family in which multiple members had developed lung squamous carcinoma. To find the causative mutations, whole exome sequencing was conducted using a peripheral blood sample of one lung squamous carcinoma patient, and certain variants were validated in more samples. Whole exome sequencing analysis obtained ~2.0 Gb of data (an average of 60x depth for each targeted base), and further validation experiments identified two functional variants in two cancer-related genes (c.1218delA:p.E406fs in PDE4DIP and C1342A:p.L448I in CLTCL1). This study therefore provides useful sources for the further study of hereditary lung cancer. PMID:26622902

  19. Primary lung cancer associated with Werner syndrome.

    PubMed

    Ohnishi, Shunichiro; Fujimoto, Masaki; Oide, Takashi; Nakatani, Yukio; Tsurutani, Yuya; Koshizaka, Masaya; Mezawa, Morito; Ishikawa, Takahiro; Takemoto, Minoru; Yokote, Koutaro

    2010-10-01

    A 52-year-old man with Werner Syndrome (WS) was admitted to our hospital for the treatment of skin ulcers on his thighs. Routine chest radiography revealed an abnormal shadow in the left upper lung field. Computed tomography (CT) revealed a poorly demarcated homogeneous mass (diameter, 4 cm) in the S1 + 2 lung area; no pleural effusion was observed. CT-guided percutaneous needle biopsy revealed the presence of an adenocarcinoma. Other imaging studies did not reveal any lymph-node involvement or presence of metastatic lesions. The patient was diagnosed with stage IB adenocarcinoma (T2N0M0), and a left upper lobectomy was successfully carried out; postoperative wound healing was steady and uneventful, with no obvious ulcer formation. Primary lung cancers very rarely develop in patients with WS; non-epithelial tumors are usually observed in such patients. Patients with WS usually develop severe skin problems, such as refractory skin ulcers in the extremities; however, our patient did not develop any skin-related complications after surgery. As the expected lifespan of patients with WS is increasing, we need to pay attention not only to the rare non-epithelial malignancy, but also cancer. Further, the expected short lifespan of patients with WS, as well as the possibility of skin-related problems after surgery, should not be considered while deciding whether to take the option of surgery in the case of malignancy. PMID:20887625

  20. Lung cancer in asbestos cement workers in Denmark.

    PubMed Central

    Raffn, E; Villadsen, E; Engholm, G; Lynge, E

    1996-01-01

    OBJECTIVES: To study the relative and absolute risks of main types of lung cancer in a cohort of asbestos cement workers from Denmark. METHOD: A cohort of 7887 men and 576 women employed between 1928 and 1984 was compiled from the personnel files of Danish Eternit Production. The cohort was followed up for deaths, emigrations, and incident cancer cases during the period 1943-90. The observed number of lung cancer cases in the cohort was compared with the expected number based on incidences for the Danish population. Internal comparison was made with Poisson modelling. RESULTS: A total of 226 lung cancer cases were observed (223 men and three women). The standardised incidence ratio (SIR) for all lung cancer among men was 1.7 (observed number 223, expected number 129.7, 95% confidence interval (95% CI) 1.5-2.0). The SIRs were raised for all main types of lung cancer; adenocarcinoma 2.6, squamous cell carcinoma 1.7, and anaplastic carcinoma 1.5. The higher SIR for adenocarcinomas was found particularly with a latency period of 25 years or more. Among the 93 excess lung cancer cases, 36 were squamous cell carcinomas and 32 were adenocarcinomas. CONCLUSION: Asbestos cement work is associated with an increased risk of lung cancer of all main types. During the first 25 years after the start of employment this excess risk is shared almost equally between the different histological types of lung cancer, but the risk of adenocarcinomas is clearly higher after this point. PMID:8758035

  1. Association Between COX-2 Polymorphisms and Lung Cancer Risk

    PubMed Central

    Wang, Weiwei; Fan, Xinyun; Zhang, Yong; Yang, Yi; Yang, Siyuan; Li, Gaofeng

    2015-01-01

    Background Multiple relevant risk factors for lung cancer have been reported in different populations, but results of previous studies were not consistent. Therefore, a meta-analysis is necessary to summarize these outcomes and reach a relatively comprehensive conclusion. Material/Methods STATA 12.0 software was used for all statistical of the relationship between COX-2 polymorphisms and lung cancer risk. Inter-study heterogeneity was examined with the Q statistic (significance level at P<0.1). The publication bias among studies in the meta-analysis was analyzed with Begg’s funnel plot and Egger’s test. Hardy-Weinberg equilibrium was tested in all controls of the studies. Results COX-2 rs20417 polymorphism had a significant association with reduced risk of lung cancer under homozygous and recessive models, and similar results were observed in white and population-based subgroups under 2 and 3 contrasts, respectively. Additionally, rs2066826 polymorphism manifested a strong correlation with increased risk of lung cancer under 5 genetic models. Conclusions In COX-2 gene, rs20417 may have a certain relationship with reduced risk of lung cancer, while rs2066826 may increase the risk of lung cancer. PMID:26624903

  2. Trends of lung cancer mortality in Mexico.

    PubMed

    Lazcano Ponce, E C; Tovar Guzman, V; Meneses Gonzalez, F; Rascon Pacheco, R A; Hernandez Avila, M

    1997-01-01

    Lung cancer (LC) is one of the most important public health problems in the world; 1,035,000 annual deaths are estimated each year and more than 80% of these are attributed to tobacco. The trend of lung cancer mortality in Mexico City from 1979 - 1993 was determined, as was the rate ratio of lung cancer mortality in 31 states in Mexico, taking Mexico City as a reference by means of a Poisson model. A strong linear regression model was used to evaluate the rate, where the dependent variable was LC mortality rate and the independent variable the year observed. In 15 years, 73,807 deaths from LC were reported, with an increase in mortality from 5.01 - 7.25 per 100,000 inhabitants. Mortality increases significantly after 60 years of age (B not equal to 0), p<.05) in men and in women. Mortality from LC was 70% in men, and more than 60% of deaths were reported after 65 years of age. Mortality risk is higher in the northern states of the country (e.g., Sonora, RR=2.40) than in the southern region (e.g., Oaxaca RR=0.40). In Mexico, almost 10,000 deaths by LC are estimated for the year 2010. Therefore, changes in lifestyle should be encouraged in order to decrease the smoking habit. The governmental tax on cigarettes should be increased, smoking restricted in squares and public spaces, and the risks should be announced on cigarette packages, among other measures. With respect to other emergent risk factors, the sources of industrial pollution and toxic emissions should be regulated. PMID:9428585

  3. Metallothioneins in the lung cancer.

    PubMed

    Werynska, Bozena; Pula, Bartosz; Kobierzycki, Christopher; Dziegiel, Piotr; Podhorska-Okolow, Marzenna

    2015-01-01

    Metallothioneins (MTs) are low weight proteins involved in several key cellular processes such as metal ions homeostasis, detoxification and scavenging of free radicals. Four groups of MTs are distinguished: MT-1, MT-2, MT-3 and MT-4. Regardless of the type, MTs are characterized by high content of cysteine, responsible for their biological properties such as binding of relevant zinc and copper ions, as well as toxic ions such as lead and cadmium. MTs were additionally shown to protect cells against oxidative stress damage and participate in differentiation, proliferation and/or apoptosis of normal and cancer cells. Many studies of different neoplasms showed association of elevated MTs levels with occurrence of chemo- and radiotherapy resistance and poor patients' outcome. In this review, we summarize and discuss the potential mechanism of action of metallotioneins in lung physiology and pathology. PMID:25815626

  4. [Epidemiologic aspects of the histologic types of lung cancer].

    PubMed

    Wilde, J; Matthäi, C; Wilde, J

    1990-01-01

    An epidemiological study was performed in the county of Erfurt including all lung cancer patients of the years 1963, 1968, and 1972 to 1977, together 2,585 males and 358 females. The following results were found: 1. The incidence of lung cancer increased significantly from 1963 to 1977. 2. About 60% of all lung cancer patients were younger than 70 years. 3. In male patients squamous cell carcinomas prevailed with 44.8%. Small cell cancers came up to 34.6% and adenocarcinomas to 10.1%. Large cell cancers reached 10.5%. These types in female patients had a proportion to each other like 26.9%: 30.8%: 30.4%: 11.9%. The proportion of adenocarcinomas increased significantly during 1963 to 1977. 4. We found a non significant age relation of histological types. The adenocarcinoma and the small cell cancers dropped with rising age. 5. The classification of histological types and the conditions of detection of lung cancers did not change in the study interval. Therefore the altering of patterns of histological types, especially the increase of adenocarcinomas was attached to the beginning of cigarette smoking in younger ages and the increasing proportion of filter tipped brands as well to a variation of exposition against professional cancerogens. 6. Patients with adenocarcinomas have the highest survival rate after 5 years: 8.1%. Squamous cell lung cancer patients have a 5 year survival rate of 6.8%. Patients with small cell cancers and large cell cancers ranged at 2.7% or 2.6%. 7. Peripheral tumors of each histological type will be detected earlier by fluorographic screening than central carcinomas. Therefore the 5 year survival rates of peripheral cancers always are more favourable than that of central cancers. 8. For the problems in exact typing and staging we propose an internationally adjusted definition of tumor localization as a third parameter for prognosis. PMID:2171236

  5. Lung Cancer:Symptoms, Diagnosis, Treatments & Research | NIH MedlinePlus the Magazine

    MedlinePlus

    ... of this page please turn Javascript on. Feature: Lung Cancer Lung Cancer: Symptoms, Diagnosis, Treatments & Research Past Issues / Winter 2013 ... lung cancer are given intravenously or by mouth. Lung Cancer Research The large-scale National Lung Screening Trial, ...

  6. Microdosimetric considerations of lung cancer risks from plutonium.

    PubMed

    Simmons, Jack A

    2015-03-01

    New data from the workers at the Mayak nuclear facility near Chelyabinsk, Russia, apparently show a linear increase in the risk of lung cancer with increasing dose. Furthermore, this increase occurs without a threshold. However, these conclusions are at variance with the results reported by other investigators. A possible cause of these inconsistencies could be the lack of application of microdosimetric considerations when discussing "dose" to the lung. PMID:25627951

  7. Cryptogenic fibrosing alveolitis and lung cancer.

    PubMed

    Turner-Warwick, M; Lebowitz, M; Burrows, B; Johnson, A

    1980-07-01

    Lung cancer was found in 20 (9.8%) of 205 patients with cryptogenic fibrosing alveolitis (CFA) or 12.9% of the 155 patients in this series followed to death. An excess relative risk of lung cancer of 14.1 was found in patients with CFA compared to the general population of comparable age and sex, allowing for the lengths of follow-up of the CFA patients. The relative risk for male smokers was (observed/expected) 15+1.06 = 14.2, and for female smokers (O/E) 2/0.3 = 6.7. Only one male and one female non-smoker had lung cancer. These data suggest that there is an excess risk of lung cancer not wholly accounted for by age, sex, or smoking habit. The distribution of histological types was not obviously different from that found in lung cancer without pulmonary fibrosis. Large opacities suggestive of lung cancer were present at the time of first hospital attendance for symptoms relating to CFA in four of the 20 patients. Finger clubbing was present in 19 (95%) compared with 116/185 (63%) of those so far not developing cancer. There were no other clinical differences at presentation. In particular, cancer was not found especially in those with longer survival from the onset of symptoms of CFA or with a greater initial radiographic change. PMID:7434310

  8. Recent evidence, advances, and current practices in surgical treatment of lung cancer.

    PubMed

    Suda, Kenichi; Sato, Katsuaki; Mizuuchi, Hiroshi; Kobayashi, Yoshihisa; Shimoji, Masaki; Tomizawa, Kenji; Takemoto, Toshiki; Iwasaki, Takuya; Sakaguchi, Masahiro; Mitsudomi, Tetsuya

    2014-11-01

    In the last 10-15 years, strategies and modalities of lung cancer treatment have changed dramatically. Meanwhile, the treatment objectives, the lung cancers themselves, have also changed, probably owing to early detection by computed tomography and aging of the population. In particular, the proportions of smaller lung cancers, lung adenocarcinomas with ground-glass opacity, and lung cancers in older patients are increasing. Along with these changes, surgeons have innovated and evaluated novel procedures for pulmonary resection. These include the application of minimally invasive surgical techniques, such as video-assisted thoracoscopic surgery (VATS) and robotic surgery, and sub-lobar resection, such as wedge resection and segmentectomy, for small peripheral lung cancers. Currently, VATS has gained wide acceptance and several institutions in Japan have started using robotic surgery for lung cancers. Two important clinical trials of sub-lobar resection for small peripheral lung cancers are now underway in Japan. In addition, surgery itself is of growing importance in lung cancer treatment. In particular, recent evidence supports the use of surgery in strictly selected patients with locally advanced disease, lung cancers with N2 lymph node metastases, small cell lung cancers, recurrent oligo-metastasis after pulmonary resection, or relapsed tumors after drug treatment. Surgical treatment also provides abundant tumor samples for molecular analysis, which can be used for drug selection in the adjuvant setting or after disease relapse. In the era of personalized treatment, surgery is still one of the most important treatment modalities to combat lung cancer. PMID:25453375

  9. Immune checkpoint blockade in lung cancer.

    PubMed

    Somasundaram, Aswin; Socinski, Mark A; Villaruz, Liza C

    2016-08-01

    Immunotherapy has revolutionized the therapeutic landscape of advanced lung cancer. The adaptive immune system has developed a sophisticated method of tumor growth control, but T-cell activation is regulated by various checkpoints. Blockade of the immune checkpoints with therapies targeting the PD-1 pathway, such as nivolumab and pembrolizumab, has been validated as a therapeutic approach in non-small cell lung cancer. Newer therapies and novel combinations are also being evaluated, and the use of biomarkers in conjunction with these drugs is an area of active investigation. This review summarizes the current evidence for the efficacy and safety of the above approaches in the treatment of lung cancer. PMID:27585231

  10. The Canadian Lung Cancer Conference 2016

    PubMed Central

    Melosky, B.; Ho, C.

    2016-01-01

    Each February, the Canadian Lung Cancer Conference brings together lung cancer researchers, clinicians, and care professionals who are united in their commitment to improve the care of patients with lung cancer. This year’s meeting, held 11–12 February, featured a resident education session, a welcome dinner, networking sessions, lectures, breakout sessions, debates, and a satellite symposium. Key themes from this year’s meeting included innovations across the care spectrum and results of recent clinical trials with targeted agents, immuno-oncology agents, and novel drug combinations.

  11. CMTM7 knockdown increases tumorigenicity of human non-small cell lung cancer cells and EGFR-AKT signaling by reducing Rab5 activation

    PubMed Central

    Li, Ting; Yuan, Wanqiong; Mo, Xiaoning; Li, Henan; He, Qihua; Ma, Dalong; Han, Wenling

    2015-01-01

    The dysregulation of epidermal growth factor receptor (EGFR) signaling has been well documented to contribute to the progression of non-small cell lung cancer (NSCLC), the leading cause of cancer death in the world. EGF-stimulated EGFR activation induces receptor internalization and degradation, which plays an important role in EGFR signaling. This process is frequently deregulated in cancer cells, leading to enhanced EGFR levels and signaling. Our previous study on CMTM7 is only limited to a brief description of the relationship of overexpressed CMTM7 with EGFR-AKT signaling. The biological functions of endogenous CMTM7 and its molecular mechanism remained unclear. In this study, we show that the stable knockdown of CMTM7 augments the malignant potential of NSCLC cells and enhances EGFR-AKT signaling by decreasing EGFR internalization and degradation. Mechanistically, CMTM7 knockdown reduces the activation of Rab5, a protein known to be required for early endosome fusion. In NSCLC, the loss of CMTM7 would therefore serve to sustain aberrant EGFR-mediated oncogenic signaling. Together, our findings highlight the role of CMTM7 in the regulation of EGFR signaling in tumor cells, revealing CMTM7 as a novel molecule related to Rab5 activation. PMID:26528697

  12. Perceptions of lung cancer and potential impacts on funding and patient care: a qualitative study.

    PubMed

    Tran, Kim; Delicaet, Kendra; Tang, Theresa; Ashley, Leslie Beard; Morra, Dante; Abrams, Howard

    2015-03-01

    The objective of this study was to explore health-care professionals', health administrators', and not-for-profit cancer organization representatives' perceptions of lung cancer-related stigma and nihilism and the perceived impacts on funding and patient care. This is a qualitative descriptive study using semi-structured interviews, which was conducted in Ontario, Canada. Seventy-four individuals from medical oncology, radiation oncology, thoracic surgery, respirology, pathology, radiology, primary care, palliative care, nursing, pharmacy, social work, genetics, health administration, and not-for-profit cancer organizations participated in this study. Participants described lung cancer-related stigma and nihilism and its negative impact on patients' psychological health, lung cancer funding, and patient care. The feeling of guilt and shame experienced by lung cancer patients as a result of the stigma associated with the disease was described. In terms of lung cancer funding, stigma was described as a reason lung cancer receives significantly less research funding compared to other cancers. In terms of patient care, lung cancer-related nihilism was credited with negatively impacting physician referral patterns with the belief that lung cancer patients were less likely to receive referrals for medical treatment. Health-care professionals, health administrators, and not-for-profit cancer organization representatives described lung cancer-related stigma and nihilism with far-reaching consequences. Further work is needed to increase education and awareness about lung cancer to reduce the stigma and nihilism associated with the disease. PMID:24882441

  13. Elastin-derived peptides increase invasive capacities of lung cancer cells by post-transcriptional regulation of MMP-2 and uPA.

    PubMed

    Toupance, Simon; Brassart, Bertrand; Rabenoelina, Fanja; Ghoneim, Christelle; Vallar, Laurent; Polette, Myriam; Debelle, Laurent; Birembaut, Philippe

    2012-06-01

    Elastin-rich lung extracellular matrix is largely remodeled during tumor invasion. Elastin degradation produces peptides displaying a wide range of biological activities. These elastin derived peptides (EP) interact with the elastin receptor complex (ERC) but also bind to α(V)β(3) integrin and galectin-3. In this study, we explored the role of EP and their receptors in tumor progression of lung carcinomas. Non-invasive and invasive lung tumor cell lines were incubated in presence of kappa-elastin (κE) or with synthetic peptides displaying receptor-specific sequences (VGVAPG, GRKRK, AGVPGLGVG and AGVPGFGAG). Modified Boyden chamber assays revealed an increased invasive capacity of invasive cells induced by κE. EP treatment had no effect on cell proliferation but zymography analysis revealed an increase of pro-MMP-2 and uPA levels in the conditioned media of treated cells. Moreover, the active form of MMP-2 was increased in invasive cells. Interestingly, this regulation was not observed at the mRNA level and actinomycin D was unable to inhibit κE effects. We also observed that the regulation of proteases protein level following κE treatment was an early process detectable after 1 h. All these effects could not be inhibited by lactose and V14, two ERC antagonists, or by blocking antibodies against α(V)β(3) integrin and galectin-3. Finally, VGVAPG and GRKRK failed to reproduce κE effects whereas nonapeptides partially mimicked them. These results demonstrate that treatment with EP up-regulates invasiveness of lung tumor cells via the release of proteolytic enzymes. This modulation involves post-transcriptional mechanisms and a nonapeptide-receptor different from the ERC, α(V)β(3) integrin and galectin-3. PMID:22434583

  14. Lung and Upper Aerodigestive Cancer | Division of Cancer Prevention

    Cancer.gov

    This group conducts and supports research on the prevention and early detection of lung and head and neck cancers, as well as new approac | Conducts and supports research on the prevention and early detection of lung and head and neck cancers.

  15. Lung Cancer Care Before and After Medicare Eligibility.

    PubMed

    Huesch, Marco D; Ong, Michael K

    2016-01-01

    Uninsured and underinsured near-elderly may not have timely investigation, diagnosis, or care of cancer. Prior studies suggest Medicare eligibility confers significant and substantial reductions in mortality and increases in health service utilization. We compared 2245 patients diagnosed with lung cancer at ages 64.5 to 65 years and 2512 patients aged 65 to 65.5 years, with 2492 patients aged 65.5 to 66 years (controls) in 2000 to 2005. Compared with controls, patients diagnosed with lung cancer before Medicare eligibility had no statistically significant differences in cancer stage, time to treatment, type of treatment, and survival. Study power was sufficient to exclude mortality reductions and health service utilization changes of the magnitude found in prior work, suggesting that typically, appropriate lung cancer care may be sought and delivered regardless of insurance status. PMID:27166413

  16. Lung cancer mutations and use of targeted agents in Hispanics.

    PubMed

    Cress, W Douglas; Chiappori, Alberto; Santiago, Pedro; Muñoz-Antonia, Teresita

    2014-01-01

    Hispanic/Latinos (H/L) are expected to grow to over 24% of the USA population by 2050 and lung cancer is the number one cause of cancer death among H/L men. Due to the information that is becoming available via genetic testing, lung cancer molecular profiling is allowing for increasing application of personalized lung cancer therapies. However, to benefit the most people, development of these therapies and genetic tests must include research on as many racial and ethnic groups as possible. The purpose of this review is to bring attention to the fact that the mutations driving lung cancer in H/Ls differ in frequency and nature relative to the non-Hispanic White (WNH) majority that dominate current databases and participate in clinical trials that test new therapies. Clinical trials using new agents targeting genetic alterations (driver mutations) in lung cancer have demonstrated significant improvements in patient outcomes (for example, gefitinib, erlotinib or crizotinib for lung adenocarcinomas harboring EGFR mutations or EML4-ALK fusions, respectively). The nature and frequencies of some lung cancer driver mutations have been shown to be considerably different among racial and ethnic groups. This is particularly true for H/Ls. For example, several reports suggest a dramatic shift in the mutation pattern from predominantly KRAS in a WNH population to predominantly EGFR in multiple H/L populations. However, these studies are limited, and the effects of racial and ethnic differences on the incidence of mutations in lung cancer remain incompletely understood. This review serves as a call to address this problem. PMID:25626064

  17. Protein Signature of Lung Cancer Tissues

    PubMed Central

    Mehan, Michael R.; Ayers, Deborah; Thirstrup, Derek; Xiong, Wei; Ostroff, Rachel M.; Brody, Edward N.; Walker, Jeffrey J.; Gold, Larry; Jarvis, Thale C.; Janjic, Nebojsa; Baird, Geoffrey S.; Wilcox, Sheri K.

    2012-01-01

    Lung cancer remains the most common cause of cancer-related mortality. We applied a highly multiplexed proteomic technology (SOMAscan) to compare protein expression signatures of non small-cell lung cancer (NSCLC) tissues with healthy adjacent and distant tissues from surgical resections. In this first report of SOMAscan applied to tissues, we highlight 36 proteins that exhibit the largest expression differences between matched tumor and non-tumor tissues. The concentrations of twenty proteins increased and sixteen decreased in tumor tissue, thirteen of which are novel for NSCLC. NSCLC tissue biomarkers identified here overlap with a core set identified in a large serum-based NSCLC study with SOMAscan. We show that large-scale comparative analysis of protein expression can be used to develop novel histochemical probes. As expected, relative differences in protein expression are greater in tissues than in serum. The combined results from tissue and serum present the most extensive view to date of the complex changes in NSCLC protein expression and provide important implications for diagnosis and treatment. PMID:22509397

  18. [New biological treatments for lung cancer].

    PubMed

    Zalcman, G; Richard, N; Bergot, E

    2007-02-01

    Therapies targeted on cell signal pathways that control cell division and tumor angiogenesis have been developed over the last five years for non small cell lung cancer (NSCLC) with some amazing results, in subgroups of selected patients, predicting more significant success in the upcoming years. Compounds targeted on EGF tyrosine kinase receptor have been tested in large clinical phase 2 and 3 trials including thousands of patients. Their efficacy has been proved, in second and third line trials, after first line cisplatin-based chemotherapy for non-mucinous adenocarcinoma in non-smokers, women and Asian patients. Response rates vary from 10% in non selected Caucasian patients to 40% in non-smoking Asian patients with long survivals. Therapeutic targeting improves success rates, either relying on EGFR gene amplification detection by FISH, or search for EGFR tyrosine kinase domain mutations. Commercial kits are available for routine molecular diagnosis of domain mutations potentially enabling molecular targeting in addition to clinical targeting. Angiogenesis inhibitors, especially monoclonal antibody to VEGF, bevacizumab, have also been developed in the last few years. Bevacizumab associated with classical cytotoxic chemotherapy led, in selected patients (with non squamous cell lung cancer and no past history of cardiovascular disease) to an increase of median survival to more than 12 months with tolerable toxicity. Other drugs that have both anti-EGFR activity and anti-angiogenic properties will be soon developed, since future bioactive anti-cancer drugs will probably be multi-targeted drugs. PMID:17457280

  19. Lung cancer screening guidelines: common ground and differences

    PubMed Central

    Gulati, Swati

    2014-01-01

    Lung cancer accounts for almost one-third of all cancer related deaths. Lung cancer risk persists even after smoking cessation and so many lung cancers now are diagnosed in former smokers. Five-year survival of lung cancer has marginally improved over decades and significantly lags behind that of colon, breast and prostate cancer. Over the past one decade, lung cancer screening trials have shown promising results. Results from National Lung Cancer Screening Trial (NLST), have shown a significant 20% reduction in mortality with annual low dose computed tomography (LDCT) screening. Based on these results, annual LDCT testing has been recommended for lung cancer screening in high risk population. However, development and acceptance of lung cancer screening as a public health policy is still in the nascent stages. Major concerns relate to risk of radiation, overdiagnosis bias, proportion of false positives and cost benefit analysis. This article reviews the literature pertaining to lung cancer screening guidelines and above mentioned concerns. PMID:25806292

  20. Lung cancer screening guidelines: common ground and differences.

    PubMed

    Gulati, Swati; Mulshine, James L

    2014-06-01

    Lung cancer accounts for almost one-third of all cancer related deaths. Lung cancer risk persists even after smoking cessation and so many lung cancers now are diagnosed in former smokers. Five-year survival of lung cancer has marginally improved over decades and significantly lags behind that of colon, breast and prostate cancer. Over the past one decade, lung cancer screening trials have shown promising results. Results from National Lung Cancer Screening Trial (NLST), have shown a significant 20% reduction in mortality with annual low dose computed tomography (LDCT) screening. Based on these results, annual LDCT testing has been recommended for lung cancer screening in high risk population. However, development and acceptance of lung cancer screening as a public health policy is still in the nascent stages. Major concerns relate to risk of radiation, overdiagnosis bias, proportion of false positives and cost benefit analysis. This article reviews the literature pertaining to lung cancer screening guidelines and above mentioned concerns. PMID:25806292

  1. Lung cancer in ferrous foundry workers: a review.

    PubMed

    Palmer, W G; Scott, W D

    1981-05-01

    Epidemiologic studies indicate that an increased incidence of lung cancer may be associated with specific work areas in ferrous foundries. With the exception of crane operators, who were found to have an elevated lung cancer rate in one foundry, the excess lung cancer incidence is generally confined to molders, casters, and cleaning room operators whose lung cancer risk is two- to threefold higher than that of standard populations. These studies reflect conditions that existed in the foundries several decades ago. The lung cancer risk today may differ as a result of the introduction of new foundry practices and the use of new molding materials. Benzo(a)pyrene and certain other polycyclic aromatic hydrocarbons have been found in many locations in the foundries. It is not known if tumor promoters, co-carcinogens, or other classes of chemical carcinogens are present. The contribution of tobacco smoke to the lung cancer risk of ferrous foundry workers is also unknown. Current studies are examining the composition and long-term health effects of emissions from molds composed of modern synthetic chemical molding materials as well as those from the more traditional green sand molds. PMID:7013460

  2. Management of Lung Cancer in the Elderly.

    PubMed

    Rao, Archana; Sharma, Namita; Gajra, Ajeet

    2016-01-01

    Lung cancer is the leading cause of cancer-associated mortality in the USA. The median age at diagnosis of lung cancer is 70 years, and thus, about one-half of patients with lung cancer fall into the elderly subgroup. There is dearth of high level of evidence regarding the management of lung cancer in the elderly in the three broad stages of the disease including early-stage, locally advanced, and metastatic disease. A major reason for the lack of evidence is the underrepresentation of elderly in prospective randomized clinical trials. Due to the typical decline in physical and physiologic function associated with aging, most elderly do not meet the stringent eligibility criteria set forth in age-unselected clinical trials. In addition to performance status, ideally, comorbidity, cognitive, and psychological function, polypharmacy, social support, and patient preferences should be taken into account before applying prevailing treatment paradigms often derived in younger, healthier patients to the care of the elderly patient with lung cancer. The purpose of this chapter was to review the existing evidence of management of early-stage, locally advanced disease, and metastatic lung cancer in the elderly. PMID:27535398

  3. Antioxidants accelerate lung cancer progression in mice.

    PubMed

    Sayin, Volkan I; Ibrahim, Mohamed X; Larsson, Erik; Nilsson, Jonas A; Lindahl, Per; Bergo, Martin O

    2014-01-29

    Antioxidants are widely used to protect cells from damage induced by reactive oxygen species (ROS). The concept that antioxidants can help fight cancer is deeply rooted in the general population, promoted by the food supplement industry, and supported by some scientific studies. However, clinical trials have reported inconsistent results. We show that supplementing the diet with the antioxidants N-acetylcysteine (NAC) and vitamin E markedly increases tumor progression and reduces survival in mouse models of B-RAF- and K-RAS-induced lung cancer. RNA sequencing revealed that NAC and vitamin E, which are structurally unrelated, produce highly coordinated changes in tumor transcriptome profiles, dominated by reduced expression of endogenous antioxidant genes. NAC and vitamin E increase tumor cell proliferation by reducing ROS, DNA damage, and p53 expression in mouse and human lung tumor cells. Inactivation of p53 increases tumor growth to a similar degree as antioxidants and abolishes the antioxidant effect. Thus, antioxidants accelerate tumor growth by disrupting the ROS-p53 axis. Because somatic mutations in p53 occur late in tumor progression, antioxidants may accelerate the growth of early tumors or precancerous lesions in high-risk populations such as smokers and patients with chronic obstructive pulmonary disease who receive NAC to relieve mucus production. PMID:24477002

  4. Passive smoking and lung cancer in nonsmoking women.

    PubMed Central

    Brownson, R C; Alavanja, M C; Hock, E T; Loy, T S

    1992-01-01

    OBJECTIVES. The causes of lung cancer among nonsmokers are not clearly understood. To further evaluate the relation between passive smoke exposure and lung cancer in nonsmoking women, we conducted a population-based, case-control study. METHODS. Case patients (n = 618), identified through the Missouri Cancer Registry for the period 1986 through 1991, included 432 lifetime nonsmokers and 186 ex-smokers who had stopped at least 15 years before diagnosis or who had smoked for less than 1 pack-year. Control subjects (n = 1402) were selected from driver's license and Medicare files. RESULTS. No increased risk of lung cancer was associated with childhood passive smoke exposure. Adulthood analyses showed an increased lung cancer risk for lifetime nonsmokers with exposure of more than 40 pack-years from all household members (odds ratio [OR] = 1.3; 95% confidence interval [CI] = 1.0, 1.8) or from spouses only (OR = 1.3; 95% CI = 1.0, 1.7). When the time-weighted product of pack-years and average hours exposed per day was considered, a 30% excess risk was shown at the highest quartile of exposure among lifetime nonsmokers. CONCLUSIONS. Ours and other recent studies suggest a small but consistent increased risk of lung cancer from passive smoking. Comprehensive actions to limit smoking in public places and worksites are well-advised. PMID:1443304

  5. Lung cancer in the Indian subcontinent.

    PubMed

    Noronha, Vanita; Pinninti, Rakesh; Patil, Vijay M; Joshi, Amit; Prabhash, Kumar

    2016-01-01

    Smoking tobacco, both cigarettes and beedis, is the principal risk factor for causation of lung cancer in Indian men; however, among Indian women, the association with smoking is not strong, suggesting that there could be other risk factors besides smoking. Despite numerous advances in recent years in terms of diagnostic methods, molecular changes, and therapeutic interventions, the outcomes of the lung cancer patients remain poor; hence, a better understanding of the risk factors may impact the preventive measures to be implemented at the community level. There is a lack of comprehensive data on lung cancer in India. In this review, we attempt to collate the available data on lung cancer from India. PMID:27606290

  6. Lung cancer in the Indian subcontinent

    PubMed Central

    Noronha, Vanita; Pinninti, Rakesh; Patil, Vijay M.; Joshi, Amit; Prabhash, Kumar

    2016-01-01

    Smoking tobacco, both cigarettes and beedis, is the principal risk factor for causation of lung cancer in Indian men; however, among Indian women, the association with smoking is not strong, suggesting that there could be other risk factors besides smoking. Despite numerous advances in recent years in terms of diagnostic methods, molecular changes, and therapeutic interventions, the outcomes of the lung cancer patients remain poor; hence, a better understanding of the risk factors may impact the preventive measures to be implemented at the community level. There is a lack of comprehensive data on lung cancer in India. In this review, we attempt to collate the available data on lung cancer from India. PMID:27606290

  7. Lung cancer in patients diagnosed with silicosis should be investigated.

    PubMed

    Güngen, Adil Can; Aydemir, Yusuf; Çoban, Hikmet; Düzenli, Hasan; Tasdemir, Canantan

    2016-01-01

    Silicosis is an interstitial lung disease developing as a result of inhalation of inorganic silica particles. In silicosis cases developing as a result of environmental and occupational exposure, an increase is observed in Turkey especially depending upon denim sandblasting. We present a 35-year-old female case who was applied to our hospital due to complaint of progressive dyspnea, had a history of working in denim sandblasting for 18 months, were diagnosed with silicosis as a result of high resolution computed tomography (HRCT) and diagnosed with lung adenocarcinoma as a result of transbronchial lung biopsy made due to clinical deterioration and radiological progression within three months. The purpose of this report was to point out that lung cancer can develop in patients followed up with diagnosis of silicosis or radiologic findings in silicosis can be confused with lung cancer. PMID:27330963

  8. Surgery for small cell lung cancer.

    PubMed

    de Hoyos, Alberto; DeCamp, Malcolm M

    2014-11-01

    Small-cell lung cancer (SCLC) comprises approximately 14% of all lung cancer cases. Most patients present with locally advanced or metastatic disease and are therefore treated nonoperatively with chemotherapy, radiotherapy, or both. A small subset of patients with SCLC present with early-stage disease and will benefit from surgical resection plus chemotherapy. The rationale for radiotherapy in these patients remains controversial. PMID:25441133

  9. Advances in bronchoscopy for lung cancer

    PubMed Central

    Dhillon, Samjot Singh; Dexter, Elisabeth U.

    2012-01-01

    Bronchoscopic techniques have seen significant advances in the last decade. The development and refinement of different types of endobronchial ultrasound and navigation systems have led to improved diagnostic yield and lung cancer staging capabilities. The complication rate of these minimally invasive procedures is extremely low as compared to traditional transthoracic needle biopsy and surgical sampling. These advances augment the safe array of methods utilized in the work up and management algorithms of lung cancer. PMID:23346012

  10. [Lung cancer: psychological and psychiatric aspects].

    PubMed

    Domingues, Vera; Albuquerque, Emília

    2008-01-01

    According to the literature, lung cancer patients experience greater emotional distress than other cancer patients, with scores as high as 61,6%. Poor prognosis, guilt and stigma associated with a history of smoking, may be related with this morbidity. Several studies mention the prevalence of depression to be between 16 and 22%. As distress affects the family as well, mostly those members involved in the patient care, they should not be forgotten and must be involved in the treatment plan. The authors conclude that lung cancer patients' distress is highly prevalent and interferes with quality of live and, possibly, prognosis. Therefore, psychosocial care should be integrated early in cancer treatment. PMID:18363022

  11. Immunotherapy for lung cancer: advances and prospects.

    PubMed

    Yang, Li; Wang, Liping; Zhang, Yi

    2016-01-01

    Lung cancer is the most commonly diagnosed cancer as well as the leading cause of cancer-related deaths worldwide. To date, surgery is the first choice treatment, but most clinically diagnosed cases are inoperable. While chemotherapy and/or radiotherapy are the next considered options for such cases, these treatment modalities have adverse effects and are sometimes lethal to patients. Thus, new effective strategies with minimal side effects are urgently needed. Cancer immunotherapy provides either active or passive immunity to target tumors. Multiple immunotherapy agents have been proposed and tested for potential therapeutic benefit against lung cancer, and some pose fewer side effects as compared to conventional chemotherapy and radiotherapy. In this article, we discuss studies focusing on interactions between lung cancer and the immune system, and we place an emphasis on outcome evidence in order to create a knowledge base well-grounded in clinical reality. Overall, this review highlights the need for new lung cancer treatment options, with much ground to be paved for future advances in the field. We believe that immunotherapy agents alone or with other forms of treatment can be recognized as next modality of lung cancer treatment. PMID:27168951

  12. Immunotherapy for lung cancer: advances and prospects

    PubMed Central

    Yang, Li; Wang, Liping; Zhang, Yi

    2016-01-01

    Lung cancer is the most commonly diagnosed cancer as well as the leading cause of cancer-related deaths worldwide. To date, surgery is the first choice treatment, but most clinically diagnosed cases are inoperable. While chemotherapy and/or radiotherapy are the next considered options for such cases, these treatment modalities have adverse effects and are sometimes lethal to patients. Thus, new effective strategies with minimal side effects are urgently needed. Cancer immunotherapy provides either active or passive immunity to target tumors. Multiple immunotherapy agents have been proposed and tested for potential therapeutic benefit against lung cancer, and some pose fewer side effects as compared to conventional chemotherapy and radiotherapy. In this article, we discuss studies focusing on interactions between lung cancer and the immune system, and we place an emphasis on outcome evidence in order to create a knowledge base well-grounded in clinical reality. Overall, this review highlights the need for new lung cancer treatment options, with much ground to be paved for future advances in the field. We believe that immunotherapy agents alone or with other forms of treatment can be recognized as next modality of lung cancer treatment. PMID:27168951

  13. Lung Cancer Screening with Low Dose CT

    PubMed Central

    Caroline, Chiles

    2014-01-01

    SUMMARY The announcement of the results of the NLST, showing a 20% reduction in lung-cancer specific mortality with LDCT screening in a high risk population, marked a turning point in lung cancer screening. This was the first time that a randomized controlled trial had shown a mortality reduction with an imaging modality aimed at early detection of lung cancer. Current guidelines endorse LDCT screening for smokers and former smokers ages 55 to 74, with at least a 30 pack year smoking history. Adherence to published algorithms for nodule follow-up is strongly encouraged. Future directions for screening research include risk stratification for selection of the screening population, and improvements in the diagnostic follow-up for indeterminate pulmonary nodules. As with screening for other malignancies, screening for lung cancer with LDCT has revealed that there are indolent lung cancers which may not be fatal. More research is necessary if we are to maximize the risk-benefit ratio in lung cancer screening. PMID:24267709

  14. Current Controversies in Lung Cancer Staging.

    PubMed

    Carter, Brett W; Godoy, Myrna C B; Wu, Carol C; Erasmus, Jeremy J; Truong, Mylene T

    2016-07-01

    Lung cancer remains the leading cause of cancer-related mortality in the United States, and accurate staging of disease plays an important role in the formulation of treatment strategies and optimization of patient outcomes. The International Association for the Study of Lung Cancer has recently proposed changes to the upcoming eighth edition of the tumor, node, and metastasis (TNM-8) staging system used for lung cancer. This revised classification is based on significant differences in patient survival identified on analysis of a new large international database of lung cancer cases. Key changes include: further modifications to the T descriptors based on 1 cm increments in tumor size; grouping of tumors resulting in partial or complete lung atelectasis/pneumonitis; grouping of tumors involving a main bronchus with respect to distance from the carina; reassignment of diaphragmatic invasion; elimination of mediastinal pleural invasion as a descriptor; and further subdivision of metastatic disease into distinct descriptors based on the number of extrathoracic metastases and involved organs. Because of these changes, several new stage groups have been developed, and others have shifted. Although TNM-8 represents continued improvement upon modifications previously made to the staging system, reflecting an evolving understanding of tumor behavior and patient management, several limitations and unaddressed issues persist. Understanding the proposed revisions to TNM-8 and awareness of key limitations and potential controversial issues still unaddressed will allow radiologists to accurately stage patients with lung cancer and optimize treatment decisions. PMID:27306388

  15. Lung cancer screening overdiagnosis: reports of overdiagnosis in screening for lung cancer are grossly exaggerated.

    PubMed

    Mortani Barbosa, Eduardo J

    2015-08-01

    The National Lung Cancer Screening Trial (NLST) demonstrated a mortality reduction benefit associated with low-dose computed tomography (LDCT) screening for lung cancer. There has been considerable debate regarding the benefits and harms of LDCT lung cancer screening, including the challenges related to its practical implementation. One of the controversies regards overdiagnosis, which conceptually denotes diagnosing a cancer that, either because of its indolent, low-aggressiveness biologic behavior or because of limited life expectancy, is unlikely to result in significant morbidity during the patient's remainder lifetime. In theory, diagnosing and treating these cancers offer no measurable benefit while incurring costs and risks. Therefore, if a screening test detects a substantial number of overdiagnosed cancers, it is less likely to be effective. It has been argued that LDCT screening for lung cancer results in an unacceptably high rate of overdiagnosis. This article aims to defend the opposite stance. Overdiagnosis does exist and to a certain extent is inherent to any cancer-screening test. Nonetheless, the concept is less dualistic and more nuanced than it has been suggested. Furthermore, the average estimates of overdiagnosis in LDCT lung cancer screening based on the totality of published data are likely much lower than the highest published estimates, if a careful definition of a positive screening test reflecting our current understanding of lung cancer biology is utilized. This article presents evidence on why reports of overdiagnosis in lung cancer screening have been exaggerated. PMID:25772581

  16. Role of STAT3 in lung cancer

    PubMed Central

    Dutta, Pranabananda; Sabri, Nafiseh; Li, Jinghong; Li, Willis X

    2014-01-01

    Lung cancer remains a challenging disease. It is responsible for the high cancer mortality rates in the US and worldwide. Elucidation of the molecular mechanisms operative in lung cancer is an important first step in developing effective therapies. Accumulating evidence over the last 2 decades suggests a critical role for Signal Transducer and Activator of Transcription 3 (STAT3) as a point of convergence for various signaling pathways that are dysregulated in the disease. In this review, we discuss possible molecular mechanisms involving STAT3 in lung tumorigenesis based on recent literature. We consider possible roles of STAT3 in cancer cell proliferation and survival, in the tumor immune environment, and in epigenetic regulation and interaction of STAT3 with other transcription factors. We also discuss the potential role of STAT3 in tumor suppression, which complicates strategies of targeting STAT3 in cancer therapy. PMID:26413424

  17. Mineral particles, mineral fibers, and lung cancer

    SciTech Connect

    Churg, A.; Wiggs, B.

    1985-08-01

    The total fibrous and nonfibrous mineral content of the lung has been analyzed in a series of 14 men with lung cancer but no history of occupational dust exposure, and in a series of 14 control men matched for age, smoking history, and general occupational class. The lung cancer patients had an average of 525 +/- 369 X 10(6) exogenous mineral particles and 17.4 +/- 19.6 X 10(6) exogenous mineral fibers/g dry lung, while the controls had averages of 261 +/- 175 mineral particles and 4.7 +/- 3.2 X 10(6) mineral fibers/g dry lung. These differences are statistically significant for both particles and fibers. Kaolinite, talc, mica, feldspars, and crystalline silica comprised the majority of particles of both groups. Approximately 90% of the particles were smaller than 2 micron in diameter and approximately 60% smaller than 1 micron. In both groups, patients who had smoked more than 35 pack years had greater numbers of particles than patients who had smoked less than 35 pack years. It is concluded that, in this study, lungs from patients with lung cancer had statistically greater numbers of mineral particles and fibers than lungs from controls, and that smoking influences total long-term retention of particles from all sources.

  18. Diesel engine exhaust and lung cancer: An unproven association

    SciTech Connect

    Muscat, J.E.; Wynder, E.L.

    1995-09-01

    The risk of lung cancer associated with diesel exhaust has been calculated from 14 case-control or cohort studies. We evaluated the findings from these studies to determine whether there is sufficient evidence to implicate diesel exhaust as a human lung carcinogen. Four studies found increased risks associated with long-term exposure, although two of the four studies were based on the same cohort of railroad workers. Six studies were inconclusive due to missing information on smoking habits, internal inconsistencies, or inadequate characterization of diesel exposure. Four studies found no statistically significant association. It can be concluded that short-term exposure to diesel engine exhaust (<20 years) does not have a causative role in human lung cancer. There is statistical but no causal evidence that long-term exposure to diesel exhaust (>20 years) increases the risk of lung cancer for locomotive engineers, brakemen, and diesel engine mechanics. There is inconsistent evidence on the effects of long-term exposure to diesel exhaust in the trucking industry. There is no evidence for a joint effect of diesel exhaust and cigarette smoking on lung cancer risk. Using common criteria for determining causal associations, the epidemiologic evidence is insufficient to establish diesel engine exhaust as a human lung carcinogen. 77 refs., 1 tab.

  19. Lung cancer treatment rates and the role of the lung cancer nurse specialist: a qualitative study

    PubMed Central

    Redman, Judy; McDonnell, Ann; Borthwick, Diana; White, John

    2015-01-01

    Objectives This qualitative study examines how the Lung Cancer Nurse Specialist (LCNS) role operates and why they may be able to increase access to treatment. Setting 4 Hospital NHS Foundation Trusts in England. Design A multiple case study design using semistructured interviews, observation and Framework Analysis techniques. Participants Four LCNSs, comprised the ‘cases’. Twenty four clinicians who worked with the LCNS participated in individual interviews. Six LCNSs took part in a group interview and 60 lung cancer multidisciplinary team (MDT) members and co-ordinators were observed in the MDT meeting. Results The LCNS is crucial within the MDT and can act as a catalyst to patient access to treatment. The study identified the clinical activity (assessment, managing symptoms, psychological support and information provision) and role characteristics that can facilitate treatment access. These characteristics are the LCNS's presence across the patient pathway, acting as the ‘hub’ of the MDT, maintaining a holistic patient focus and working to an advanced level of practice. The findings indicate how factors may have a cumulative impact on treatment access. Conclusions If UK patient with lung cancer survival rates are to improve in line with comparable countries, we need to employ every advantage. This study demonstrates how the LCNS role may open doors to positive patient outcomes, including treatment. Further research is required to explore patients’ experiences, decision-making and attitudes to treatment. PMID:26685023

  20. Silicosis and risk of lung cancer or lung tuberculosis: a cohort study

    SciTech Connect

    Westerholm, P.; Ahlmark, A.; Maasing, R.; Segelberg, I.

    1986-10-01

    This is a study of cancer mortality, cancer incidence, and incidence of lung tuberculosis among cases of silicosis reported to the National Swedish Pneumoconiosis Register during 1959-1977. Two occupational categories were extracted - mining, tunneling, and quarrying (n = 284) and iron and steel foundries (n = 428), respectively. Control groups were drawn from a national register of persons undergoing periodic health examinations with regard to silicosis risk. The controls were matched for occupation, age, and time of first exposure. In cases drawn from mining, quarrying, and tunneling workers seven deaths in lung cancer were observed and two among the controls. Among iron and steel foundry workers the corresponding numbers were 10 and 6. The values for expected numbers, based on general population statistics, were 1.3 and 2.6, respectively, for these two occupational groups. When cancer incidence statistics were used, the case/control ratio for lung cancer was 2.1 for mining, quarrying, and tunneling and 0.6 for iron and steel foundries. There were 29 cases of lung tuberculosis registered among the silicosis cases during the follow-up period. Only one tuberculosis case was observed among the controls. The results demonstrate that persons with silicosis contracted in the mining, quarrying, and tunneling occupations are subject to an increased risk of lung cancer.

  1. Paraneoplastic syndromes associated with lung cancer

    PubMed Central

    Kanaji, Nobuhiro; Watanabe, Naoki; Kita, Nobuyuki; Bandoh, Shuji; Tadokoro, Akira; Ishii, Tomoya; Dobashi, Hiroaki; Matsunaga, Takuya

    2014-01-01

    Paraneoplastic syndromes are signs or symptoms that occur as a result of organ or tissue damage at locations remote from the site of the primary tumor or metastases. Paraneoplastic syndromes associated with lung cancer can impair various organ functions and include neurologic, endocrine, dermatologic, rheumatologic, hematologic, and ophthalmological syndromes, as well as glomerulopathy and coagulopathy (Trousseau’s syndrome). The histological type of lung cancer is generally dependent on the associated syndrome, the two most common of which are humoral hypercalcemia of malignancy in squamous cell carcinoma and the syndrome of inappropriate antidiuretic hormone secretion in small cell lung cancer. The symptoms often precede the diagnosis of the associated lung cancer, especially when the symptoms are neurologic or dermatologic. The proposed mechanisms of paraneoplastic processes include the aberrant release of humoral mediators, such as hormones and hormone-like peptides, cytokines, and antibodies. Treating the underlying cancer is generally the most effective therapy for paraneoplastic syndromes, and treatment soon after symptom onset appears to offer the best potential for symptom improvement. In this article, we review the diagnosis, potential mechanisms, and treatments of a wide variety of paraneoplastic syndromes associated with lung cancer. PMID:25114839

  2. MicroRNA-106b-25 cluster targets β-TRCP2, increases the expression of Snail and enhances cell migration and invasion in H1299 (non small cell lung cancer) cells.

    PubMed

    Savita, Udainiya; Karunagaran, Devarajan

    2013-05-17

    Lung cancer causes high mortality without a declining trend and non small cell lung cancer represents 85% of all pulmonary carcinomas. MicroRNAs (miRNAs) serve as fine regulators of proliferation, migration, invasion/metastasis and angiogenesis of normal and cancer cells. Using TargetScan6.2, we predicted that the ubiquitin ligase, β-TRCP2, could be a target for two of the constituent miRNAs of the miR-106b-25 cluster (miR-106b and miR-93). We generated a stable clone of miR-106b-25 cluster (CL) or the empty vector (EV) in H1299 (non small cell lung cancer) cells. The expression of β-TRCP2 mRNA was significantly lower in CL than that in EV cells. Transient expression of miR-93 but not antimiR-93 decreased the expression of β-TRCP2 mRNA in H1299 cells. β-TRCP2-3'UTR reporter assay revealed that its activity in CL cells was only 60% of that in EV cells. Snail protein expression was higher in CL than that in EV cells and H1299 cells exhibited an increase in the expression of Snail upon transient transfection with miR-93. miR-106b-25 cluster-induced migration of CL measured by scratch assay was more than that in EV cells and no significant difference in migration was observed between antimiR-93-transfected H1299 cells and the corresponding control-oligo-transfected cells. miR-106b-25 cluster-induced migration of CL cells was again confirmed in a Boyden chamber assay without the matrigel. CL cells were more invasive than EV cells when assessed using Boyden chambers with matrigel but there were no significant changes in the cell viabilities between EV and CL cells. Colony formation assay revealed that the CL cells formed more number of colonies than EV cells but they were smaller in size than those formed by EV cells. The supernatant from CL cells was more effective than that from EV cells in inducing tube formation in endothelial cells. Taken together, our data indicate that miR-106b-25 cluster may play an important role in the metastasis of human non-small cell

  3. Transbronchial Dissemination of Squamous Cell Lung Cancer

    PubMed Central

    Tadokoro, Akira; Kanaji, Nobuhiro; Ishii, Tomoya; Watanabe, Naoki; Inoue, Takuya; Kadowaki, Norimitsu; Bandoh, Shuji

    2015-01-01

    We report a case of squamous cell lung cancer with transbronchial dissemination in a 73-year-old man. Bronchoscopic examination revealed multiple bronchial mucosal nodules that existed independently of one another. We reviewed 16 previous cases of endobronchial metastasis in lung cancer. All patients were men. Among the reports that described the smoking history, most patients were smokers (6/7), and the most frequent histological type of cancer was squamous cell carcinoma (11/17). Although hematogenous and lymphogenous routes have been reported as metastatic mechanisms, no previous cases involving transbronchial dissemination have been described. Transbronchial dissemination may be an alternative pathway of endobronchial metastasis. PMID:26672760

  4. 28 CFR 79.54 - Proof of primary lung cancer.

    Code of Federal Regulations, 2011 CFR

    2011-07-01

    ... 28 Judicial Administration 2 2011-07-01 2011-07-01 false Proof of primary lung cancer. 79.54... cancer. (a) In determining whether a claimant developed primary lung cancer following pertinent... conclusion that a claimant developed primary lung cancer must be supported by medical documentation. To...

  5. 28 CFR 79.54 - Proof of primary lung cancer.

    Code of Federal Regulations, 2014 CFR

    2014-07-01

    ... 28 Judicial Administration 2 2014-07-01 2014-07-01 false Proof of primary lung cancer. 79.54... cancer. (a) In determining whether a claimant developed primary lung cancer following pertinent... conclusion that a claimant developed primary lung cancer must be supported by medical documentation. To...

  6. 28 CFR 79.54 - Proof of primary lung cancer.

    Code of Federal Regulations, 2012 CFR

    2012-07-01

    ... 28 Judicial Administration 2 2012-07-01 2012-07-01 false Proof of primary lung cancer. 79.54... cancer. (a) In determining whether a claimant developed primary lung cancer following pertinent... conclusion that a claimant developed primary lung cancer must be supported by medical documentation. To...

  7. 28 CFR 79.64 - Proof of primary lung cancer.

    Code of Federal Regulations, 2012 CFR

    2012-07-01

    ... 28 Judicial Administration 2 2012-07-01 2012-07-01 false Proof of primary lung cancer. 79.64... cancer. (a) In determining whether a claimant developed primary lung cancer following pertinent... claimant. A conclusion that a claimant developed primary lung cancer must be supported by...

  8. 28 CFR 79.64 - Proof of primary lung cancer.

    Code of Federal Regulations, 2013 CFR

    2013-07-01

    ... 28 Judicial Administration 2 2013-07-01 2013-07-01 false Proof of primary lung cancer. 79.64... cancer. (a) In determining whether a claimant developed primary lung cancer following pertinent... claimant. A conclusion that a claimant developed primary lung cancer must be supported by...

  9. 28 CFR 79.45 - Proof of primary lung cancer.

    Code of Federal Regulations, 2011 CFR

    2011-07-01

    ... 28 Judicial Administration 2 2011-07-01 2011-07-01 false Proof of primary lung cancer. 79.45... cancer. (a) In determining whether a claimant developed primary lung cancer following pertinent... conclusion that a claimant developed primary lung cancer must be supported by medical documentation. To...

  10. 28 CFR 79.45 - Proof of primary lung cancer.

    Code of Federal Regulations, 2014 CFR

    2014-07-01

    ... 28 Judicial Administration 2 2014-07-01 2014-07-01 false Proof of primary lung cancer. 79.45... cancer. (a) In determining whether a claimant developed primary lung cancer following pertinent... conclusion that a claimant developed primary lung cancer must be supported by medical documentation. To...

  11. 28 CFR 79.54 - Proof of primary lung cancer.

    Code of Federal Regulations, 2010 CFR

    2010-07-01

    ... 28 Judicial Administration 2 2010-07-01 2010-07-01 false Proof of primary lung cancer. 79.54... cancer. (a) In determining whether a claimant developed primary lung cancer following pertinent... conclusion that a claimant developed primary lung cancer must be supported by medical documentation. To...

  12. 28 CFR 79.64 - Proof of primary lung cancer.

    Code of Federal Regulations, 2010 CFR

    2010-07-01

    ... 28 Judicial Administration 2 2010-07-01 2010-07-01 false Proof of primary lung cancer. 79.64... cancer. (a) In determining whether a claimant developed primary lung cancer following pertinent... claimant. A conclusion that a claimant developed primary lung cancer must be supported by...

  13. 28 CFR 79.45 - Proof of primary lung cancer.

    Code of Federal Regulations, 2013 CFR

    2013-07-01

    ... 28 Judicial Administration 2 2013-07-01 2013-07-01 false Proof of primary lung cancer. 79.45... cancer. (a) In determining whether a claimant developed primary lung cancer following pertinent... conclusion that a claimant developed primary lung cancer must be supported by medical documentation. To...

  14. 28 CFR 79.64 - Proof of primary lung cancer.

    Code of Federal Regulations, 2011 CFR

    2011-07-01

    ... 28 Judicial Administration 2 2011-07-01 2011-07-01 false Proof of primary lung cancer. 79.64... cancer. (a) In determining whether a claimant developed primary lung cancer following pertinent... claimant. A conclusion that a claimant developed primary lung cancer must be supported by...

  15. 28 CFR 79.45 - Proof of primary lung cancer.

    Code of Federal Regulations, 2010 CFR

    2010-07-01

    ... 28 Judicial Administration 2 2010-07-01 2010-07-01 false Proof of primary lung cancer. 79.45... cancer. (a) In determining whether a claimant developed primary lung cancer following pertinent... conclusion that a claimant developed primary lung cancer must be supported by medical documentation. To...

  16. 28 CFR 79.64 - Proof of primary lung cancer.

    Code of Federal Regulations, 2014 CFR

    2014-07-01

    ... 28 Judicial Administration 2 2014-07-01 2014-07-01 false Proof of primary lung cancer. 79.64... cancer. (a) In determining whether a claimant developed primary lung cancer following pertinent... claimant. A conclusion that a claimant developed primary lung cancer must be supported by...

  17. 28 CFR 79.54 - Proof of primary lung cancer.

    Code of Federal Regulations, 2013 CFR

    2013-07-01

    ... 28 Judicial Administration 2 2013-07-01 2013-07-01 false Proof of primary lung cancer. 79.54... cancer. (a) In determining whether a claimant developed primary lung cancer following pertinent... conclusion that a claimant developed primary lung cancer must be supported by medical documentation. To...

  18. 28 CFR 79.45 - Proof of primary lung cancer.

    Code of Federal Regulations, 2012 CFR

    2012-07-01

    ... 28 Judicial Administration 2 2012-07-01 2012-07-01 false Proof of primary lung cancer. 79.45... cancer. (a) In determining whether a claimant developed primary lung cancer following pertinent... conclusion that a claimant developed primary lung cancer must be supported by medical documentation. To...

  19. Molecular understanding of lung cancers-A review

    PubMed Central

    Singh, Chinnappan Ravinder; Kathiresan, Kandasamy

    2014-01-01

    Lung cancer is considered to be the most common cancer in the world. The purpose of this paper is to review scientific evidence, particularly epidemiologic evidence of overall lung cancer burden in the world. And molecular understanding of lung cancer at various levels by dominant and suppressor oncogenes. PMID:25183110

  20. Combination Chemotherapy, Radiation Therapy, and Bevacizumab in Treating Patients With Newly Diagnosed Stage III Non-Small Cell Lung Cancer That Cannot Be Removed By Surgery

    ClinicalTrials.gov

    2016-05-26

    Adenocarcinoma of the Lung; Adenosquamous Cell Lung Cancer; Bronchoalveolar Cell Lung Cancer; Large Cell Lung Cancer; Squamous Cell Lung Cancer; Stage IIIA Non-small Cell Lung Cancer; Stage IIIB Non-small Cell Lung Cancer

  1. Explorations of lung cancer stigma for female long term survivors

    PubMed Central

    Brown, Cati; Cataldo, Janine

    2013-01-01

    Lung cancer is the leading cause of cancer death in women, accompanied by greater psychological distress than other cancers. There is minimal but increasing awareness of the impact of lung cancer stigma (LCS) on patient outcomes. LCS is associated with increased symptom burden and decreased quality of life. The purpose of this study was to explore the experience of female long term lung cancer survivors in the context of LCS and examine how participants discursively adhere to or reject stigmatizing beliefs. Findings situated within Cataldo et al.’s theoretical model include: 1) addiction and tobacco marketing as possible precursors for LCS, 2) the possible role of expert providers as LCS enhancers, 3) response of overlapping complicated identity shifts, 4) simultaneous rejection and assumption of LCS, and 5) information control via advocacy activities as a LCS mitigation response. These findings expand the current understanding of LCS, and call for future conceptual exploration and theoretical revision, particularly with respect to the possibility of interaction between relevant related stigma(s) and LCS. As the number of women living with lung cancer increases, with longer survival times, the effect of LCS and other experiences of discrimination on patient outcomes could be substantial. PMID:23414179

  2. Small activating ribonucleic acid reverses tyrosine kinase inhibitor resistance in epidermal growth factor receptor‐mutant lung cancer by increasing the expression of phosphatase and tensin homolog

    PubMed Central

    Li, Meng; Peng, Zhongmin; Ren, Wangang

    2016-01-01

    Background Epidermal growth factor receptor‐tyrosine kinase inhibitors (TKI‐EGFRs) present a new prospect for the treatment of lung cancer. However, in clinical application, the majority of patients become TKI resistant within a year. More and more studies have shown that a loss of phosphatase and tensin homolog (PTEN) expression is associated with TKI resistance. An alternative method of upregulating PTEN expression may reverse TKI resistance. Methods We designed five candidate small activating ribonucleic acids (saRNAs) to target PTEN, and transfected them into H‐157 cells to screen out functional saRNA. We used reverse transcriptase‐polymerase chain reaction and Western blot to evaluate the effect of saRNA to PTEN expression. We then analyzed the growth and apoptosis of cells transfected with saRNA under the treatment of TKI to investigate whether saRNAs can reverse TKI resistance by upregulating PTEN expression. Results The functional saRNA we designed could upregulate PTEN expression. The H‐157 cells transfected with saRNA grew slower in the presence of TKI drugs than the cells that were not transfected with saRNA. The apoptosis rate was also obviously higher. Conclusions Our study proves that loss of PTEN expression is an important mechanism of TKI resistance. It is possible to control TKI resistance by upregulating PTEN expression using RNA activation technology. PMID:27385992

  3. Targeted therapy for squamous cell lung cancer

    PubMed Central

    Liao, Rachel G.; Watanabe, Hideo; Meyerson, Matthew; Hammerman, Peter S.

    2013-01-01

    SUMMARY Lung squamous cell carcinoma (SqCC) is the second most common subtype of non-small-cell lung cancer and leads to 40,000–50,000 deaths per year in the USA. Management of non-small-cell lung cancer has dramatically changed over the past decade with the introduction of targeted therapeutic agents for genotypically selected individuals with lung adenocarcinoma. These agents lead to improved outcomes, and it has now become the standard of care to perform routine molecular genotyping of lung adenocarcinomas. By contrast, progress in lung SqCC has been modest, and there has yet to be a successful demonstration of targeted therapy in this disease. Here, we review exciting work from ongoing genomic characterization and biomarker validation efforts that have nominated several likely therapeutic targets in lung SqCCs. These studies suggest that targeted therapies are likely to be successful in the treatment of lung SqCCs and should be further explored in both preclinical models and in clinical trials. PMID:23956794

  4. Intermediate endpoint biomarkers for lung cancer chemoprevention

    NASA Astrophysics Data System (ADS)

    MacAulay, Calum E.; Lam, Stephen; Klein-Parker, Helga; Gazdar, Adi; Guillaud, Martial; Payne, Peter W.; Le Riche, Jean C.; Dawe, Chris; Band, Pierre; Palcic, Branko

    1998-04-01

    Given the demographics of current and ex-smoking populations in North America, lung cancer will be a major problem in the foreseeable future. Early detection and treatment of lung cancer holds great promise for the management of this disease. Unlike cervical cancer, the physical, complete removal/destruction of all dysplastic lesions in the bronchial tree is not possible; however, treatment of the lesions using a chemopreventive agent is. Intermediate biomarkers have been used to screen promising chemopreventive agents for larger population studies. We have examined the natural history of lung cancer development by following a group of subjects at high risk of developing lung cancer using fluorescence endoscopy to identify the areas of abnormality for biopsy. Approximately 900 biopsies have been collected in this fashion and graded by at least two experienced, expert pathologists. Using an interactive version of the Cyto-Savant (Oncometrics Imaging Corp.), cytometric and tissue architectural data were collected from these biopsies. Using only the data from the normal and invasive cancer biopsies, quantitative morphometric and architectural indices were generated and calculated for all the collected biopsies. These indices were compared with Loss of Heterozygosity (LOH) of ten sites commonly associated with cancer. These results and the application of these quantitative measures to two small chemoprevention studies will be reported.

  5. Detection and minimally invasive treatment of early squamous lung cancer

    PubMed Central

    Sutedja, Thomas G.

    2013-01-01

    Non-small cell lung cancer (NSCLC) is the most common cause of cancer deaths worldwide. The majority of patents presenting with NSCLC have advanced disease, which precludes curative treatment. Early detection and treatment might result in the identification of more patients with early central lung cancer and improve survival. In addition, the study of early lung cancer improves understanding of lung carcinogenesis and might also reveal new treatment targets for advanced lung cancer. Bronchoscopic investigation of the central airways can reveal both early central lung cancer in situ (stage 0) and other preinvasive lesions such as dysplasia. In the current review we discuss the detection of early squamous lung cancer, the natural history of preinvasive lesions and whether biomarkers can be used to predict progression to cancer. Finally we will review the staging and management of preinvasive lung cancer lesions and the different therapeutic modalities that are available. PMID:23858332

  6. Isolating and Testing Circulating Tumor DNA and Soluble Immune Markers During the Course of Treatment for Lung Cancer

    ClinicalTrials.gov

    2016-07-11

    Lung Cancer; Lung Neoplasms; Cancer of Lung; Cancer of the Lung; Neoplasms, Lung; Neoplasms, Pulmonary; Pulmonary Cancer; Pulmonary Neoplasms; Carcinoma, Non-small-cell Lung; Adenocarcinoma; Squamous Cell Carcinoma

  7. Occupational associations with lung cancer in two Ontario cities.

    PubMed

    Finkelstein, M M

    1995-01-01

    A death certificate based case-control study of lung cancer in two Ontario cities was performed to estimate the risk of lung cancer attributable to occupation in Ontario, and to estimate the proportion of occupational lung cancers receiving compensation from the Workers' Compensation Board. Occupation and industry were identified from the death certificate. A priori occupations for analysis were those whose members had received compensation for occupational cancer from the Ontario Workers' Compensation Board. Population attributable risks were computed using the relative risks observed in this study and employment data from the 1986 Census of Canada. Subjects were all men (N = 967) between the ages of 45 and 75 years resident in the cities of Hamilton and Sault Ste-Marie who died of lung cancer from 1979 to 1988. Controls (2,821) were matched on age, year of death, and city of residence. In agreement with other studies, an increased risk of lung cancer was observed for workers in the construction sector, for miners, and for truck drivers. It was estimated that only a small proportion of lung cancers attributable to occupation are compensated in Ontario. It is believed that many occupational cancers go uncompensated because of the failure to file claims, rather than because claims are rejected by Compensation Boards. Physicians are in a position to advise patients about the possibility of compensable disease and to act as advocates for them. By recognizing compensable illness, physicians have the opportunity to ease the financial burden of patients and their families. The challenge is a difficult one, but it is well worth pursuing. PMID:7900730

  8. Targeted Therapies for Lung Cancer.

    PubMed

    Stinchcombe, Thomas E

    2016-01-01

    Targeted therapies have become standard therapies for patients with non-small cell lung cancer (NSCLC). A phase III trial of carboplatin and paclitaxel with and without bevacizumab in patients with advanced NSCLC with non-squamous histology demonstrated a statistically significant improvement in efficacy. In patients with NSCLC with an activating epidermal growth factor receptor (EGFR) mutation (defined as exon 19 deletion and exon 21 L858R point mutation), phase III trials of EGFR tyrosine kinase inhibitors (TKI) compared to platinum-based chemotherapy have demonstrated superior efficacy in the first-line setting. In patients with NSCLC with anaplastic lymphoma kinase (ALK) rearrangements, phase III trials of crizotinib have demonstrated superior efficacy compared to platinum-pemetrexed in the first-line setting and standard chemotherapy in the second-line setting. A second-generation ALK inhibitor, ceritinib, is available for patients who have progressed after or were intolerant of crizotinib. Crizotinib has also demonstrated activity on patients with ROS1 rearrangements, and BRAF inhibitors (dabrafenib, vemurafenib) have demonstrated activity in patients with NSCLC with BRAF V600E mutation. The oncogenic mutations that are susceptible to targeted therapy are mainly found in non-squamous NSCLC. The development of targeted therapy in patients with squamous NSCLC has been more challenging due to the genomic complexity observed in the squamous histology and the low prevalence of EGFR, ALK, and ROS1 molecular alterations. A phase III trial of cisplatin and gemcitabine with and without necitumumab in patients with advanced NSCLC with squamous histology demonstrated a statistically significant improvement in progression-free and overall survival. PMID:27535394

  9. The equivalent efficacy of multiple operations for multiple primary lung cancer and a single operation for single primary lung cancer

    PubMed Central

    Dai, Liang; Yang, He-Li; Yan, Wan-Pu; Liang, Zhen; Xiong, Hong-Chao; Kang, Xiao-Zheng; Yang, Yong-Bo; Fu, Hao; Fan, Meng-Ying

    2016-01-01

    Background The incidence of synchronous and metachronous multiple primary lung cancers (MPLCs) has been increasing recently. The new multidisciplinary classification of lung adenocarcinoma and TNM Classification of Lung Cancer (7th edition, 2009), have improved the understanding of MPLC. Most researchers recommend that surgical therapy should be actively pursued if the patient’s physical condition and lung function permit it and if a complete cure can be achieved. However, few studies have reported the long-term efficacy of surgical treatment for MPLC, which we explored in this study. Methods A total of 1,290 Lung cancer patients from a prospectively maintained database, treated by a single surgeon group between January 2000 and July 2013, at Beijing Cancer Hospital, Peking University, were reviewed. We retrospectively analyzed the clinical data of 31 patients diagnosed with MPLC out of 1290 lung cancer patients, focusing on long-term survival. Results MPLC patients accounted for 2.4% (31/1,290) of the patient cohort: 27 had synchronous MPLC (87.1%) and 4 had metachronous MPLC (12.9%). The 1-, 3- and 5-year postoperative survival rates were 100%, 75.8% and 75.8%. On stratification according to TNM stage, the 1-, 3- and 5-year of patients with stage I cancer (20 patients) were 100%, 77.2% and 77.2%, not statistically significant with those for the entire cohort (1,290 patients; 95.4%, 80.5% and 66.2%, P=0.455). Conclusions When the patient’s physical condition and tumor-related factors permit it, surgery should be the first choice of treatment for MPLC; it is associated with an equivalent efficacy to that of surgery for single primary lung cancer. PMID:27162659

  10. Follow-up and surveillance of the lung cancer patient following curative-intent therapy.

    PubMed

    Colice, Gene L; Rubins, Jeffrey; Unger, Michael

    2003-01-01

    The following two distinctly different issues should be taken into account when planning patient care following curative-intent therapy for lung cancer: adequate follow-up to manage complications related to the curative-intent therapy; and surveillance to detect recurrences of the primary lung cancer and/or development of a new primary lung cancer early enough to allow potentially curative retreatment. Follow-up for complications should be performed by the specialist responsible for the curative-intent therapy and should last 3 to 6 months. Recurrences of the original lung cancer will be more likely during the first 2 years after curative-intent therapy, but there will be an increased lifelong risk of approximately 1 to 2% per year of developing a metachronous, or new primary, lung cancer. A standard surveillance program for these patients is recommended based on periodic visits, with chest-imaging studies and counseling patients on symptom recognition. Whether subgroups of patients with a higher risk of developing a metachronous lung cancer (eg, those patients whose primary lung cancer was radiographically occult or central and those patients surviving for > 2 years after treatment for small cell lung cancer) should have a more intensive surveillance program is presently unclear. The surveillance program should be coordinated by a multidisciplinary tumor board and overseen by the physician who diagnosed and initiated therapy for the original lung cancer. Smoking cessation is recommended for all patients following curative-intent therapy for lung cancer. PMID:12527585

  11. Genetic Evidence for XPC-KRAS Interactions During Lung Cancer Development.

    PubMed

    Zhang, Xiaoli; He, Nonggao; Gu, Dongsheng; Wickliffe, Jeff; Salazar, James; Boldogh, Istavan; Xie, Jingwu

    2015-10-20

    Lung cancer causes more deaths than breast, colorectal and prostate cancers combined. Despite major advances in targeted therapy in a subset of lung adenocarcinomas, the overall 5-year survival rate for lung cancer worldwide has not significantly changed for the last few decades. DNA repair deficiency is known to contribute to lung cancer development. In fact, human polymorphisms in DNA repair genes such as xeroderma pigmentosum group C (XPC) are highly associated with lung cancer incidence. However, the direct genetic evidence for the role of XPC for lung cancer development is still lacking. Mutations of the Kirsten rat sarcoma viral oncogene homolog (Kras) or its downstream effector genes occur in almost all lung cancer cells, and there are a number of mouse models for lung cancer with these mutations. Using activated Kras, Kras(LA1), as a driver for lung cancer development in mice, we showed for the first time that mice with Kras(LA1) and Xpc knockout had worst outcomes in lung cancer development, and this phenotype was associated with accumulated DNA damage. Using cultured cells, we demonstrated that induced expression of oncogenic KRAS(G12V) led to increased levels of reactive oxygen species (ROS) as well as DNA damage, and both can be suppressed by anti-oxidants. Our results suggest that XPC may help repair DNA damage caused by KRAS-mediated production of ROS. PMID:26554912

  12. Pollutional haze as a potential cause of lung cancer

    PubMed Central

    Shi, Xuefei; Liu, Hongbing

    2015-01-01

    Along with fast economic growth over the past few decades, the world is faced with cumulatively serious environmental pollution and now is paying increased attention to pollutional haze. In the last few years, multiple epidemiological studies and animal models have provided compelling evidences that inhalation of pollutional haze could be linked to several adverse health effects. Since the respiratory tract is the crucial passageway of entry of pollutional haze, the lung is the main affected organ. Therefore, here, we reviewed some of the important information around long-term exposure to pollutional haze and lung cancer, as well as highlight important roles of pollutional haze in human lung carcinogenesis, providing evidence for pollutional haze acting as another risk factor for lung cancer. PMID:26623118

  13. Photoradiation Therapy Of Obstructing Endobronchial Lung Cancer

    NASA Astrophysics Data System (ADS)

    Balchum, Oscar J.; Doiron, Daniel R.

    1982-12-01

    Clinical trials of photoradiation therapy (PRT) have been carried out in 32 patients with lung cancer, 10 of which are reported here. The aim is the palliative treatment and control of cancer lesions obstructing an airway, whether in the trachea or in a large bronchus leading to a lung or to a lobe of a lung. The objective or patient benefit is the opening up of the lumen of the airway to improve ventilation to relieve shortness of breath, and to prevent the retention of secretions containing bacteria, that cause lung infections. Immediate results (one to several weeks) were uniformly good. Air passageways were opened up as revealed by subsequent bronchoscopy, after clearing away tumor debris. Short-term (several months) observations were limited in number but indicate potentially good results. Future research is directed toward better criteria for patient selection improved patient evaluation that will reveal potential cardiac and pulmonary complications, and the devising of more suitable laser light delivery techniques.

  14. The pivotal role of pathology in the management of lung cancer.

    PubMed

    Davidson, Morgan R; Gazdar, Adi F; Clarke, Belinda E

    2013-10-01

    The last decade has seen significant advances in our understanding of lung cancer biology and management. Identification of key driver events in lung carcinogenesis has contributed to the development of targeted lung cancer therapies, heralding the era of personalised medicine for lung cancer. As a result, histological subtyping and molecular testing has become of paramount importance, placing increasing demands on often small diagnostic specimens. This has triggered the review and development of the first structured classification of lung cancer in small biopsy/cytology specimens and a new classification of lung adenocarcinoma from the IASLC/ATS/ERS. These have enhanced the clinical relevance of pathological diagnosis, and emphasise the role of the modern surgical pathologist as an integral member of the multidisciplinary team, playing a crucial role in clinical trials and determining appropriate and timely management for patients with lung cancer. PMID:24163740

  15. Successes and limitations of targeted cancer therapy in lung cancer.

    PubMed

    Suda, Kenichi; Mitsudomi, Tetsuya

    2014-01-01

    Human cancers usually evolve through multistep processes. These processes are driven by the accumulation of abundant genetic and epigenetic abnormalities. However, some lung cancers depend on a single activated oncogene by somatic mutation, termed 'driver oncogenic mutations', for their proliferation and survival. EGFR(epidermal growth factor receptor) mutations and ALK(anaplastic lymphoma kinase) rearrangement are typical examples of such driver oncogenic mutations found in lung adenocarcinomas. EGFR-tyrosine kinase inhibitors (TKIs) or ALK-TKIs significantly improved treatment outcomes compared with conventional cytotoxic chemotherapy in patients with lung cancers harboring EGFR mutations or ALK rearrangement, respectively. Therefore, treatment strategies for lung cancers have dramatically changed from a 'general and empiric' to a 'personalized and evidence-based' approach according to the driver oncogenic mutation. Several novel driver oncogenic mutations, which are candidates as novel targets, such as ERBB2, BRAF, ROS1, and RET, have been discovered. Despite these successes, several limitations have arisen. One example is that some lung cancers do not respond to treatments targeting driver oncogenic mutations, as exemplified in KRAS-mutated lung cancers. Another is resistance to molecular-targeted drugs. Such resistance includes de novo resistance and acquired resistance. A number of molecular mechanisms underlying such resistance have been reported. These mechanisms can be roughly divided into three categories: alteration of the targeted oncogenes themselves by secondary mutations or amplification, activation of an alternative oncogenic signaling track, and conversion of cellular characteristics. Overcoming resistance is a current area of urgent clinical research. PMID:24727987

  16. Non-coding RNAs in lung cancer

    PubMed Central

    Ricciuti, Biagio; Mecca, Carmen; Crinò, Lucio; Baglivo, Sara; Cenci, Matteo; Metro, Giulio

    2014-01-01

    The discovery that protein-coding genes represent less than 2% of all human genome, and the evidence that more than 90% of it is actively transcribed, changed the classical point of view of the central dogma of molecular biology, which was always based on the assumption that RNA functions mainly as an intermediate bridge between DNA sequences and protein synthesis machinery. Accumulating data indicates that non-coding RNAs are involved in different physiological processes, providing for the maintenance of cellular homeostasis. They are important regulators of gene expression, cellular differentiation, proliferation, migration, apoptosis, and stem cell maintenance. Alterations and disruptions of their expression or activity have increasingly been associated with pathological changes of cancer cells, this evidence and the prospect of using these molecules as diagnostic markers and therapeutic targets, make currently non-coding RNAs among the most relevant molecules in cancer research. In this paper we will provide an overview of non-coding RNA function and disruption in lung cancer biology, also focusing on their potential as diagnostic, prognostic and predictive biomarkers. PMID:25593996

  17. Lung cancer: chemoprevention and intermediate effect markers.

    PubMed

    Tockman, M S

    2001-01-01

    Even after smoking cessation, genetic damage in the airways epithelium may lead to focal progression of lung carcinogenesis. Some centres now report as many new lung cancer cases among former smokers as among current smokers. Chemoprevention is a potential approach to diminish the progression of pre-clinical genetic damage. The most intensively studied lung cancer chemoprevention agents are the retinoids, including vitamin A and its synthetic analogues and precursors. While effective in suppressing lung carcinogenesis in animal models, retinoids have failed to inhibit carcinogenesis in human chemoprevention trials with premalignant end-points (sputum atypia, bronchial metaplasia). In trials with lung cancer end-points, administration of retinoids either was ineffective or, in the case of beta-carotene, led to greater lung cancer incidence and mortality. In view of these findings, markers of specific retinoid effect (i.e., levels of RAR-beta) become less relevant. Other markers of genetic instability and proliferation may be useful for both early detection and potentially as intermediate-effect markers for new chemoprevention trials. Cytological atypia, bronchial metaplasia, protein (hnRNP A2/B1) overexpression, ras oncogene activation and tumour-suppressor gene deletion, genomic instability (loss of heterozygosity, microsatellite alterations), abnormal methylation, helical CT detection of atypical adenomatous hyperplasia and fluorescent bronchoscopic detection of angiogenic squamous dysplasia offer great promise for molecular diagnosis of lung cancer far in advance of clinical presentation. These end-points can now be evaluated as monitors of response to chemoprevention as potential intermediate-effect markers. PMID:11220665

  18. Lung cancer in relation to airborne radiation levels

    SciTech Connect

    Helsing, K.J.; Natta, P.V.; Comstock, G.W. ); Kalin, Heidi ) Chee, E. )

    1992-01-01

    A 1986 aeroradiometric survey of the eastern two-thirds of Washington County, Maryland provided and opportunity to study lung cancers in relation to gamma radiation levels. In the first approach, lung cancer deaths between 1963 and 1975 in four areas of the county categorized as low, moderately low, moderately high, and high showed relative risks of 1.00, 0.93, 1.01, and 1.43, respectively, after adjustment of sex, age, and smoking. A second approach used lung cancer cases diagnosed between 1975 and 1989, controls matched to cases by race, sex, and age, and aerometric radiation readings above the individual residences. In four levels of increasing gamma radiation, odds ratios adjusted for smoking were 1.00, 0.84, 0.90, and 0.92, respectively. No differences were statistically significant.

  19. Better Lung Cancer Survival? There's an App for That

    MedlinePlus

    ... nih.gov/medlineplus/news/fullstory_159289.html Better Lung Cancer Survival? There's an App for That Study found ... HealthDay News) -- A new smartphone app may help lung cancer patients live longer and better by monitoring their ...

  20. Do Too Many Lung Cancer Patients Miss Out on Surgery?

    MedlinePlus

    ... medlineplus/news/fullstory_159488.html Do Too Many Lung Cancer Patients Miss Out on Surgery? Study evaluates treatment ... 21, 2016 (HealthDay News) -- Many patients with advanced lung cancer might live longer if treated surgically, but few ...

  1. General Information about Non-Small Cell Lung Cancer

    MedlinePlus

    ... most patients with non-small cell lung cancer, current treatments do not cure the cancer. If lung ... professional versions have detailed information written in technical language. The patient versions are written in easy-to- ...

  2. Treatment Option Overview (Non-Small Cell Lung Cancer)

    MedlinePlus

    ... lung cancer include a cough that doesn't go away and shortness of breath. Sometimes lung cancer ... discomfort or pain. A cough that doesn’t go away or gets worse over time. Trouble breathing. ...

  3. Treatment Options by Stage (Non-Small Cell Lung Cancer)

    MedlinePlus

    ... lung cancer include a cough that doesn't go away and shortness of breath. Sometimes lung cancer ... discomfort or pain. A cough that doesn’t go away or gets worse over time. Trouble breathing. ...

  4. Stages of Non-Small Cell Lung Cancer

    MedlinePlus

    ... lung cancer include a cough that doesn't go away and shortness of breath. Sometimes lung cancer ... discomfort or pain. A cough that doesn’t go away or gets worse over time. Trouble breathing. ...

  5. Better Lung Cancer Survival? There's an App for That

    MedlinePlus

    ... https://medlineplus.gov/news/fullstory_159289.html Better Lung Cancer Survival? There's an App for That Study ... HealthDay News) -- A new smartphone app may help lung cancer patients live longer and better by monitoring ...

  6. New genes linked to lung cancer susceptibility in Asian women

    Cancer.gov

    An international group of scientists has identified three genes that predispose Asian women who have never smoked to lung cancer. The discovery of specific genetic variations, which have not previously been associated with lung cancer risk in other popul

  7. Xalkori Approved for Rare Genetic Form of Lung Cancer

    MedlinePlus

    ... html Xalkori Approved For Rare Genetic Form of Lung Cancer ROS-1 positive NSCLC To use the sharing ... Drug Administration to treat advanced non-small cell lung cancer (NSCLC) with tumors that have a rare ROS- ...

  8. Smoking cessation and lung cancer screening

    PubMed Central

    Pedersen, Jesper Holst; Tønnesen, Philip

    2016-01-01

    Smoking behavior may have a substantial influence on the overall effect of lung cancer screening. Non-randomized studies of smoking behavior during screening have indicated that computer tomography (CT) screening induces smoking cessation. Randomized studies have further elaborated that this effect has to do with participation in screening alone and not dependent on the CT scan. Participants in both CT and control arm in randomized screening trials had higher smoking abstinence rate compared to that of the general population. A positive screening test seems to further promote smoking cessation and decrease smoking relapse rate. Also low smoking dependency and high motivation to quit smoking at baseline predicted smoking abstinence in screening trials. Lung cancer screening therefore seems to be a teachable moment for smoking cessation. Targeted smoking cessation counselling should be an integrated part of future lung cancer screening trials. PMID:27195275

  9. Contemplating Genetic Feedback Regarding Lung Cancer Susceptibility

    PubMed Central

    Shepperd, James A.; Novell, Corinne A.; O'Neill, Suzanne C.; Docherty, Sharron L.; Sanderson, Saskia C.; McBride, Colleen M.; Lipkus, Isaac M.

    2013-01-01

    Background and Purpose We examined three theoretical models (self-enhancement theory, consistency theory, and combined model) for understanding how expectations and test result favorability influence smokers' desire for a retest following hypothetical genetic test results. Method College smokers (N = 128) read a brochure describing a biomarker for lung cancer (the GSTM1 gene) then reported whether they thought they had the gene (indicating lower lung cancer risk) or were missing the gene (indicating higher lung cancer risk). Participants then reported whether they would get retested if they received favorable GSTM1 results versus unfavorable GSTM1 results. Results Participants were most likely to want a retest, suggesting rejection of the results, if they expected favorable news yet received unfavorable news. Conclusion The findings supported the combined model such that smokers expressed greatest interest in a retest when they imagined genetic risk feedback that challenges both enhancement and consistency motives. PMID:24222509

  10. Narcissus, the Beam, and lung cancer.

    PubMed

    Rocco, Gaetano

    2016-08-01

    In the management of lung cancer, the rules of engagement of stereotactic ablative radiotherapy (SABR) are not clearly defined. The potential for SABR to affect to an unprecedented level current protocols and in all disease stages emerges vehemently from the literature. However, in a time when the role of surgery is being reassessed, surgeons need to take a closer look at the evidence for the use of SABR in lung cancer patients and clearly define their indisputable role within the context of multidisciplinary teams. The myth of Narcissus exemplified in the absolute masterpiece by Caravaggio seems to represent an ideal metaphor to explain the ever-evolving interaction between surgery and SABR in lung cancer management. PMID:27209014

  11. Silicosis and risk of lung cancer or lung tuberculosis: a cohort study.

    PubMed

    Westerholm, P; Ahlmark, A; Maasing, R; Segelberg, I

    1986-10-01

    This is a study of cancer mortality, cancer incidence, and incidence of lung tuberculosis among cases of silicosis reported to the National Swedish Pneumoconiosis Register during 1959-1977. Two occupational categories were extracted--"mining, tunneling, and quarrying" (n = 284) and "iron and steel foundries" (n = 428), respectively. Control groups were drawn from a national register of persons undergoing periodic health examinations with regard to silicosis risk. The controls were matched for occupation, age, and time of first exposure. The follow-up was performed through record-linkage operations to computerized information in Swedish Death Statistics, Swedish Cancer Register, and the Swedish Tuberculosis Index. End of follow-up was set at December 31, 1980. In cases drawn from mining, quarrying, and tunneling workers seven deaths in lung cancer were observed and two among the controls. Among iron and steel foundry workers the corresponding numbers were 10 and 6. The values for expected numbers, based on general population statistics, were 1.3 and 2.6, respectively, for these two occupational groups. When cancer incidence statistics were used, the case/control ratio for lung cancer was 2.1 for "mining, quarrying, and tunneling" and 0.6 for "iron and steel foundries." There were 29 cases of lung tuberculosis registered among the silicosis cases during the follow-up period. Only one tuberculosis case was observed among the controls. The results demonstrate that persons with silicosis contracted in the mining, quarrying, and tunneling occupations are subject to an increased risk of lung cancer. The risk is observed when both the general population and a closely matched control population from the same occupations are used for values of reference. The results also demonstrate the high risk of persons with silicosis to contract lung tuberculosis. PMID:3757978

  12. Cloning of human lung cancer cells.

    PubMed Central

    Walls, G. A.; Twentyman, P. R.

    1985-01-01

    We have carried out a comparison of two different methods for cloning human lung cancer cells. The method of Courtenay & Mills (1978) generally gave higher plating efficiencies (PE) than the method of Carney et al. (1980). The number of colonies increased with incubation time in both methods and the weekly medium replenishment in the Courtenay method was advantageous for longer incubation times of several weeks. In the Courtenay method, the use of August rat red blood cells (RBC) and low oxygen tension were both found to be necessary factors for maximum plating efficiency. The usefulness of heavily irradiated feeder cells in improving PE is less certain; each cell type may have its own requirement. PMID:3904799

  13. Fluorescence imaging of early lung cancer

    NASA Astrophysics Data System (ADS)

    Lam, Stephen; MacAulay, Calum E.; Le Riche, Jean C.; Ikeda, Norihiko; Palcic, Branko

    1995-01-01

    The performance of a fluorescence imaging device was compared with conventional white-light bronchoscopy in 100 patients with lung cancer, 46 patients with resected State I nonsmall cell lung cancer, 10 patients with head and neck cancer, and 67 volunteers who had smoked at least one pack of cigarettes per day for twenty-five years or more. Using differences in tissue autofluorescence between premalignant, malignant and normal tissues, fluorescence bronchoscopy was found to detect more than twice as many moderate-severe dysplasia and carcinoma in situ sites than conventional white-light bronchoscopy. The use of fluorescence imaging to detect small peripheral lung nodules was investigated in a micro metastatic lung model of mice implanted with Lewis lung tumor cells. Fluorescence imaging was found to be able to detect small malignant lung lesions. The use of (delta) -aminolevulinic acid (ALA) to enhance fluorescence detection of CIS was investigated in a patient after oral administration of 60 mg/kg of ALA four hours prior to bronchoscopy, although ALA enhanced the tumor's visibility, multiple sites of false positive fluorescence were observed in areas of inflammation or metaplasia.

  14. Gene mutation discovery research of non-smoking lung cancer patients due to indoor radon exposure.

    PubMed

    Choi, Jung Ran; Park, Seong Yong; Noh, O Kyu; Koh, Young Wha; Kang, Dae Ryong

    2016-01-01

    Although the incidence and mortality for most cancers such as lung and colon are decreasing in several countries, they are increasing in several developed countries because of an unhealthy western lifestyles including smoking, physical inactivity and consumption of calorie-dense food. The incidences for lung and colon cancers in a few of these countries have already exceeded those in the United States and other western countries. Among them, lung cancer is the main cause of cancer death in worldwide. The cumulative survival rate at five years differs between 13 and 21 % in several countries. Although the most important risk factors are smoking for lung cancer, however, the increased incidence of lung cancer in never smokers(LCINS) is necessary to improve knowledge concerning other risk factors. Environmental factors and genetic susceptibility are also thought to contribute to lung cancer risk. Patients with lung adenocarcinoma who have never smoking frequently contain mutation within tyrosine kinase domain of the epidermal growth factor receptor(EGFR) gene. Also, K-ras mutations are more common in individuals with a history of smoking use and are related with resistance to EFGR-tyrosine kinase inhibitors. Recently, radon(Rn), natural and noble gas, has been recognized as second common reason of lung cancer. In this review, we aim to know whether residential radon is associated with an increased risk for developing lung cancer and regulated by several genetic polymorphisms. PMID:26985396

  15. The importance of exercise in lung cancer treatment

    PubMed Central

    2016-01-01

    There is emerging evidence that exercise can help in a variety of different ways for people with lung cancer. Exercise can be beneficial at any stage of the patient journey through increasing strength, endurance and decreasing emotional issues. A recovery fitness program is described and provides guidance on breathing, stretching, aerobic exercise and strength training. There are more people surviving lung cancer with services needing to cater for the varying requirements of each patient. Promoting physical activity is an important facet of health care management and collaboration between providers of services is required. PMID:27413700

  16. Survivorship Care Planning in Patients With Colorectal or Non-Small Cell Lung Cancer

    ClinicalTrials.gov

    2013-12-16

    Stage I Colon Cancer; Stage I Rectal Cancer; Stage IA Non-small Cell Lung Cancer; Stage IB Non-small Cell Lung Cancer; Stage IIA Colon Cancer; Stage IIA Non-small Cell Lung Cancer; Stage IIA Rectal Cancer; Stage IIB Colon Cancer; Stage IIB Non-small Cell Lung Cancer; Stage IIB Rectal Cancer; Stage IIC Colon Cancer; Stage IIC Rectal Cancer; Stage IIIA Colon Cancer; Stage IIIA Non-small Cell Lung Cancer; Stage IIIA Rectal Cancer; Stage IIIB Colon Cancer; Stage IIIB Non-small Cell Lung Cancer; Stage IIIB Rectal Cancer; Stage IIIC Colon Cancer; Stage IIIC Rectal Cancer

  17. Cancers of the Lung and Nasal Sinuses in Nickel Workers

    PubMed Central

    Doll, R.; Morgan, L. G.; Speizer, F. E.

    1970-01-01

    Men employed in a nickel refinery in South Wales were investigated to determine whether the specific risks of developing carcinoma of the bronchi and nasal sinuses, which had been associated with the refining of nickel, are still present. The data obtained were also used to compare the effect of age at exposure on susceptibility to cancer induction and to determine the rate of change of mortality after exposure to a carcinogenic agent had ceased. Eight hundred and forty five men were studied who had been employed in the industry for at least 5 years and whose first employment was in or before April 1994. All but 27 (3.2 per cent) were traced until death or January 1, 1967. Altogether 482 of the men had died: 113 from lung cancer and 39 from nasal cancer. In men employed before 1925, deaths from lung cancer varied from about 5 to 10 times the numbers that would have been expected from the corresponding national mortality rates, while the deaths from nasal cancer varied from about 100 to 900 times the expected numbers. Among men first employed in 1925 or after there were 8 deaths from lung cancer against 6.2 expected and no deaths from nasal cancer. The death rate from causes other than cancer was similar to that experienced by men in the same geographical area irrespective of their date of first employment. Susceptibility to the induction of nasal cancer increased with age at first exposure, but susceptibility to the induction of lung cancer varied irregularly. The trends in susceptibility showed some similarity to the trends in the national mortality among men employed at similar ages. It is suggested that susceptibility to cancer induction is determined by the amount of previous exposure to other agents. The risk of developing nasal cancer persisted with little change 15 to 42 years after the carcinogen was eliminated whereas the risk of developing lung cancer decreased. If the effects of cigarette smoking and the specific occupational hazard interact, the

  18. Lung Cancer and Vehicle Exhaust in Trucking Industry Workers

    PubMed Central

    Garshick, Eric; Laden, Francine; Hart, Jaime E.; Rosner, Bernard; Davis, Mary E.; Eisen, Ellen A.; Smith, Thomas J.

    2008-01-01

    Background An elevated risk of lung cancer in truck drivers has been attributed to diesel exhaust exposure. Interpretation of these studies specifically implicating diesel exhaust as a carcinogen has been limited because of limited exposure measurements and lack of work records relating job title to exposure-related job duties. Objectives We established a large retrospective cohort of trucking company workers to assess the association of lung cancer mortality and measures of vehicle exhaust exposure. Methods Work records were obtained for 31,135 male workers employed in the unionized U.S. trucking industry in 1985. We assessed lung cancer mortality through 2000 using the National Death Index, and we used an industrial hygiene review and current exposure measurements to identify jobs associated with current and historical use of diesel-, gas-, and propane-powered vehicles. We indirectly adjusted for cigarette smoking based on an industry survey. Results Adjusting for age and a healthy-worker survivor effect, lung cancer hazard ratios were elevated in workers with jobs associated with regular exposure to vehicle exhaust. Mortality risk increased linearly with years of employment and was similar across job categories despite different current and historical patterns of exhaust-related particulate matter from diesel trucks, city and highway traffic, and loading dock operations. Smoking behavior did not explain variations in lung cancer risk. Conclusions Trucking industry workers who have had regular exposure to vehicle exhaust from diesel and other types of vehicles on highways, city streets, and loading docks have an elevated risk of lung cancer with increasing years of work. PMID:18941573

  19. The lung cancer nurse role in the management of paraneoplastic syndromes in lung cancer

    PubMed Central

    2016-01-01

    Paraneoplastic syndromes (PNS) associated with lung cancer are well recognised, are often complex to diagnose, and have minimal evidence to promote nursing and medical management. This paper aims to help guide lung cancer nurses to identify the most common and rarer PNS together with basic clinical management advice to help develop nursing assessments and interventions. The issues regarding the pathway of care at diagnosis together with palliative and supportive care requirements will be addressed and will aim to promote best practice in patients diagnosed with PNS and lung cancer. PMID:27413699

  20. Aryl Hydrocarbon Receptor and Lung Cancer

    PubMed Central

    Tsay, Junchieh J.; Tchou-Wong, Kam-Meng; Greenberg, Alissa K.; Pass, Harvey; Rom, William N.

    2013-01-01

    The leading cause of lung cancer is exposure to cigarette smoke and other environmental pollutants, which include formaldehyde, acrolein, benzene, dioxin, and polycyclic aromatic hydrocarbons (PAHs). PAHs and dioxins are exogenous ligands that directly bind to the aryl hydrocarbon receptor (AhR), a transcription factor that activates xenobiotic metabolism, histone modification (an important step in DNA methylation), and, ultimately, tumorigenesis. Here we summarize the current understanding of AhR and its role in the development of lung cancer, including its influence on cell proliferation, angiogenesis, inflammation, and apoptosis. PMID:23564762

  1. VOC breath biomarkers in lung cancer.

    PubMed

    Saalberg, Yannick; Wolff, Marcus

    2016-08-01

    This review provides an overview of volatile organic compounds (VOCs) which are considered lung cancer biomarkers for diagnostic breath analysis. It includes results of scientific publications from 1985 to 2015. The identified VOCs are listed and ranked according to their occurrence of nomination. The applied detection and sampling methods are specified but not evaluated. Possible reasons for the different results of the studies are stated. Among the most frequently emerging biomarkers are 2-butanone and 1-propanol as well as isoprene, ethylbenzene, styrene and hexanal. The outcome of this review may be helpful for the development of a lung cancer screening device. PMID:27221203

  2. The changing epidemiology of smoking and lung cancer histology.

    PubMed Central

    Wynder, E L; Muscat, J E

    1995-01-01

    In 1950, the first large-scale epidemiological studies demonstrated that lung cancer is causatively associated with cigarette smoking, a finding subsequently confirmed by the Royal College of Physicians in London, the U.S. Surgeon General, and the World Health Organization. Although cigarette consumption has gradually decreased in the United States from a high of about 3800 cigarettes per adult per year in 1965 to about 2800 cigarettes in 1993, death from lung cancer has reached a high among males at the rate of 74.9/100,000/year and among females at the rate of 28.5. However, in the younger cohorts, the lung cancer death rate is decreasing in both men and women. In this overview we discuss the steeper increase during recent decades of lung adenocarcinoma incidence compared with squamous cell carcinoma of the lung. In 1950, the ratio of these two major types of lung cancer in males was about 1:18; today it is about 1:1.2-1.4. This overview discusses two concepts that are regarded as contributors to this change in the histological types of lung cancer. One factor is the decrease in average nicotine and tar delivery of cigarettes from about 2.7 and 38 mg in 1955 to 1.0 and 13.5 mg in 1993, respectively. Other major factors for the reduced emission of smoke relate to changes in the composition of the cigarette tobacco blend and general acceptance of cigarettes with filter tips; the latter constitute 97% of all cigarettes currently sold. However, smokers of low-yield cigarettes compensate for the low delivery of nicotine by inhaling the smoke more deeply and by smoking more intensely; such smokers may be taking up to 5 puffs/min with puff volumes up to 55 ml. Under these conditions, the peripheral lung is exposed to increased amounts of smoke carcinogens that are suspected to lead to lung adenocarcinoma. Among the important changes in the composition of the tobacco blend of the U.S. cigarette is a significant increase in nitrate content (0.5% to 1.2-1.5%), which raises

  3. The changing epidemiology of smoking and lung cancer histology.

    PubMed

    Wynder, E L; Muscat, J E

    1995-11-01

    In 1950, the first large-scale epidemiological studies demonstrated that lung cancer is causatively associated with cigarette smoking, a finding subsequently confirmed by the Royal College of Physicians in London, the U.S. Surgeon General, and the World Health Organization. Although cigarette consumption has gradually decreased in the United States from a high of about 3800 cigarettes per adult per year in 1965 to about 2800 cigarettes in 1993, death from lung cancer has reached a high among males at the rate of 74.9/100,000/year and among females at the rate of 28.5. However, in the younger cohorts, the lung cancer death rate is decreasing in both men and women. In this overview we discuss the steeper increase during recent decades of lung adenocarcinoma incidence compared with squamous cell carcinoma of the lung. In 1950, the ratio of these two major types of lung cancer in males was about 1:18; today it is about 1:1.2-1.4. This overview discusses two concepts that are regarded as contributors to this change in the histological types of lung cancer. One factor is the decrease in average nicotine and tar delivery of cigarettes from about 2.7 and 38 mg in 1955 to 1.0 and 13.5 mg in 1993, respectively. Other major factors for the reduced emission of smoke relate to changes in the composition of the cigarette tobacco blend and general acceptance of cigarettes with filter tips; the latter constitute 97% of all cigarettes currently sold. However, smokers of low-yield cigarettes compensate for the low delivery of nicotine by inhaling the smoke more deeply and by smoking more intensely; such smokers may be taking up to 5 puffs/min with puff volumes up to 55 ml. Under these conditions, the peripheral lung is exposed to increased amounts of smoke carcinogens that are suspected to lead to lung adenocarcinoma. Among the important changes in the composition of the tobacco blend of the U.S. cigarette is a significant increase in nitrate content (0.5% to 1.2-1.5%), which raises

  4. Changing Rates for Liver and Lung Cancer in Qidong, China

    PubMed Central

    Chen, Jian-Guo; Kensler, Thomas W.

    2013-01-01

    Residents of Qidong, China are undergoing a rapid fluctuation in cancer incidence rates at many organ sites, reflecting a dynamic interplay of socio-behavioral, economic and environmental factors. This Perspective On Statistical Trends examines the China age-standardized incidence rates (CASR), as tracked by the Qidong Cancer Registry for the past 40 years, for the two leading cancer killers in Qidong, liver and lung. Both cancer types are strongly influenced by environmental factors. The CASR for liver cancer has dropped nearly 50% in the last 4 decades, in part from access to deep-well drinking water in the 1970s with consequent diminished exposure to tumor promoting microcystins produced by blue-green algae. There have also been substantive reductions in exposures to dietary aflatoxins, as economic reform in the mid-1980s fostered a wholesale change in dietary staple from maize to rice. In men, lung cancer CASR has trebled over this period, likely driven by a high prevalence of smokers (~65%) and an ever increasing smoking frequency in this population. Qidong women, by contrast, rarely smoke and have exhibited a flat CASR until the last decade where lung cancer rates have now doubled. This upturn may reflect an increasing burden of indoor and outdoor air pollution. PMID:24215631

  5. Changing rates for liver and lung cancers in Qidong, China.

    PubMed

    Chen, Jian-Guo; Kensler, Thomas W

    2014-01-21

    Residents of Qidong, China are undergoing a rapid fluctuation in cancer incidence rates at many organ sites, reflecting a dynamic interplay of socio-behavioral, economic, and environmental factors. This Perspective On Statistical Trends examines the China age-standardized incidence rates (CASR), as tracked by the Qidong Cancer Registry for the past 40 years, for the two leading cancer killers in Qidong, liver and lung. Both cancer types are strongly influenced by environmental factors. The CASR for liver cancer has dropped nearly 50% in the last 4 decades, in part from access to deep-well drinking water in the 1970s with consequent diminished exposure to tumor promoting microcystins produced by blue-green algae. There have also been substantive reductions in exposures to dietary aflatoxins, as economic reform in the mid-1980s fostered a wholesale change in dietary staple from maize to rice. In men, lung cancer CASR has trebled over this period, likely driven by a high prevalence of smokers (∼65%) and an ever increasing smoking frequency in this population. Qidong women, by contrast, rarely smoke and have exhibited a flat CASR until the past decade where lung cancer rates have now doubled. This upturn may reflect an increasing burden of indoor and outdoor air pollution. PMID:24215631

  6. Photodynamic therapy in lung and gastrointestinal cancers.

    PubMed

    Karanov, S; Kostadinov, D; Shopova, M; Kurtev, P

    1990-06-01

    Twelve central bronchial carcinoma patients and two gastrointestinal (GI) tract (oesophageal and colonic) early-stage cancer patients were treated with photodynamic therapy (PDT). Haematoporphyrin (HP/5, Jacopo Monico, Italy) at a dose of 5 mg kg-1 body weight was used as photosensitizer. Laser light at 628.2-630 nm generated by two different laser systems (gold vapour laser (I.P. Optics, Sofia, Bulgaria) in lung cancer cases and an argon dye laser system (Spectra Physics, Mountain View, U.S.A.) in GI tract cancers) was used. Lung cancers were irradiated 48 h after drug administration and GI tract cancers were irradiated 72 h after infusion of the photosensitizer. Both tumour sites were treated with a total energy dose in the range 350-600 J cm-2. Efficiency of PDT in lung cancer was evaluated by X-rays and endoscopic and functional respiratory tests for bronchial de-obstruction. Complete remission after PDT of GI tract cancers was considered to be tumour eradication (histologically and cytologically proved) and a tumour-free interval of at least 12 months. PMID:2121932

  7. Bone-targeted agents in the treatment of lung cancer

    PubMed Central

    Silva, Shobha C.; Wilson, Caroline

    2015-01-01

    Over a third of patients with lung cancer will develop bone metastases during the course of their disease, resulting in symptoms of pain and immobility, and skeletal-related events (SREs) such as fracture, hypercalcaemia, surgery or radiotherapy to bones, and malignant spinal cord compression. These reduce quality of life and increase mortality. Preclinical research has identified the interactions between tumour cells and bone that are key to tumour cell survival and associated osteolysis. These data have led to the development of drugs to prevent osteoclast-mediated bone breakdown, such as zoledronic acid and denosumab, which are now licensed for use in patients with bone metastases from solid tumours. Both zoledronic acid and denosumab reduce the risk of SREs and increase time to first SRE, with minimal side effects. In addition, denosumab improved survival in patients with lung cancer compared with zoledronic acid. Ongoing trials are testing whether these drugs can prevent the development of bone metastases from lung cancer. New bone-targeted agents showing promise in breast and prostate cancer include radium-223, cabozantinib and Src inhibitors. These agents require further evaluation in patients with lung cancer. PMID:26136853

  8. Targeting Lung Cancer Stem Cells with Antipsychological Drug Thioridazine

    PubMed Central

    Yue, Haiying; Huang, Dongning; Qin, Li; Zheng, Zhiyong; Hua, Li; Wang, Guodong; Huang, Jian

    2016-01-01

    Lung cancer stem cells are a subpopulation of cells critical for lung cancer progression, metastasis, and drug resistance. Thioridazine, a classical neurological drug, has been reported with anticancer ability. However, whether thioridazine could inhibit lung cancer stem cells has never been studied. In our current work, we used different dosage of thioridazine to test its effect on lung cancer stem cells sphere formation. The response of lung cancer stem cells to chemotherapy drug with thioridazine treatment was measured. The cell cycle distribution of lung cancer stem cells after thioridazine treatment was detected. The in vivo inhibitory effect of thioridazine was also measured. We found that thioridazine could dramatically inhibit sphere formation of lung cancer stem cells. It sensitized the LCSCs to chemotherapeutic drugs 5-FU and cisplatin. Thioridazine altered the cell cycle distribution of LCSCs and decreased the proportion of G0 phase cells in lung cancer stem cells. Thioridazine inhibited lung cancer stem cells initiated tumors growth in vivo. This study showed that thioridazine could inhibit lung cancer stem cells in vitro and in vivo. It provides a potential drug for lung cancer therapy through targeting lung cancer stem cells. PMID:27556038

  9. Lung Cancer Gene Signatures and Clinical Perspectives

    PubMed Central

    Kuner, Ruprecht

    2013-01-01

    Microarrays have been used for more than two decades in preclinical research. The tumor transcriptional profiles were analyzed to select cancer-associated genes for in-deep functional characterization, to stratify tumor subgroups according to the histopathology or diverse clinical courses, and to assess biological and cellular functions behind these gene sets. In lung cancer—the main type of cancer causing mortality worldwide—biomarker research focuses on different objectives: the early diagnosis of curable tumor diseases, the stratification of patients with prognostic unfavorable operable tumors to assess the need for further therapy regimens, or the selection of patients for the most efficient therapies at early and late stages. In non-small cell lung cancer, gene and miRNA signatures are valuable to differentiate between the two main subtypes’ squamous and non-squamous tumors, a discrimination which has further implications for therapeutic schemes. Further subclassification within adenocarcinoma and squamous cell carcinoma has been done to correlate histopathological phenotype with disease outcome. Those tumor subgroups were assigned by diverse transcriptional patterns including potential biomarkers and therapy targets for future diagnostic and clinical applications. In lung cancer, none of these signatures have entered clinical routine for testing so far. In this review, the status quo of lung cancer gene signatures in preclinical and clinical research will be presented in the context of future clinical perspectives.

  10. Video-assisted thoracoscopic surgery lobectomy for lung cancer.

    PubMed

    Puri, Varun; Meyers, Bryan F

    2013-01-01

    Surgical resection is currently the gold standard in operable patients with early-stage lung cancer. Video-assisted thoracoscopic surgery (VATS) lobectomy is a technique that has technically evolved and grown increasingly popular over the past two decades. This article presents the evolution, definition, current application, and some of the controversies surrounding VATS lobectomy. PMID:23158083

  11. Exposure to diesel exhaust linked to lung cancer in miners

    Cancer.gov

    In a study of non-metal miners in the United States, federal government scientists reported that heavy exposure to diesel exhaust increased risk of death from lung cancer. The research, all part of the Diesel Exhaust in Miners Study, was designed to evalu

  12. Genetically engineered mouse models for lung cancer.

    PubMed

    Kwak, I; Tsai, S Y; DeMayo, F J

    2004-01-01

    The lung is a complex organ consisting of numerous cell types that function to ensure sufficient gas exchange to oxygenate the blood. In order to accomplish this function, the lung must be exposed to the external environment and at the same time maintain a homeostatic balance between its function in gas exchange and the maintenance of inflammatory balance. During the past two decades, as molecular methodologies have evolved with the sequencing of entire genomes, the use of in vivo models to elucidate the molecular mechanisms involved in pulmonary physiology and disease have increased. The mouse has emerged as a potent model to investigate pulmonary physiology due to the explosion in molecular methods that now allow for the developmental and tissue-specific regulation of gene transcription. Initial efforts to manipulate gene expression in the mouse genome resulted in the generation of transgenic mice characterized by the constitutive expression of a specific gene and knockout mice characterized by the ablation of a specific gene. The utility of these original mouse models was limited, in many cases, by phenotypes resulting in embryonic or neonatal lethality that prevented analysis of the impact of the genetic manipulation on pulmonary biology. Second-generation transgenic mouse models employ multiple strategies that can either activate or silence gene expression thereby providing extensive temporal and spatial control of the experimental parameters of gene expression. These highly regulated mouse models are intended to serve as a foundation for further investigation of the molecular basis of human disease such as tumorigenesis. This review describes the principles, progress, and application of systems that are currently employed in the conditional regulation of gene expression in the investigation of lung cancer. PMID:14977417

  13. Radiation Therapy, Chemotherapy, and Soy Isoflavones in Treating Patients With Stage IIIA-IIIB Non-Small Cell Lung Cancer

    ClinicalTrials.gov

    2016-02-08

    Adenocarcinoma of the Lung; Adenosquamous Cell Lung Cancer; Bronchoalveolar Cell Lung Cancer; Large Cell Lung Cancer; Recurrent Non-small Cell Lung Cancer; Squamous Cell Lung Cancer; Stage IIIA Non-small Cell Lung Cancer; Stage IIIB Non-small Cell Lung Cancer

  14. Low-Dose Acetylsalicylic Acid in Treating Patients With Stage I-III Non-Small Cell Lung Cancer

    ClinicalTrials.gov

    2016-06-28

    Adenocarcinoma of the Lung; Recurrent Non-small Cell Lung Cancer; Stage IA Non-small Cell Lung Cancer; Stage IB Non-small Cell Lung Cancer; Stage IIA Non-small Cell Lung Cancer; Stage IIB Non-small Cell Lung Cancer; Stage IIIA Non-small Cell Lung Cancer; Stage IIIB Non-small Cell Lung Cancer

  15. [Therapeutic strategy for secondary lung cancer].

    PubMed

    Miura, Hiroyuki; Nakajima, Norio; Takahashi, Hidenobu; Kinoshita, Masao; Ikeda, Norihiko

    2010-10-01

    Among 659 resected lung cancer cases from 1994 to 2009, 57 secondary lung cancers (8.6%) were evaluated. The secondary tumors were synchronous, located in the same lobe in 10, the ipsilateral different lobe in 17, and the contralateral lobe in 13, or metachronous, located in the contralateral lobe in 15, and the ipsilateral different lobe in 5. Both the tumors were removed in 49 cases. Chemotherapy, stereotactic radiotherapy (SRT), photo dynamic therapy (PDT), or best supportive care (BSC) was selected after a lobectomy or segmentectomy of the 1st tumor in 8 cases considering the patient's condition. Lobectomy or segmentectomy should be indicated for the 1st tumor considering curability. Bilobectomy is adopted for multiple cancers involving middle lobe. According to the operability or pulmonary function, the same strategy is adopted for secondary cancer. Considering the patient's condition, possibility of metastases and the tumor location and histologic type, partial resection, SRT, PDT, or BSC could be selected. PMID:20954350

  16. Asthma and lung cancer risk: a systematic investigation by the International Lung Cancer Consortium

    PubMed Central

    Rosenberger, Albert; Bickeböller, Heike; McCormack, Valerie; Brenner, Darren R.; Duell, Eric J.; Tjønneland, Anne; Friis, Soren; Muscat, Joshua E.; Yang, Ping; Wichmann, H-Erich; Heinrich, Joachim; Szeszenia-Dabrowska, Neonila; Lissowska, Jolanta; Zaridze, David; Rudnai, Peter; Fabianova, Eleonora; Janout, Vladimir; Bencko, Vladimir; Brennan, Paul; Mates, Dana; Schwartz, Ann G.; Cote, Michele L.; Zhang, Zuo-Feng; Morgenstern, Hal; Oh, Sam S.; Field, John K.; Raji, Olaide; McLaughlin, John R.; Wiencke, John; LeMarchand, Loic; Neri, Monica; Bonassi, Stefano; Andrew, Angeline S.; Lan, Qing; Hu, Wei; Orlow, Irene; Park, Bernard J.; Boffetta, Paolo

    2012-01-01

    Asthma has been hypothesized to be associated with lung cancer (LC) risk. We conducted a pooled analysis of 16 studies in the International Lung Cancer Consortium (ILCCO) to quantitatively assess this association and compared the results with 36 previously published studies. In total, information from 585 444 individuals was used. Study-specific measures were combined using random effects models. A meta-regression and subgroup meta-analyses were performed to identify sources of heterogeneity. The overall LC relative risk (RR) associated with asthma was 1.28 [95% confidence intervals (CIs) = 1.16–1.41] but with large heterogeneity (I2 = 73%, P < 0.001) between studies. Among ILCCO studies, an increased risk was found for squamous cell (RR = 1.69, 95%, CI = 1.26–2.26) and for small-cell carcinoma (RR = 1.71, 95% CI = 0.99–2.95) but was weaker for adenocarcinoma (RR = 1.09, 95% CI = 0.88–1.36). The increased LC risk was strongest in the 2 years after asthma diagnosis (RR = 2.13, 95% CI = 1.09–4.17) but subjects diagnosed with asthma over 10 years prior had no or little increased LC risk (RR = 1.10, 95% CI = 0.94–1.30). Because the increased incidence of LC was chiefly observed in small cell and squamous cell lung carcinomas, primarily within 2 years of asthma diagnosis and because the association was weak among never smokers, we conclude that the association may not reflect a causal effect of asthma on the risk of LC. PMID:22198214

  17. Expression of a phosphorylated form of ATF4 in lung and non-small cell lung cancer tissues.

    PubMed

    Fan, Chui-Feng; Miao, Yuan; Lin, Xu-Yong; Zhang, Di; Wang, En-Hua

    2014-01-01

    ATF4 is a member of the cAMP-responsive element-binding protein family of basic zipper-containing proteins, a family of transcription factors phosphorylated at serines residues by protein kinase A. The family has been proved to be able to stimulate the transcription of the genes containing CRE elements. Elevated ATF4 expression was detected in some tumors including breast carcinoma compared to their corresponding nontumor tissues. p-ATF4 (ser 245), a phosphorylated form of ATF4 protein at serine 245 site, was believed to be an active type of this protein. However, its expression and clinical significance in malignant tumors including non-small cell lung cancer were not reported up to date. In the current study, we investigate the expression of p-ATF4 (ser 245) in non-small cell lung cancer using tissue microarray and immunohistochemistry. p-ATF4 (ser 245) immunostaining was detected in nucleus and cytoplasm in cancer cells and normal lung epithelial cells. Compared to bronchial epithelium and submucosal glands (total positive rate, 14.6% (12/82)), there was increased expression of p-ATF4 (ser 245) in non-small cell lung cancer cells (total positive rate, 42.7% (35/82)) (p < 0.05). In addition, increased expression of p-ATF4 (ser 245) was associated with lymph node metastasis and advanced TNM stages (III and IV) in non-small cell lung cancer (p < 0.05). Immunofluorescent staining confirmed nuclear and cytoplasmic expression of p-ATF4 (ser 245) in lung and cancer tissues, and also in non-small cell lung cancer cell lines including NCI-H157 and LTE cells. These results indicate that increased expression of p-ATF4 (ser 245) may contribute to cancer development of non-small cell lung cancer and may be a potential cancer marker. PMID:23975372

  18. Hedgehog Pathway Inhibition Radiosensitizes Non-Small Cell Lung Cancers

    PubMed Central

    Zeng, Jing; Aziz, Khaled; Chettiar, Sivarajan T.; Aftab, Blake T.; Armour, Michael; Gajula, Rajendra; Gandhi, Nishant; Salih, Tarek; Herman, Joseph M.; Wong, John; Rudin, Charles M.; Tran, Phuoc T.; Hales, Russell K.

    2012-01-01

    Purpose Despite improvements in chemoradiation, local control remains a major clinical problem in locally advanced non-small cell lung cancer. The Hedgehog pathway has been implicated in tumor recurrence by promoting survival of tumorigenic precursors and through effects on tumor-associated stroma. Whether Hedgehog inhibition can affect radiation efficacy in vivo has not been reported. Methods and Materials We evaluated the effects of a targeted Hedgehog inhibitor (HhAntag) and radiation on clonogenic survival of human non-small cell lung cancer lines in vitro. Using an A549 cell line xenograft model, we examined tumor growth, proliferation, apoptosis, and gene expression changes after concomitant HhAntag and radiation. In a transgenic mouse model of KrasG12D-induced and Twist1-induced lung adenocarcinoma, we assessed tumor response to radiation and HhAntag by serial micro-computed tomography (CT) scanning. Results In 4 human lung cancer lines in vitro, HhAntag showed little or no effect on radio-sensitivity. By contrast, in both the human tumor xenograft and murine inducible transgenic models, HhAntag enhanced radiation efficacy and delayed tumor growth. By use of the human xenograft model to differentiate tumor and stromal effects, mouse stromal cells, but not human tumor cells, showed significant and consistent downregulation of Hedgehog pathway gene expression. This was associated with increased tumor cell apoptosis. Conclusions Targeted Hedgehog pathway inhibition can increase in vivo radiation efficacy in lung cancer preclinical models. This effect is associated with pathway suppression in tumor-associated stroma. These data support clinical testing of Hedgehog inhibitors as a component of multimodality therapy for locally advanced non-small cell lung cancer. PMID:23182391

  19. Hedgehog Pathway Inhibition Radiosensitizes Non-Small Cell Lung Cancers

    SciTech Connect

    Zeng, Jing; Aziz, Khaled; Chettiar, Sivarajan T.; Aftab, Blake T.; Armour, Michael; Gajula, Rajendra; Gandhi, Nishant; Salih, Tarek; Herman, Joseph M.; Wong, John; Rudin, Charles M.; Tran, Phuoc T.; Hales, Russell K.

    2013-05-01

    Purpose: Despite improvements in chemoradiation, local control remains a major clinical problem in locally advanced non-small cell lung cancer. The Hedgehog pathway has been implicated in tumor recurrence by promoting survival of tumorigenic precursors and through effects on tumor-associated stroma. Whether Hedgehog inhibition can affect radiation efficacy in vivo has not been reported. Methods and Materials: We evaluated the effects of a targeted Hedgehog inhibitor (HhAntag) and radiation on clonogenic survival of human non-small cell lung cancer lines in vitro. Using an A549 cell line xenograft model, we examined tumor growth, proliferation, apoptosis, and gene expression changes after concomitant HhAntag and radiation. In a transgenic mouse model of Kras{sup G12D}-induced and Twist1-induced lung adenocarcinoma, we assessed tumor response to radiation and HhAntag by serial micro-computed tomography (CT) scanning. Results: In 4 human lung cancer lines in vitro, HhAntag showed little or no effect on radiosensitivity. By contrast, in both the human tumor xenograft and murine inducible transgenic models, HhAntag enhanced radiation efficacy and delayed tumor growth. By use of the human xenograft model to differentiate tumor and stromal effects, mouse stromal cells, but not human tumor cells, showed significant and consistent downregulation of Hedgehog pathway gene expression. This was associated with increased tumor cell apoptosis. Conclusions: Targeted Hedgehog pathway inhibition can increase in vivo radiation efficacy in lung cancer preclinical models. This effect is associated with pathway suppression in tumor-associated stroma. These data support clinical testing of Hedgehog inhibitors as a component of multimodality therapy for locally advanced non-small cell lung cancer.

  20. Personalizing Therapy in Advanced Non–Small Cell Lung Cancer

    PubMed Central

    Villaruz, Liza C.; Burns, Timothy F.; Ramfidis, Vasilis S.; Socinski, Mark A.

    2016-01-01

    The recognition that non–small cell lung cancer (NSCLC) is not a single disease entity, but rather a collection of distinct molecularly driven neoplasms, has permanently shifted the therapeutic landscape of NSCLC to a personalized approach. This personalization of NSCLC therapy is typified by the dramatic response rates seen in EGFR mutant NSCLC when treated with targeted tyrosine kinase inhibitor therapy and in ALK translocation–driven NSCLC when treated with ALK inhibitors. Targeted therapeutic approaches in NSCLC necessitate consideration of more invasive biopsy techniques aimed at providing sufficient tissue for both histological determination and molecular profiling in all patients with stage IV disease both at the time of diagnosis and at the time of disease progression. Comprehensive genotyping efforts have identified oncogenic drivers in 62% lung adenocarcinomas and an increasing proportion of squamous cell carcinomas of the lung. The identification of these oncogenic drivers and the triage of patients to clinical trials evaluating novel targeted therapeutic approaches will increasingly mold a landscape of personalized lung cancer therapy where each genotype has an associated targeted therapy. This review outlines the state of personalized lung cancer therapy as it pertains to individual NSCLC genotypes. PMID:24258572

  1. Magnetic resonance imaging for lung cancer screen.

    PubMed

    Wang, Yi-Xiang J; Lo, Gladys G; Yuan, Jing; Larson, Peder E Z; Zhang, Xiaoliang

    2014-09-01

    Lung cancer is the leading cause of cancer related death throughout the world. Lung cancer is an example of a disease for which a large percentage of the high-risk population can be easily identified via a smoking history. This has led to the investigation of lung cancer screening with low-dose helical/multi-detector CT. Evidences suggest that early detection of lung cancer allow more timely therapeutic intervention and thus a more favorable prognosis for the patient. The positive relationship of lesion size to likelihood of malignancy has been demonstrated previously, at least 99% of all nodules 4 mm or smaller are benign, while noncalcified nodules larger than 8 mm diameter bear a substantial risk of malignancy. In the recent years, the availability of high-performance gradient systems, in conjunction with phased-array receiver coils and optimized imaging sequences, has made MR imaging of the lung feasible. It can now be assumed a threshold size of 3-4 mm for detection of lung nodules with MRI under the optimal conditions of successful breath-holds with reliable gating or triggering. In these conditions, 90% of all 3-mm nodules can be correctly diagnosed and that nodules 5 mm and larger are detected with 100% sensitivity. Parallel imaging can significantly shorten the imaging acquisition time by utilizing the diversity of sensitivity profile of individual coil elements in multi-channel radiofrequency receive coil arrays or transmit/receive coil arrays to reduce the number of phase encoding steps required in imaging procedure. Compressed sensing technique accelerates imaging acquisition from dramatically undersampled data set by exploiting the sparsity of the images in an appropriate transform domain. With the combined imaging algorithm of parallel imaging and compressed sensing and advanced 32-channel or 64-channel RF hardware, overall imaging acceleration of 20 folds or higher can then be expected, ultimately achieve free-breathing and no ECG gating acquisitions

  2. Magnetic resonance imaging for lung cancer screen

    PubMed Central

    Lo, Gladys G.; Yuan, Jing; Larson, Peder E. Z.

    2014-01-01

    Lung cancer is the leading cause of cancer related death throughout the world. Lung cancer is an example of a disease for which a large percentage of the high-risk population can be easily identified via a smoking history. This has led to the investigation of lung cancer screening with low-dose helical/multi-detector CT. Evidences suggest that early detection of lung cancer allow more timely therapeutic intervention and thus a more favorable prognosis for the patient. The positive relationship of lesion size to likelihood of malignancy has been demonstrated previously, at least 99% of all nodules 4 mm or smaller are benign, while noncalcified nodules larger than 8 mm diameter bear a substantial risk of malignancy. In the recent years, the availability of high-performance gradient systems, in conjunction with phased-array receiver coils and optimized imaging sequences, has made MR imaging of the lung feasible. It can now be assumed a threshold size of 3-4 mm for detection of lung nodules with MRI under the optimal conditions of successful breath-holds with reliable gating or triggering. In these conditions, 90% of all 3-mm nodules can be correctly diagnosed and that nodules 5 mm and larger are detected with 100% sensitivity. Parallel imaging can significantly shorten the imaging acquisition time by utilizing the diversity of sensitivity profile of individual coil elements in multi-channel radiofrequency receive coil arrays or transmit/receive coil arrays to reduce the number of phase encoding steps required in imaging procedure. Compressed sensing technique accelerates imaging acquisition from dramatically undersampled data set by exploiting the sparsity of the images in an appropriate transform domain. With the combined imaging algorithm of parallel imaging and compressed sensing and advanced 32-channel or 64-channel RF hardware, overall imaging acceleration of 20 folds or higher can then be expected, ultimately achieve free-breathing and no ECG gating acquisitions

  3. Genomics of Squamous Cell Lung Cancer

    PubMed Central

    Rooney, Melissa; Devarakonda, Siddhartha

    2013-01-01

    Approximately 30% of patients with non-small cell lung cancer have the squamous cell carcinoma (SQCC) histological subtype. Although targeted therapies have improved outcomes in patients with adenocarcinoma, no agents are currently approved specifically for use in SQCC. The Cancer Genome Atlas (TCGA) recently published the results of comprehensive genomic analyses of tumor samples from 178 patients with SQCC of the lung. In this review, we briefly discuss key molecular aberrations reported by TCGA and other investigators and their potential therapeutic implications. Carefully designed preclinical and clinical studies based on these large-scale genomic analyses are critical to improve the outcomes of patients with SQCC of lung in the near future. PMID:23728941

  4. Expanding a Comprehensive Lung Cancer Screening Program.

    PubMed

    Jansak, Buffy

    2015-01-01

    The OhioHealth Lung Cancer Screening Program is a high quality multi-disciplinary program that was launched in July 2013 at OhioHealth Riverside Methodist Hospital, OhioHealth Doctors Hospital, and OhioHealth Grant Medical Center in Columbus, Ohio. With the assistance of the AHRA & Toshiba Putting Patients First grant, we were able to expand community access for people at high risk of developing lung cancer by opening several more programs at OhioHealth Marion General and OhioHealth Grady Memorial Hospitals. A subsequent patient educational video was developed to highlight the comprehensive program, nurse navigational involvement, potential risks, benefits, and tobacco cessation. The tobacco cessation educational skills of the OhioHealth Lung Nurse Navigators were enhanced with the completion of the Tobacco Treatment Specialist certification. PMID:26710574

  5. ESR/ERS white paper on lung cancer screening.

    PubMed

    Kauczor, Hans-Ulrich; Bonomo, Lorenzo; Gaga, Mina; Nackaerts, Kristiaan; Peled, Nir; Prokop, Mathias; Remy-Jardin, Martine; von Stackelberg, Oyunbileg; Sculier, Jean-Paul

    2015-07-01

    Lung cancer is the most frequently fatal cancer, with poor survival once the disease is advanced. Annual low dose computed tomography has shown a survival benefit in screening individuals at high risk for lung cancer. Based on the available evidence, the European Society of Radiology and the European Respiratory Society recommend lung cancer screening in comprehensive, quality-assured, longitudinal programmes within a clinical trial or in routine clinical practice at certified multidisciplinary medical centres. Minimum requirements include: standardised operating procedures for low dose image acquisition, computer-assisted nodule evaluation, and positive screening results and their management; inclusion/exclusion criteria; expectation management; and smoking cessation programmes. Further refinements are recommended to increase quality, outcome and cost-effectiveness of lung cancer screening: inclusion of risk models, reduction of effective radiation dose, computer-assisted volumetric measurements and assessment of comorbidities (chronic obstructive pulmonary disease and vascular calcification). All these requirements should be adjusted to the regional infrastructure and healthcare system, in order to exactly define eligibility using a risk model, nodule management and quality assurance plan. The establishment of a central registry, including biobank and image bank, and preferably on a European level, is strongly encouraged. PMID:25929956

  6. ESR/ERS white paper on lung cancer screening

    PubMed Central

    Bonomo, Lorenzo; Gaga, Mina; Nackaerts, Kristiaan; Peled, Nir; Prokop, Mathias; Remy-Jardin, Martine; von Stackelberg, Oyunbileg; Sculier, Jean-Paul

    2015-01-01

    Lung cancer is the most frequently fatal cancer, with poor survival once the disease is advanced. Annual low dose computed tomography has shown a survival benefit in screening individuals at high risk for lung cancer. Based on the available evidence, the European Society of Radiology and the European Respiratory Society recommend lung cancer screening in comprehensive, quality-assured, longitudinal programmes within a clinical trial or in routine clinical practice at certified multidisciplinary medical centres. Minimum requirements include: standardised operating procedures for low dose image acquisition, computer-assisted nodule evaluation, and positive screening results and their management; inclusion/exclusion criteria; expectation management; and smoking cessation programmes. Further refinements are recommended to increase quality, outcome and cost-effectiveness of lung cancer screening: inclusion of risk models, reduction of effective radiation dose, computer-assisted volumetric measurements and assessment of comorbidities (chronic obstructive pulmonary disease and vascular calcification). All these requirements should be adjusted to the regional infrastructure and healthcare system, in order to exactly define eligibility using a risk model, nodule management and quality assurance plan. The establishment of a central registry, including biobank and image bank, and preferably on a European level, is strongly encouraged. PMID:25929956

  7. PET/CT imaging in lung cancer: indications and findings*

    PubMed Central

    Hochhegger, Bruno; Alves, Giordano Rafael Tronco; Irion, Klaus Loureiro; Fritscher, Carlos Cezar; Fritscher, Leandro Genehr; Concatto, Natália Henz; Marchiori, Edson

    2015-01-01

    The use of PET/CT imaging in the work-up and management of patients with lung cancer has greatly increased in recent decades. The ability to combine functional and anatomical information has equipped PET/CT to look into various aspects of lung cancer, allowing more precise disease staging and providing useful data during the characterization of indeterminate pulmonary nodules. In addition, the accuracy of PET/CT has been shown to be greater than is that of conventional modalities in some scenarios, making PET/CT a valuable noninvasive method for the investigation of lung cancer. However, the interpretation of PET/CT findings presents numerous pitfalls and potential confounders. Therefore, it is imperative for pulmonologists and radiologists to familiarize themselves with the most relevant indications for and limitations of PET/CT, seeking to protect their patients from unnecessary radiation exposure and inappropriate treatment. This review article aimed to summarize the basic principles, indications, cancer staging considerations, and future applications related to the use of PET/CT in lung cancer. PMID:26176525

  8. Treatment of Brain Metastasis from Lung Cancer

    PubMed Central

    Chi, Alexander; Komaki, Ritsuko

    2010-01-01

    Brain metastases are not only the most common intracranial neoplasm in adults but also very prevalent in patients with lung cancer. Patients have been grouped into different classes based on the presence of prognostic factors such as control of the primary tumor, functional performance status, age, and number of brain metastases. Patients with good prognosis may benefit from more aggressive treatment because of the potential for prolonged survival for some of them. In this review, we will comprehensively discuss the therapeutic options for treating brain metastases, which arise mostly from a lung cancer primary. In particular, we will focus on the patient selection for combined modality treatment of brain metastases, such as surgical resection or stereotactic radiosurgery (SRS) combined with whole brain irradiation; the use of radiosensitizers; and the neurocognitive deficits after whole brain irradiation with or without SRS. The benefit of prophylactic cranial irradiation (PCI) and its potentially associated neuro-toxicity for both small cell lung cancer (SCLC) and non-small cell lung cancer (NSCLC) are also discussed, along with the combined treatment of intrathoracic primary disease and solitary brain metastasis. The roles of SRS to the surgical bed, fractionated stereotactic radiotherapy, WBRT with an integrated boost to the gross brain metastases, as well as combining WBRT with epidermal growth factor receptor (EGFR) inhibitors, are explored as well. PMID:24281220

  9. Parathyroid adenoma upstaging the lung cancer.

    PubMed

    Okuyucu, Kursat; Kavakli, Kuthan; Ozaydın, Sukru; Karahatay, Serdar; Karatas, Okan; Doğan, Deniz

    2015-05-01

    Mediastinal staging of NSCLC with noninvasive methods such as PET/CT can be misleading when a mediastinal disease accompany. Histopathologic confirmation should be made before any treatment plan. Herein, we presented a case of parathyroid adenoma upstaging the lung cancer. PMID:25618011

  10. [Immunotherapy in lung cancer: checkpoint inhibitors].

    PubMed

    Wehler, Thomas; Wehler, Beatrice; Stehle, Ingo

    2015-12-01

    Monoclonal antibodies against the PD-1 receptor or its ligands result in a recovery of T cell responses against tumor antigens. Nivolumab is the first antibody that has been approved in lung cancer. This mode of action is very intersting, especially because of long term responses and the moderate toxicity. PMID:26625234

  11. Outdoor air pollution and lung cancer.

    PubMed Central

    Cohen, A J

    2000-01-01

    In the 1950s evidence of an ongoing epidemic of lung cancer in the United States and Western Europe led researchers to examine the role of outdoor air pollution, which was considered by some to be a likely cause. Although epidemiologic research quickly identified the central role of cigarette smoking in this epidemic, and despite progress in reducing outdoor air pollution in Western industrialized countries, concerns that ambient air pollution is causing lung cancer have persisted to the present day. This concern is based on the fact that known carcinogens continue to be released into outdoor air from industrial sources, power plants, and motor vehicles, and on a body of epidemiologic research that provides some evidence for an association between outdoor air pollution and lung cancer. This article reviews the epidemiologic evidence for this association and discusses the limitations of current studies for estimating the lung cancer risk in the general population. It also identifies research needs and suggests possible approaches to addressing outstanding questions. PMID:10931793

  12. Screening and early detection of lung cancer.

    PubMed

    Vansteenkiste, J; Dooms, C; Mascaux, C; Nackaerts, K

    2012-09-01

    The greatest news of the past year in this field was the first large-scale early detection trial that could prove a 20% reduction in lung cancer-related mortality by screening high-risk individuals with low-dose computed tomography (LDCT). Several expert groups and medical societies have assessed the data and concluded that LDCT screening for lung cancer is, however, not ready for large-scale population-based implementation. Too many open questions remain, such as definition of the at-risk population, timing and intervals of screening, optimal method of acquisition and interpretation of the images, how to handle (false) positive findings, and especially cost-effectiveness in relation to other lung cancer prevention strategies, mainly smoking cessation. Further analyses and several ongoing European trials are eagerly awaited. Much hope also resides in the use of biomarkers, as their use in, e.g., blood or exhaled air may provide more easy-to-use tests to better stratify high-risk populations for screening studies. While exciting research is ongoing in this domain--e.g. with microRNAs--none of the tests has yet reached sufficient validation for clinical use. Early central lung cancers are more difficult to visualise by CT. For these patients, standard bronchoscopy, complemented by autofluoresence endoscopy, has been studied in different screening and follow-up settings. PMID:22987984

  13. The wind god promotes lung cancer.

    PubMed

    Frisch, Steven M; Schaller, Michael D

    2014-05-12

    In this issue of Cancer Cell, Li and colleagues demonstrate that the hematopoietic transcription factor Aiolos (named after the Wind God of Greek mythology) confers anoikis resistance in lung tumor cells through repression of cell adhesion-related genes including the mechanosensor p66Shc. PMID:24823631

  14. Aiolos and Lymphocyte Mimicry in Lung Cancer

    PubMed Central

    Terada, Lance S; Liu, Zhe

    2014-01-01

    Aggressive carcinomas tend to adopt behaviors normally restricted to lymphocytes, including anchorage-independent mobilization, response to chemokines, and modulation of local inflammatory conditions. In a recent study we identified the lymphocyte-restricted chromatin regulator Aiolos as an epigenetic driver of lymphocyte mimicry in lung cancer that links immune cell development to metastatic behavior. PMID:27308319

  15. Gene variant linked to lung cancer risk

    Cancer.gov

    A variation of the gene NFKB1, called rs4648127, is associated with an estimated 44 percent reduction in lung cancer risk. When this information, derived from samples obtained as part of a large NCI-sponsored prevention clinical trial, was compared with d

  16. Global trends of lung cancer mortality and smoking prevalence

    PubMed Central

    Torre, Lindsey A.; Jemal, Ahmedin

    2015-01-01

    Lung cancer killed approximately 1,590,000 persons in 2012 and currently is the leading cause of cancer death worldwide. There is large variation in mortality rates across the world in both males and females. This variation follows trend of smoking, as tobacco smoking is responsible for the majority of lung cancer cases. In this article, we present estimated worldwide lung cancer mortality rates in 2012 using the World Health Organization (WHO) GLOBOCAN 2012 and changes in the rates during recent decades in select countries using WHO Mortality Database. We also show smoking prevalence and trends globally and at the regional level. By region, the highest lung cancer mortality rates (per 100,000) in 2012 were in Central and Eastern Europe (47.6) and Eastern Asia (44.8) among males and in Northern America (23.5) and Northern Europe (19.1) among females; the lowest rates were in sub-Saharan Africa in both males (4.4) and females (2.2). The highest smoking prevalence among males is generally in Eastern and South-Eastern Asia and Eastern Europe, and among females is in European countries, followed by Oceania and Northern and Southern America. Many countries, notably high-income countries, have seen a considerable decrease in smoking prevalence in both males and females, but in many other countries there has been little decrease or even an increase in smoking prevalence. Consequently, depending on whether or when smoking prevalence has started to decline, the lung cancer mortality trend is a mixture of decreasing, stable, or increasing. Despite major achievements in tobacco control, with current smoking patterns lung cancer will remain a major cause of death worldwide for several decades. The main priority to reduce the burden of lung cancer is to implement or enforce effective tobacco control policies in order to reduce smoking prevalence in all countries and prevent an increase in smoking in sub-Saharan Africa and women in low- and middle-income countries (LMICs). PMID

  17. Vaccine Therapy in Treating Patients With Colon, Pancreatic, or Lung Cancer

    ClinicalTrials.gov

    2015-04-27

    Recurrent Colon Cancer; Extensive Stage Small Cell Lung Cancer; Stage III Pancreatic Cancer; Stage III Rectal Cancer; Limited Stage Small Cell Lung Cancer; Recurrent Pancreatic Cancer; Recurrent Rectal Cancer; Stage III Non-small Cell Lung Cancer; Stage I Pancreatic Cancer; Stage II Non-small Cell Lung Cancer; Stage IVB Pancreatic Cancer; Stage II Pancreatic Cancer; Stage III Colon Cancer; Stage IVA Pancreatic Cancer

  18. Enhanced expression of G-protein coupled estrogen receptor (GPER/GPR30) in lung cancer

    PubMed Central

    2012-01-01

    Background G-protein-coupled estrogen receptor (GPER/GPR30) was reported to bind 17β-estradiol (E2), tamoxifen, and ICI 182,780 (fulvestrant) and promotes activation of epidermal growth factor receptor (EGFR)-mediated signaling in breast, endometrial and thyroid cancer cells. Although lung adenocarcinomas express estrogen receptors α and β (ERα and ERβ), the expression of GPER in lung cancer has not been investigated. The purpose of this study was to examine the expression of GPER in lung cancer. Methods The expression patterns of GPER in various lung cancer lines and lung tumors were investigated using standard quantitative real time PCR (at mRNA levels), Western blot and immunohistochemistry (IHC) methods (at protein levels). The expression of GPER was scored and the pairwise comparisons (cancer vs adjacent tissues as well as cancer vs normal lung tissues) were performed. Results Analysis by real-time PCR and Western blotting revealed a significantly higher expression of GPER at both mRNA and protein levels in human non small cell lung cancer cell (NSCLC) lines relative to immortalized normal lung bronchial epithelial cells (HBECs). The virally immortalized human small airway epithelial cell line HPL1D showed higher expression than HBECs and similar expression to NSCLC cells. Immunohistochemical analysis of tissue sections of murine lung adenomas as well as human lung adenocarcinomas, squamous cell carcinomas and non-small cell lung carcinomas showed consistently higher expression of GPER in the tumor relative to the surrounding non-tumor tissue. Conclusion The results from this study demonstrate increased GPER expression in lung cancer cells and tumors compared to normal lung. Further evaluation of the function and regulation of GPER will be necessary to determine if GPER is a marker of lung cancer progression. PMID:23273253

  19. Ouabain enhances lung cancer cell detachment.

    PubMed

    Ruanghirun, Thidarat; Pongrakhananon, Varisa; Chanvorachote, Pithi

    2014-05-01

    A human steroid hormone, ouabain, has been shown to play a role in several types of cancer cell behavior; however, its effects on cancer metastasis are largely unknown. Herein, we demonstrate that sub-toxic concentrations of ouabain facilitate cancer cell detachment from the extracellular matrix in human lung cancer cells. Ouabain at concentrations of 0-10 pM significantly enhanced cell detachment in dose- and time- dependent manners, while having minimal effect on cell viability. The detachment-inducing effect of ouabain was found to be mediated through focal-adhesion kinase and ATP-dependent tyrosine kinase pathways. Alpha-5 and beta-1 integrins were found to be down-regulated in response to ouabain treatment. Since detachment of cancer cells is a prerequisite process for metastasis to begin, these insights benefit our understanding over the molecular basis of cancer biology. PMID:24778025

  20. Challenges in defining radiation pneumonitis in patients with lung cancer

    SciTech Connect

    Kocak, Zafer; Evans, Elizabeth S.; Zhou Sumin; Miller, Keith L.; Folz, Rodney J.; Shafman, Timothy D.; Marks, Lawrence B. . E-mail: marks@radonc.duke.edu

    2005-07-01

    Purpose: To assess the difficulty of assigning a definitive clinical diagnosis of radiation (RT)-induced lung injury in patients irradiated for lung cancer. Methods: Between 1991 and 2003, 318 patients were enrolled in a prospective study to evaluate RT-induced lung injury. Only patients with lung cancer who had a longer than 6-month follow-up (251 patients) were considered in the current analysis. Of these, 47 of 251 patients had Grade {>=}2 (treated with steroids) increasing shortness of breath after RT, thought possibly consistent with pneumonitis/fibrosis. The treating physician, and one to three additional reviewing physicians, evaluated the patients or their medical records, or both. The presence or absence of confounding clinical factors that made the diagnosis of RT-induced uncertain lung injury were recorded. Results: Thirty-one of 47 patients (66%) with shortness of breath had 'classic' pneumonitis, i.e., they responded to steroids and had a definitive diagnosis of pneumonitis. In 13 of 47 patients (28%), the diagnosis of RT-induced toxicity was confounded by possible infection; exacerbation of preexisting lung disease (chronic obstructive pulmonary disease); tumor regrowth/progression; and cardiac disease in 6, 8, 5, and 1 patients, respectively (some of the patients had multiple confounding factors and were counted more than once). An additional 3 patients (6%) had progressive shortness of breath and an overall clinical course more consistent with fibrosis. All 3 had evidence of bronchial stenosis by bronchoscopy. Conclusions: Scoring of radiation pneumonitis was challenging in 28% of patients treated for lung cancer owing to confounding medical conditions. Recognition of this uncertainty is needed and may limit our ability to understand RT-induced lung injury.

  1. Role of acetylcholinesterase in lung cancer

    PubMed Central

    Xi, Hui-Jun; Wu, Ren-Pei; Liu, Jing-Jing; Zhang, Ling-Juan; Li, Zhao-Shen

    2015-01-01

    Acetylcholinesterase (AChE) plays a key role in catalytic hydrolysis of cholinergic neurotransmitters. Intensive research has proven the involvement of this protein in novel functions, such as cell adhesion, differentiation, and proliferation. In addition, several recent studies have indicated that acetylcholinesterase is potentially a marker and regulator of apoptosis. Importantly, AChE is also a promising tumor suppressor. In this review, we briefly summarize the involvement of AChE in apoptosis and cancer, focusing on the role of AChE in lung cancer, as well as the therapeutic consideration of AChE for cancer therapy. PMID:26273392

  2. Lung Cancer and Elemental Carbon Exposure in Trucking Industry Workers

    PubMed Central

    Laden, Francine; Hart, Jaime E.; Davis, Mary E.; Eisen, Ellen A.; Smith, Thomas J.

    2012-01-01

    Background: Diesel exhaust has been considered to be a probable lung carcinogen based on studies of occupationally exposed workers. Efforts to define lung cancer risk in these studies have been limited in part by lack of quantitative exposure estimates. Objective: We conducted a retrospective cohort study to assess lung cancer mortality risk among U.S. trucking industry workers. Elemental carbon (EC) was used as a surrogate of exposure to engine exhaust from diesel vehicles, traffic, and loading dock operations. Methods: Work records were available for 31,135 male workers employed in the unionized U.S. trucking industry in 1985. A statistical model based on a national exposure assessment was used to estimate historical work-related exposures to EC. Lung cancer mortality was ascertained through the year 2000, and associations with cumulative and average EC were estimated using proportional hazards models. Results: Duration of employment was inversely associated with lung cancer risk consistent with a healthy worker survivor effect and a cohort composed of prevalent hires. After adjusting for employment duration, we noted a suggestion of a linear exposure–response relationship. For each 1,000-µg/m3 months of cumulative EC, based on a 5-year exposure lag, the hazard ratio (HR) was 1.07 [95% confidence interval (CI): 0.99, 1.15] with a similar association for a 10-year exposure lag [HR = 1.09 (95% CI: 0.99, 1.20)]. Average exposure was not associated with relative risk. Conclusions: Lung cancer mortality in trucking industry workers increased in association with cumulative exposure to EC after adjusting for negative confounding by employment duration. PMID:22739103

  3. Breath sensors for lung cancer diagnosis.

    PubMed

    Adiguzel, Yekbun; Kulah, Haluk

    2015-03-15

    The scope of the applications of breath sensors is abundant in disease diagnosis. Lung cancer diagnosis is a well-fitting health-related application of this technology, which is of utmost importance in the health sector, because lung cancer has the highest death rate among all cancer types, and it brings a high yearly global burden. The aim of this review is first to provide a rational basis for the development of breath sensors for lung cancer diagnostics from a historical perspective, which will facilitate the transfer of the idea into the rapidly evolving sensors field. Following examples with diagnostic applications include colorimetric, composite, carbon nanotube, gold nanoparticle-based, and surface acoustic wave sensor arrays. These select sensor applications are widened by the state-of-the-art developments in the sensors field. Coping with sampling sourced artifacts and cancer staging are among the debated topics, along with the other concerns like proteomics approaches and biomimetic media utilization, feature selection for data classification, and commercialization. PMID:25461148

  4. Relationship Between Lung Cancer and Mycobacterium Avium Complex Isolated Using Bronchoscopy

    PubMed Central

    Tamura, Atsuhisa; Hebisawa, Akira; Kusaka, Kei; Hirose, Takashi; Suzuki, Junko; Yamane, Akira; Nagai, Hideaki; Fukami, Takeshi; Ohta, Ken; Takahashi, Fumiaki

    2016-01-01

    Introduction: The incidence of Mycobacterium avium complex (MAC)-positive respiratory specimen cultures and MAC lung disease (MACLD) is increasing worldwide. This retrospective study aimed to assess the association between MAC culture-positive bronchoscopy specimens and lung cancer. Materials and Methods: The medical records of 1382 untreated lung cancer patients between 2003 and 2011 were collected using our hospital database. Of them, records for 1258 that had undergone bronchoscopy together with sampling for mycobacterial culture were reviewed. Patient characteristics were compared between those with MAC-positive/other nontuberculous mycobacteria (NTM)-negative bronchial washings and those with MAC-negative/other NTM-negative bronchial washings. Patients with MAC-positive lung cancer were cross-sectionally divided into MACLD and non-MACLD groups, and their features were assessed. Follow-up data for patients with lung cancer but without MACLD were reviewed for subsequent development of MACLD. Results: Of the 1258 patients with lung cancer, 25 (2.0%) had MAC-positive/other NTM-negative bronchial washings. The proportion of women (52% vs 30%; P = 0.0274) and patient age (72 years vs 69 years; P = 0.0380) were significantly higher in the MAC-positive/other NTM-negative lung cancer group (n = 25) than in the MAC-negative/other NTM-negative lung cancer group (n = 1223). There were 10 patients with lung cancer and MACLD and 15 without MACLD; significant differences in patient characteristics were not found between the two groups, and none of the 15 patients without MACLD subsequently developed MACLD. Conclusion: MAC culture-positive bronchial washing is positively associated with lung cancer. Female sex and advanced age, but not lung cancer characteristics, were found to be associated with MAC infection in patients with lung cancer. PMID:27335625

  5. Air pollution: a potentially modifiable risk factor for lung cancer.

    PubMed

    Fajersztajn, Laís; Veras, Mariana; Barrozo, Ligia Vizeu; Saldiva, Paulo

    2013-09-01

    Economic growth and increased urbanization pose a new risk for cancer development: the exposure of high numbers of people to ambient air pollution. Epidemiological evidence that links air pollution to mortality from lung cancer is robust. An ability to produce high-quality scientific research that addresses these risks and the ability of local health authorities to understand and respond to these risks are basic requirements to solve the conflict between economic development and the preservation of human health. However, this is currently far from being achieved. Thus, this Science and Society article addresses the possibilities of expanding scientific networking to increase awareness of the risk of lung cancer that is promoted by air pollution. PMID:23924644

  6. MicroRNA-106b-25 cluster targets β-TRCP2, increases the expression of Snail and enhances cell migration and invasion in H1299 (non small cell lung cancer) cells

    SciTech Connect

    Savita, Udainiya; Karunagaran, Devarajan

    2013-05-17

    Highlights: •miR-106b-25 cluster directly targets the 3′UTR of the β-TRCP2 transcript. •β-TRCP2 mRNA was lower in H1299 cells stably expressing miR-106b-25 cluster. •miR-106b-25 cluster increased the expression of Snail. •miR-106b-25 cluster promoted the migration, colony formation and invasion. •miR-106b-25 cluster enhanced endothelial tube formation. -- Abstract: Lung cancer causes high mortality without a declining trend and non small cell lung cancer represents 85% of all pulmonary carcinomas. MicroRNAs (miRNAs) serve as fine regulators of proliferation, migration, invasion/metastasis and angiogenesis of normal and cancer cells. Using TargetScan6.2, we predicted that the ubiquitin ligase, β-TRCP2, could be a target for two of the constituent miRNAs of the miR-106b-25 cluster (miR-106b and miR-93). We generated a stable clone of miR-106b-25 cluster (CL) or the empty vector (EV) in H1299 (non small cell lung cancer) cells. The expression of β-TRCP2 mRNA was significantly lower in CL than that in EV cells. Transient expression of miR-93 but not antimiR-93 decreased the expression of β-TRCP2 mRNA in H1299 cells. β-TRCP2-3′UTR reporter assay revealed that its activity in CL cells was only 60% of that in EV cells. Snail protein expression was higher in CL than that in EV cells and H1299 cells exhibited an increase in the expression of Snail upon transient transfection with miR-93. miR-106b-25 cluster-induced migration of CL measured by scratch assay was more than that in EV cells and no significant difference in migration was observed between antimiR-93-transfected H1299 cells and the corresponding control-oligo-transfected cells. miR-106b-25 cluster-induced migration of CL cells was again confirmed in a Boyden chamber assay without the matrigel. CL cells were more invasive than EV cells when assessed using Boyden chambers with matrigel but there were no significant changes in the cell viabilities between EV and CL cells. Colony formation assay

  7. LUNG CANCER IN NEVER SMOKERS: MOLECULAR PROFILES AND THERAPEUTIC IMPLICATIONS

    PubMed Central

    Rudin, Charles M.; Avila-Tang, Erika; Harris, Curtis C.; Herman, James G.; Hirsch, Fred R.; Pao, William; Schwartz, Ann G.; Vahakangas, Kirsi H.; Samet, Jonathan M.

    2010-01-01

    The majority of lung cancers are caused by long term exposure to the several classes of carcinogens present in tobacco smoke. While a significant fraction of lung cancers in never smokers may also be attributable to tobacco, many such cancers arise in the absence of detectable tobacco exposure, and may follow a very different cellular and molecular pathway of malignant transformation. Recent studies summarized here suggest that lung cancers arising in never smokers have a distinct natural history, profile of oncogenic mutations, and response to targeted therapy. The majority of molecular analyses of lung cancer have focused on genetic profiling of pathways responsible for metabolism of primary tobacco carcinogens. Limited research has been conducted evaluating familial aggregation and genetic linkage of lung cancer, particularly among never smokers in whom such associations might be expected to be strongest. Data emerging over the past several years demonstrates that lung cancers in never smokers are much more likely to carry activating mutations of the Epidermal Growth Factor Receptor (EGFR), a key oncogenic factor and direct therapeutic target of several newer anti-cancer drugs. EGFR mutant lung cancers may represent a distinct class of lung cancers, enriched in the never smoking population, and less clearly linked to direct tobacco carcinogenesis. These insights followed initial testing and demonstration of efficacy of EGFR-targeted drugs. Focused analysis of molecular carcinogenesis in lung cancers in never smokers is needed, and may provide additional biologic insight with therapeutic implications for lung cancers in both ever smokers and never smokers. PMID:19755392

  8. Nonsmall-cell lung cancer: chemoprevention studies.

    PubMed

    Karp, Daniel D; Tsao, Anne S; Kim, Edward S

    2003-10-01

    Lung cancer is the leading cause of cancer-related death in the world. Tobacco is an addictive agent producing carcinogenic effects that have been extremely difficult to prevent or detect in a curable stage. Important randomized controlled studies have been published in "healthy" smokers (primary prevention); patients with early lesions, such as mucosal dysplasia/metaplasia (secondary prevention); and those who have already had definitive treatment for their first tobacco-related malignancy (tertiary prevention). To date, the results have been generally disappointing. It is critical to remember that lung cancer is usually diagnosed decades after the patient has begun or even stopped smoking. We must intervene with more effective agents or combinations of agents and do it earlier in the process of carcinogenesis. Approximately 10% of patients with lung cancer either never smoked or only were "passive" smokers due to their environment, workplace. These "never-smokers" may actually benefit from retinoids, while current smokers have not benefited from alpha-tocopherol, retinal, N-acetylcysteine, or isotretinoin. Smokers are actually harmed by the concurrent use of beta-carotene. We now have unprecedented knowledge regarding the control of cellular growth and senescence. New diagnostic tools also allow detection of smaller lesions. We must use all our knowledge of the cancer biology, new risk models, more refined intermediate markers, and modern detection tools to focus more clearly on the pathology of lung cancer and design research to ask more probing and relevant questions so we can begin to put an end to the worldwide scourge of this terrible killer. PMID:14710383

  9. Welding and Lung Cancer in a Pooled Analysis of Case-Control Studies

    PubMed Central

    Kendzia, Benjamin; Behrens, Thomas; Jöckel, Karl-Heinz; Siemiatycki, Jack; Kromhout, Hans; Vermeulen, Roel; Peters, Susan; Van Gelder, Rainer; Olsson, Ann; Brüske, Irene; Wichmann, H.-Erich; Stücker, Isabelle; Guida, Florence; Tardón, Adonina; Merletti, Franco; Mirabelli, Dario; Richiardi, Lorenzo; Pohlabeln, Hermann; Ahrens, Wolfgang; Landi, Maria Teresa; Caporaso, Neil; Consonni, Dario; Zaridze, David; Szeszenia-Dabrowska, Neonila; Lissowska, Jolanta; Gustavsson, Per; Marcus, Michael; Fabianova, Eleonora; ‘t Mannetje, Andrea; Pearce, Neil; Tse, Lap Ah; Yu, Ignatius Tak-sun; Rudnai, Peter; Bencko, Vladimir; Janout, Vladimir; Mates, Dana; Foretova, Lenka; Forastiere, Francesco; McLaughlin, John; Demers, Paul; Bueno-de-Mesquita, Bas; Boffetta, Paolo; Schüz, Joachim; Straif, Kurt; Pesch, Beate; Brüning, Thomas

    2013-01-01

    Several epidemiologic studies have indicated an increased risk of lung cancer among welders. We used the SYNERGY project database to assess welding as a risk factor for developing lung cancer. The database includes data on 15,483 male lung cancer cases and 18,388 male controls from 16 studies in Europe, Canada, China, and New Zealand conducted between 1985 and 2010. Odds ratios and 95% confidence intervals between regular or occasional welding and lung cancer were estimated, with adjustment for smoking, age, study center, and employment in other occupations associated with lung cancer risk. Overall, 568 cases and 427 controls had ever worked as welders and had an odds ratio of developing lung cancer of 1.44 (95% confidence interval: 1.25, 1.67) with the odds ratio increasing for longer duration of welding. In never and light smokers, the odds ratio was 1.96 (95% confidence interval: 1.37, 2.79). The odds ratios were somewhat higher for squamous and small cell lung cancers than for adenocarcinoma. Another 1,994 cases and 1,930 controls had ever worked in occupations with occasional welding. Work in any of these occupations was associated with some elevation of risk, though not as much as observed in regular welders. Our findings lend further support to the hypothesis that welding is associated with an increased risk of lung cancer. PMID:24052544

  10. Sleep, Mood, and Quality of Life in Patients Receiving Treatment for Lung Cancer

    PubMed Central

    Dean, Grace E.; Redeker, Nancy S.; Wang, Ya-Jung; Rogers, Ann E.; Dickerson, Suzanne S.; Steinbrenner, Lynn M.; Gooneratne, Nalaka S.

    2014-01-01

    Purpose/Objectives To distinguish relationships among subjective and objective characteristics of sleep, mood, and quality of life (QOL) in patients receiving treatment for lung cancer. Design Descriptive, correlational study. Setting Two ambulatory oncology clinics. Sample 35 patients with lung cancer. Methods The following instruments were used to measure the variables of interest: Pittsburgh Sleep Quality Index (PSQI), Hospital Anxiety and Depression Scale, Functional Assessment of Cancer Treatment–Lung (FACT-L), a sleep diary, and a motionlogger actigraph. Main Research Variables Sleep, mood, and QOL. Findings Significant differences were found between sleep diary and actigraph measures of sleep efficiency (p = 0.002), sleep latency (p = 0.014), sleep duration (p < 0.001), and wake after sleep onset (p < 0.001). Poor sleepers (PSQI score greater than 5) were significantly different from good sleepers (PSQI score of 5 or lower) on sleep diary measures of sleep efficiency and sleep latency and the FACT-L lung cancer symptom subscale, but not on mood or actigraphy sleep measures. Conclusions Although patients with lung cancer may report an overall acceptable sleep quality when assessed by a single question, those same patients may still have markedly increased sleep latencies or reduced total sleep time. The findings indicate the complexity of sleep disturbances in patients with lung cancer. Lung cancer symptoms had a stronger association with sleep than mood. Research using prospective methods will help to elucidate their clinical significance. Implications for Nursing Patients receiving treatment for lung cancer are at an increased risk for sleep disturbances and would benefit from routine sleep assessment and management. In addition, assessment and management of common symptoms may improve sleep and, ultimately, QOL. Knowledge Translation A high frequency of sleep disturbances in patients receiving treatment for lung cancer was evident, and poor sleepers had

  11. Cutaneous manifestations of lung cancer.

    PubMed

    Owen, Cindy England

    2016-06-01

    Skin findings can serve as a clue to internal disease. In this article, cutaneous manifestations of underlying lung malignancy are reviewed. Paraneoplastic dermatoses are rare, but when recognized early, can lead to early diagnosis of an underlying neoplasm. Malignancy-associated dermatoses comprise a broad group of hyperproliferative and inflammatory disorders, disorders caused by tumor production of hormonal or metabolic factors, autoimmune connective tissue diseases, among others. In this review, paraneoplastic syndromes associated with lung malignancy are discussed, including ectopic ACTH syndrome, bronchial carcinoid variant syndrome, secondary hypertrophic osteoarthropathy/digital clubbing, erythema gyratum repens, malignant acanthosis nigricans, sign of Leser-Trélat, tripe palms, hypertrichosis lanuginosa, acrokeratosis paraneoplastica, and dermatomyositis. PMID:27178690

  12. Molecular epidemiology of lung cancer and geographic variations with special reference to EGFR mutations

    PubMed Central

    2014-01-01

    Lung cancer is a leading cause of cancer-related mortality in many countries. Although recent advances in targeted therapy against driver oncogenes have significantly improved patient outcome, cure of this disease is still exceptional. Although tobacco is a known cause of lung cancer, not all smokers develop lung cancer, and conversely many patients, especially Asian female patients with lung cancer, are lifetime never-smokers. Therefore, efforts to understand the basis for different susceptibilities to lung cancer among individuals with different genetic, biologic, ethnic, and social backgrounds are important to help develop effective preventive measures. Lung cancer in never-smokers has many different characteristics to lung cancer in smokers, such as adenocarcinoma predominance and high frequency of epidermal growth factor receptor (EGFR) mutation yet low number of genetic changes. Epidemiologic studies suggest that East Asians are more susceptible to smoking-unrelated lung cancer but less susceptible to smoking-related lung cancer compared with Caucasians. Mutations in the EGFR gene are more common in Asian females and never-smokers. Our case-control study suggests that EGFR mutation occurs independent of smoking, and that the apparent low frequency of EGFR mutations in smokers may be the result of dilution by smoking-related lung cancer. The frequencies of three EGFR gene polymorphisms associated with increased protein expression are significantly different between East Asians and Caucasians, favoring lower protein expression in East Asians. Although these may be associated with preferred expression of the EGFR mutant allele, it is difficult to explain the frequent EGFR mutation in Asian patients. Genome wide association studies (GWAS) revealed several loci related to lung cancer susceptibility. In the future, GWAS may identify loci that are specifically related to EGFR-targeted carcinogenesis, leading to identification of carcinogens that induce EGFR

  13. Molecular epidemiology of lung cancer and geographic variations with special reference to EGFR mutations.

    PubMed

    Mitsudomi, Tetsuya

    2014-08-01

    Lung cancer is a leading cause of cancer-related mortality in many countries. Although recent advances in targeted therapy against driver oncogenes have significantly improved patient outcome, cure of this disease is still exceptional. Although tobacco is a known cause of lung cancer, not all smokers develop lung cancer, and conversely many patients, especially Asian female patients with lung cancer, are lifetime never-smokers. Therefore, efforts to understand the basis for different susceptibilities to lung cancer among individuals with different genetic, biologic, ethnic, and social backgrounds are important to help develop effective preventive measures. Lung cancer in never-smokers has many different characteristics to lung cancer in smokers, such as adenocarcinoma predominance and high frequency of epidermal growth factor receptor (EGFR) mutation yet low number of genetic changes. Epidemiologic studies suggest that East Asians are more susceptible to smoking-unrelated lung cancer but less susceptible to smoking-related lung cancer compared with Caucasians. Mutations in the EGFR gene are more common in Asian females and never-smokers. Our case-control study suggests that EGFR mutation occurs independent of smoking, and that the apparent low frequency of EGFR mutations in smokers may be the result of dilution by smoking-related lung cancer. The frequencies of three EGFR gene polymorphisms associated with increased protein expression are significantly different between East Asians and Caucasians, favoring lower protein expression in East Asians. Although these may be associated with preferred expression of the EGFR mutant allele, it is difficult to explain the frequent EGFR mutation in Asian patients. Genome wide association studies (GWAS) revealed several loci related to lung cancer susceptibility. In the future, GWAS may identify loci that are specifically related to EGFR-targeted carcinogenesis, leading to identification of carcinogens that induce EGFR

  14. Multimodal imaging of lung cancer and its microenvironment (Conference Presentation)

    NASA Astrophysics Data System (ADS)

    Hariri, Lida P.; Niederst, Matthew J.; Mulvey, Hillary; Adams, David C.; Hu, Haichuan; Chico Calero, Isabel; Szabari, Margit V.; Vakoc, Benjamin J.; Hasan, Tayyaba; Bouma, Brett E.; Engelman, Jeffrey A.; Suter, Melissa J.

    2016-03-01

    Despite significant advances in targeted therapies for lung cancer, nearly all patients develop drug resistance within 6-12 months and prognosis remains poor. Developing drug resistance is a progressive process that involves tumor cells and their microenvironment. We hypothesize that microenvironment factors alter tumor growth and response to targeted therapy. We conducted in vitro studies in human EGFR-mutant lung carcinoma cells, and demonstrated that factors secreted from lung fibroblasts results in increased tumor cell survival during targeted therapy with EGFR inhibitor, gefitinib. We also demonstrated that increased environment stiffness results in increased tumor survival during gefitinib therapy. In order to test our hypothesis in vivo, we developed a multimodal optical imaging protocol for preclinical intravital imaging in mouse models to assess tumor and its microenvironment over time. We have successfully conducted multimodal imaging of dorsal skinfold chamber (DSC) window mice implanted with GFP-labeled human EGFR mutant lung carcinoma cells and visualized changes in tumor development and microenvironment facets over time. Multimodal imaging included structural OCT to assess tumor viability and necrosis, polarization-sensitive OCT to measure tissue birefringence for collagen/fibroblast detection, and Doppler OCT to assess tumor vasculature. Confocal imaging was also performed for high-resolution visualization of EGFR-mutant lung cancer cells labeled with GFP, and was coregistered with OCT. Our results demonstrated that stromal support and vascular growth are essential to tumor progression. Multimodal imaging is a useful tool to assess tumor and its microenvironment over time.

  15. The Utility of Exercise Testing in Patients with Lung Cancer.

    PubMed

    Ha, Duc; Mazzone, Peter J; Ries, Andrew L; Malhotra, Atul; Fuster, Mark

    2016-09-01

    The harm associated with lung cancer treatment include perioperative morbidity and mortality and therapy-induced toxicities in various organs, including the heart and lungs. Optimal treatment therefore entails a need for risk assessment to weigh the probabilities of benefits versus harm. Exercise testing offers an opportunity to evaluate a patient's physical fitness/exercise capacity objectively. In lung cancer, it is most often used to risk-stratify patients undergoing evaluation for lung cancer resection. In recent years, its use outside this context has been described, including in nonsurgical candidates and lung cancer survivors. In this article we review the physiology of exercise testing and lung cancer. Then, we assess the utility of exercise testing in patients with lung cancer in four contexts (preoperative evaluation for lung cancer resection, after lung cancer resection, lung cancer prognosis, and assessment of efficiency of exercise training programs) after systematically identifying original studies involving the most common forms of exercise tests in this patient population: laboratory cardiopulmonary exercise testing and simple field testing with the 6-minute walk test, shuttle walk test, and/or stair-climbing test. Lastly, we propose a conceptual framework for risk assessment of patients with lung cancer who are being considered for therapy and identify areas for further studies in this patient population. PMID:27156441

  16. Mucins in lung cancer: diagnostic, prognostic, and therapeutic implications.

    PubMed

    Lakshmanan, Imayavaramban; Ponnusamy, Moorthy P; Macha, Muzafar A; Haridas, Dhanya; Majhi, Prabin Dhangada; Kaur, Sukhwinder; Jain, Maneesh; Batra, Surinder K; Ganti, Apar Kishor

    2015-01-01

    Aberrant expression of mucins is associated with cancer development and metastasis. An overexpression of few mucins contributes to oncogenesis by enhancing cancer cell growth and providing constitutive survival signals. This review focuses on the importance of mucins both in the normal bronchial epithelial cells and the malignant tumors of the lung and their contribution in the diagnosis and prognosis of lung cancer patients. During lung cancer progression, mucins either alone or through their interaction with many receptor tyrosine kinases mediate cell signals for growth and survival of cancer cells. Also, stage-specific expression of certain mucins, like MUC1, is associated with poor prognosis from lung cancer. Thus, mucins are emerging as attractive targets for developing novel therapeutic approaches for lung cancer. Several strategies targeting mucin expression and function are currently being investigated to control lung cancer progression. PMID:25319180

  17. Cancer stem cells: progress and challenges in lung cancer

    PubMed Central

    Templeton, Amanda K.; Miyamoto, Shinya; Babu, Anish; Munshi, Anupama

    2014-01-01

    The identification of a subpopulation of tumor cells with stem cell-like characteristics first in hematological malignancies and later in solid tumors has emerged into a novel field of cancer research. It has been proposed that this aberrant population of cells now called “cancer stem cells” (CSCs) drives tumor initiation, progression, metastasis, recurrence, and drug resistance. CSCs have been shown to have the capacity of self-renewal and multipotency. Adopting strategies from the field of stem cell research has aided in identification, localization, and targeting of CSCs in many tumors. Despite the huge progress in other solid tumors such as brain, breast, and colon cancers no substantial advancements have been made in lung cancer. This is most likely due to the current rudimentary understanding of lung stem cell hierarchy and heterogeneous nature of lung disease. In this review, we will discuss the most recent findings related to identification of normal lung stem cells and CSCs, pathways involved in regulating the development of CSCs, and the importance of the stem cell niche in development and maintenance of CSCs. Additionally, we will examine the development and feasibility of novel CSC-targeted therapeutic strategies aimed at eradicating lung CSCs.

  18. Anti-survivin antibody responses in lung cancer.

    PubMed

    Karanikas, Vaios; Khalil, Sanaa; Kerenidi, Theodora; Gourgoulianis, Konstantinos I; Germenis, Anastasios E

    2009-09-18

    Existing evidence regarding spontaneous anti-survivin humoral responses in lung cancer is inconclusive. Moreover, despite that cancer cell death elicited by radiotherapy and some chemotherapeutic agents seems to be immunogenic, information about the possible effect of treatment on these responses, is lacking. Serum samples from 33 small cell lung cancer (SCLC) and 117 non-small cell lung cancer (NSCLC) patients upon diagnosis, and from 100 controls, were tested by ELISA for anti-survivin antibodies. Cutoff was set to the mean+2SD of controls. 7.7% of NSCLC, none of the SCLC patients and 2% of the controls appeared with elevated antibody levels (OR 3.6, 95% CI 0.7-17.3 for NSCLC, OR 0.6, 95% CI 0.03-12.6 for SCLC). Measurement of antibodies in 76 NSCLC patients post therapies and during their follow-up, revealed that in 12 NSCLC patients the antibody levels increased up to 2-38 times, and in seven others, they decreased by 2-8 times. No significant correlation was uncovered between either the antibody levels upon diagnosis or their changes post therapies and during follow-up, and any clinicopathological parameter, their response to therapy and survival. Survivin does not induce considerable humoral responses in lung cancer. Potentially, however, strong anti-survivin antibody responses can be elicited during the post therapy and follow-up of the patients, whose clinical significance remains to be elucidated. These findings, together with our previous data concerning survivin expression and the related cytolytic T cell responses in lung cancer, signify a high tolerogenic potential of this tumor-associated antigen. PMID:19380192

  19. Radiation Therapy for Lung Cancer

    MedlinePlus

    ... whether surgery will be helpful for you EXTERNAL BEAM RADIATION THER APY External beam radiation therapy is the safe delivery of high- ... your cancer. A linear accelerator focuses the radiation beam to a precise location in your body for ...

  20. Smog May Shorten Lives of Lung Cancer Patients

    MedlinePlus

    ... 5, 2016 FRIDAY, Aug. 5, 2016 (HealthDay News) -- Air pollution may shorten the lives of lung cancer patients, ... the International Agency for Research on Cancer classifies air pollution as a cancer-causing agent. "This study, along ...

  1. Predicted reduction in lung cancer risk following cessation of smoking and radon exposure

    SciTech Connect

    Ennever, F.K. )

    1990-03-01

    Recently there has been considerable public and regulatory concern that radon, produced by the decay of naturally occurring uranium, can accumulate in homes, offices, and schools at levels that may substantially increase the risk of lung cancer. The major cause of lung cancer is smoking, and radon appears to interact multiplicatively with smoking in causing lung cancer. Thus, the most effective way to reduce the increased risk of lung cancer resulting from radon exposure is to cease smoking. In this paper, a model for the risks associated with radon exposure that was developed by a committee of the National Academy of Sciences is used to calculate the benefits, in terms of reduction in lifetime risk of lung cancer, of ceasing to smoke, ceasing radon exposure, or ceasing both. Ceasing to smoke is considerably more beneficial than ceasing radon exposure, and thus policymakers addressing the health effects of radon should place priority on encouraging individuals to stop smoking.

  2. Clinical significance of serum adipokines levels in lung cancer.

    PubMed

    Kerenidi, Theodora; Lada, Martha; Tsaroucha, Agori; Georgoulias, Panagiotis; Mystridou, Parthena; Gourgoulianis, Konstantinos I

    2013-06-01

    Adipokines have a significant effect on metabolism, immunoinflammatory responses as well as on carcinogenesis; therefore, we aimed at evaluating their potential predictive and prognostic significance in lung cancer. Eighty patients--mean age 62.9 ± 9.2 years--with previously untreated lung cancer (61 NSCLC and 19 SCLC) of all stages and 40 healthy individuals were enrolled in this study. Serum levels of leptin, adiponectin and ghrelin were measured using human Radioimmunoassay kits. Serum leptin levels in lung cancer patients were lower compared to control (p < 0.0001), while adiponectin and ghrelin levels were significantly increased in patients (p = 0.0003 and p = 0.0043, respectively). Additionally, the leptin/adiponectin ratio was significantly lower in the patients group compared to controls (p < 0.0001]. There was no association between serum levels of adipokines and any of the patient clinicopathological characteristics or response to therapy. Nevertheless, patients with lower values of serum leptin had shorter overall survival (p = 0.014), whereas multivariate analysis revealed leptin levels as an independent prognostic factor for survival (p = 0.024, HR 0.452, CI 95 % 0.232-0.899). These results suggest that adipokines may play a role in the pathogenesis of lung cancer, while leptin serum levels might provide useful prognostic information. PMID:23430445

  3. Constitutional CHEK2 mutations are associated with a decreased risk of lung and laryngeal cancers.

    PubMed

    Cybulski, Cezary; Masojc, Bartlomiej; Oszutowska, Dorota; Jaworowska, Ewa; Grodzki, Tomasz; Waloszczyk, Piotr; Serwatowski, Piotr; Pankowski, Juliusz; Huzarski, Tomasz; Byrski, Tomasz; Górski, Bohdan; Jakubowska, Anna; Debniak, Tadeusz; Wokolorczyk, Dominika; Gronwald, Jacek; Tarnowska, Czeslawa; Serrano-Fernández, Pablo; Lubinski, Jan; Narod, Steven A

    2008-04-01

    Mutations in the CHEK2 gene have been associated with increased risks of breast, prostate and colon cancer. In contrast, a previous report suggests that individuals with the I157T missense variant of the CHEK2 gene might be at decreased risk of lung cancer and upper aero-digestive cancers. To confirm this hypothesis, we genotyped 895 cases of lung cancer, 430 cases of laryngeal cancer and 6391 controls from Poland for four founder alleles in the CHEK2 gene, each of which has been associated with an increased risk of cancer at several sites. The presence of a CHEK2 mutation was protective against both lung cancer [odds ratio (OR) = 0.3; 95% confidence interval (CI) 0.2-0.5; P = 3 x 10(-8)] and laryngeal cancer (OR = 0.6; 95% CI 0.3-0.99; P = 0.05). The basis of the protective effect is unknown, but may relate to the reduced viability of lung cancer cells with a CHEK2 mutation. Lung cancers frequently possess other defects in genes in the DNA damage response pathway (e.g. p53 mutations) and have a high level of genotoxic DNA damage induced by tobacco smoke. We speculate that lung cancer cells with impaired CHEK2 function undergo increased rates of cell death. PMID:18281249

  4. Palliative care in patients with lung cancer

    PubMed Central

    Farbicka, Paulina

    2013-01-01

    Lung cancer accounts for 12% of all cancers and has the highest annual rate of mortality in men and women. The overall aim is cure or prolongation of life without evidence of disease. Almost 60% of patients at the moment of diagnosis are not eligible for radical treatment. Therefore soothing and supportive treatment is the only treatment of choice. Patients with lung cancer who have symptoms of dyspnea, chronic cough, severe pain, exhaustion and cachexia syndrome, fear and depression and significantly reduced physical and intellectual activities are qualified for inpatient or home palliative care. Knowledge about various methods used in palliative treatment allows one to alleviate symptoms that occur in an advanced stage of disease with an expected short survival period. Methods of oncological treatment that are often used in patients with advanced lung cancer include radiotherapy and chemotherapy. Drawing attention to the earlier implementation of palliative care is an objective of research carried out during recent years. Advances in surgical and conservative treatment of these patients have contributed to better outcomes and longer survival time. PMID:24596508

  5. Uranium miner lung cancer study. Final report

    SciTech Connect

    Saccomanno, G.

    1986-06-01

    This study on uranium miners was started in 1957 and extended through June 30, 1986. It consisted of the routine screening of sputum from uranium miners of the Colorado Plateau, and collection of surgical and autopsy material from uranium miners who developed lung cancer. The projects resulted in: (1) Proof, for the first time, that cancer takes from 10 to 15 years to develop from the maximum accumulated carcinogenic insult and can be demonstrated through progressive cellular changes of the bronchial tree; (2) Development of a method for preserving, concentrating, and processing sputum samples. This is known as the Saccomanno Technique, and is used worldwide in diagnosing lung cancer; (3) Publication of the 1st and 2nd editions of a full-color textbook entitled ''Diagnostic Pulmonary Cytology;'' (4) Presentation of conclusive data on the effects of cigarette smoking and alpha progeny radiation on uranium miners, and information on safe radiation exposure levels; (5) Development of a brush-wash tube for collecting, concentrating, and preparing bronchial brushings and washings; (6) Development of cytological criteria which has improved sensitivity from 30% to about 60%; (7) Development of criteria for cytologic identification of carcinoma in situ, making it possible to diagnose lung cancer before it can be detected on chest x-ray.

  6. Lung cancer: Current status and prospects for the future

    SciTech Connect

    Mountain, C.F.; Carr, D.T.

    1986-01-01

    This book contains 32 papers. Some of the titles are: Activation of cellular ras genes in human neoplasms; The valve of definitive radiation therapy of unresectable squamous cell carcinoma, large cell carcinoma, and adenocarcinoma of the lung; Current concepts of chemotherapy and radiotherapy for small cell lung cancer, and Current status of immunotherapy for lung cancer.

  7. Testing lung cancer drugs and therapies in mice

    Cancer.gov

    National Cancer Institute (NCI) investigators have designed a genetically engineered mouse for use in the study of human lung squamous cell carcinoma (SCC). SCC is a type of non-small cell lung carcinoma, one of the most common types of lung cancer, with

  8. Lung cancer in never smokers: change of a mindset in the molecular era.

    PubMed

    Lee, Young Joo; Kim, Joo-Hang; Kim, Se Kyu; Ha, Sang-Jun; Mok, Tony S; Mitsudomi, Tetsuya; Cho, Byoung Chul

    2011-04-01

    Lung cancer is a leading cause of cancer-related mortality across the world. Although the majority of lung cancer is attributed to tobacco smoke, approximately 25% of lung cancers worldwide occur in lifelong never smokers. Over the past decades, the bulk of research on this disease suggested that several genetic, environmental, hormonal, and viral factors might increase the risk of lung cancer among never smokers. However, there has been no dominant risk factor whose significance has been validated across racial and ethnic groups. However, this subset of lung cancers has received renewed attention due to the introduction of the epidermal growth factor receptor-tyrosine kinase (EGFR-TK) inhibitors showing the dramatic therapeutic response on selected patients with activating EGFR mutations which occur more commonly in never smokers. The treatment strategy blocking EGFR pathway in EGFR-mutant lung cancer represents a remarkable example of molecular targeted therapies which completely repress tumor by inhibition of driving oncogenes. More recently, a surprising positive effect of an ALK inhibitor on EML4-ALK-positive lung cancer has been suggested that lung cancer in never smokers is likely to be an assemblage of molecularly defined subsets which would be a good candidate for personalized diagnostic and therapeutic approaches. PMID:21272954

  9. Portable stove use is associated with lower lung cancer mortality risk in lifetime smoky coal users

    PubMed Central

    Hosgood, H D; Chapman, R; Shen, M; Blair, A; Chen, E; Zheng, T; Lee, K-M; He, X; Lan, Q

    2008-01-01

    Domestic fuel combustion from cooking and heating, to which about 3 billion people worldwide are exposed, is associated with increased lung cancer risk. Lung cancer incidence in Xuanwei is the highest in China, and the attributable risk of lung cancer from unvented smoky coal burning is greater than 90%. To evaluate any lung cancer mortality reduction after changing from unvented stoves to portable stoves, we used lifetime smoky coal users in a retrospective cohort of all farmers born during 1917–1951 and residing in Xuanwei in 1976. Of the 42 422 enrolled farmers, 4054 lifetime smoky coal users changed to portable stoves, 4364 did not change, and 1074 died of lung cancer. Lung cancer morality associated with stove change was assessed by product-limit survival curves and multivariate Cox regression models. Both men (P<0.0001) and women (P<0.0001) who changed to portable stoves had a significantly increased probability of survival compared with those who did not change. Portable stoves were associated with decreased risk of lung cancer mortality in male participants (hazard ratio (HR)=0.62, 95% confidence interval (CI)=0.46–0.82) and female participants (HR=0.41, 95% CI=0.29–0.57). Portable stove use is associated with reduced lung cancer mortality risk, highlighting a cost-effective intervention that could substantially benefit health in developing countries. PMID:19034286

  10. Epidermal Growth Factor Receptor Mutation Enhances Expression of Cadherin-5 in Lung Cancer Cells

    PubMed Central

    Hung, Ming-Szu; Chen, I-Chuan; Lung, Jr-Hau; Lin, Paul-Yann; Li, Ya-Chin; Tsai, Ying-Huang

    2016-01-01

    Epidermal growth factor receptor (EGFR) activation has been shown to play a critical role in tumor angiogenesis. In this study, we investigate the correlation between EGFR mutations and cadherin-5 (CDH5), which is an angiogenic factor, in lung cancer cells. Increased expression CDH5 is observed in lung cancer cells with EGFR mutations. Stable lung cancer cell lines expressing mutant (exon 19 deletion E746-A750, and exon 21 missense mutation L858R) and wild type EGFR genes are established. A significantly higher expression of CDH5 is observed in exon 19 deletion stable lung cancer cells and mouse xenografts. Further studies show that expression of CDH5 is decreased after the inhibition of EGFR and downstream Akt pathways in lung cancer cells with EGFR mutation. In addition, mutant EGFR genes potentiates angiogenesis in lung cancer cells, which is inhibited by CDH5 siRNA, and potentiates migration and invasion in lung cancer cells. Our study shows that mutant EGFR genes are associated with overexpression of CDH5 through increased phosphorylation of EGFR and downstream Akt pathways. Our result may provide an insight into the association of mutant EGFR and CDH5 expression in lung cancer and aid further development of target therapy for NSCLC in the future. PMID:27362942

  11. Pharmacological Modulation of Cytotoxicity and Cellular Uptake of Anti-cancer Drugs by PDE5 Inhibitors in Lung Cancer Cells

    PubMed Central

    LI, QING; SHU, YAN

    2013-01-01

    Purpose Previous research has led to the recognition of a cGMP signaling pathway governing drug transport. This study is to investigate whether inhibitors of phosphodiesterase type 5 (PDE5), which increase intracellular cGMP levels, modulate the cytotoxicity and uptake of anti-cancer drugs in cancer cells. Methods The experiments were conducted with and without PDE5 inhibitors: dipyridamole, vardenafil, and/or sildenafil. The cytotoxicity of doxorubicin, cisplatin and oxaliplatin was determined in multiple cancer cell lines derived from different tissues. The cellular uptake of structurally diverse compounds was further examined in lung cancer cells with and without various endocytotic inhibitors. The tumor accumulation and the anti-tumor effect of trastuzumab were examined in a lung cancer xenograft mouse model. Results Dipyridamole could modulate the cytotoxicity of doxorubicin, cisplatin, and oxaliplatin in cancer cells. Particularly, PDE5 inhibitors increased cellular uptake of structurally diverse compounds into lung cancer cells both in vitro and in vivo. The effect of vardenafil on drug uptake could be blocked by endocytotic inhibitors. The growth of lung cancer xenograft in nude mice was significantly suppressed by addition of vardenafil to trastuzumab treatment. Conclusion PDE5 inhibitors may increase the efficacy of anti-cancer drugs by increasing endocytosis-mediated cellular drug uptake, and thus serve as adjuvant therapy for certain cancers such as lung cancer. PMID:23884568

  12. Comparing histone deacetylase inhibitor responses in genetically engineered mouse lung cancer models and a window of opportunity trial in patients with lung cancer.

    PubMed

    Ma, Tian; Galimberti, Fabrizio; Erkmen, Cherie P; Memoli, Vincent; Chinyengetere, Fadzai; Sempere, Lorenzo; Beumer, Jan H; Anyang, Bean N; Nugent, William; Johnstone, David; Tsongalis, Gregory J; Kurie, Jonathan M; Li, Hua; Direnzo, James; Guo, Yongli; Freemantle, Sarah J; Dragnev, Konstantin H; Dmitrovsky, Ethan

    2013-08-01

    Histone deacetylase inhibitor (HDACi; vorinostat) responses were studied in murine and human lung cancer cell lines and genetically engineered mouse lung cancer models. Findings were compared with a window of opportunity trial in aerodigestive tract cancers. In human (HOP62, H522, and H23) and murine transgenic (ED-1, ED-2, LKR-13, and 393P, driven, respectively, by cyclin E, degradation-resistant cyclin E, KRAS, or KRAS/p53) lung cancer cell lines, vorinostat reduced growth, cyclin D1, and cyclin E levels, but induced p27, histone acetylation, and apoptosis. Other biomarkers also changed. Findings from transgenic murine lung cancer models were integrated with those from a window of opportunity trial that measured vorinostat pharmacodynamic responses in pre- versus posttreatment tumor biopsies. Vorinostat repressed cyclin D1 and cyclin E expression in murine transgenic lung cancers and significantly reduced lung cancers in syngeneic mice. Vorinostat also reduced cyclin D1 and cyclin E expression, but increased p27 levels in post- versus pretreatment human lung cancer biopsies. Notably, necrotic and inflammatory responses appeared in posttreatment biopsies. These depended on intratumoral HDACi levels. Therefore, HDACi treatments of murine genetically engineered lung cancer models exert similar responses (growth inhibition and changes in gene expression) as observed in lung cancer cell lines. Moreover, enhanced pharmacodynamic responses occurred in the window of opportunity trial, providing additional markers of response that can be evaluated in subsequent HDACi trials. Thus, combining murine and human HDACi trials is a strategy to translate preclinical HDACi treatment outcomes into the clinic. This study uncovered clinically tractable mechanisms to engage in future HDACi trials. PMID:23686769

  13. Targeted therapies in small cell lung cancer: a review

    PubMed Central

    Abidin, Aidalena Z.; Garassino, Marina C.; Califano, Raffaele; Harle, Amelie; Blackhall, Fiona

    2010-01-01

    Small cell lung cancer (SCLC) is an aggressive form of lung cancer that is characterized by a rapid doubling time, early onset of dissemination and high sensitivity to chemotherapy. Despite the potential for cure in patients with limited disease with concurrent chemoradiation and an initial good response to chemotherapy in extensive disease, there is a high chance of disease relapse with an overall poor median survival for both stages. With increasing translational research and a better understanding of the molecular basis of cancer, a number of molecular targets have been identified in various preclinical studies. This review summarizes potentially viable targets and new agents that have been developed and employed in recent, ongoing and future clinical trials to attempt to improve clinical outcomes in this disease. PMID:21789124

  14. Stereotactic Body Radiation Therapy in Treating Patients With Metastatic Breast Cancer, Non-small Cell Lung Cancer, or Prostate Cancer

    ClinicalTrials.gov

    2016-06-17

    Male Breast Carcinoma; Prostate Adenocarcinoma; Recurrent Breast Carcinoma; Recurrent Non-Small Cell Lung Carcinoma; Recurrent Prostate Carcinoma; Stage IV Breast Cancer; Stage IV Non-Small Cell Lung Cancer; Stage IV Prostate Cancer

  15. EYA4 is inactivated biallelically at a high frequency in sporadic lung cancer and is associated with familial lung cancer risk.

    PubMed

    Wilson, I M; Vucic, E A; Enfield, K S S; Thu, K L; Zhang, Y A; Chari, R; Lockwood, W W; Radulovich, N; Starczynowski, D T; Banáth, J P; Zhang, M; Pusic, A; Fuller, M; Lonergan, K M; Rowbotham, D; Yee, J; English, J C; Buys, T P H; Selamat, S A; Laird-Offringa, I A; Liu, P; Anderson, M; You, M; Tsao, M S; Brown, C J; Bennewith, K L; MacAulay, C E; Karsan, A; Gazdar, A F; Lam, S; Lam, W L

    2014-09-01

    In an effort to identify novel biallelically inactivated tumor suppressor genes (TSGs) in sporadic invasive and preinvasive non-small-cell lung cancer (NSCLC) genomes, we applied a comprehensive integrated multiple 'omics' approach to investigate patient-matched, paired NSCLC tumor and non-malignant parenchymal tissues. By surveying lung tumor genomes for genes concomitantly inactivated within individual tumors by multiple mechanisms, and by the frequency of disruption in tumors across multiple cohorts, we have identified a putative lung cancer TSG, Eyes Absent 4 (EYA4). EYA4 is frequently and concomitantly deleted, hypermethylated and underexpressed in multiple independent lung tumor data sets, in both major NSCLC subtypes and in the earliest stages of lung cancer. We found that decreased EYA4 expression is not only associated with poor survival in sporadic lung cancers but also that EYA4 single-nucleotide polymorphisms are associated with increased familial cancer risk, consistent with EYA4s proximity to the previously reported lung cancer susceptibility locus on 6q. Functionally, we found that EYA4 displays TSG-like properties with a role in modulating apoptosis and DNA repair. Cross-examination of EYA4 expression across multiple tumor types suggests a cell-type-specific tumorigenic role for EYA4, consistent with a tumor suppressor function in cancers of epithelial origin. This work shows a clear role for EYA4 as a putative TSG in NSCLC. PMID:24096489

  16. EYA4 is inactivated biallelically at a high frequency in sporadic lung cancer and is associated with familial lung cancer risk

    PubMed Central

    Wilson, Ian M.; Vucic, Emily A.; Enfield, Katey S.S.; Thu, Kelsie L.; Zhang, Yu-An; Chari, Raj; Lockwood, William W.; Radulovich, Niki; Starczynowski, Daniel T.; Banáth, Judit P.; Zhang, May; Pusic, Andrea; Fuller, Megan; Lonergan, Kim M.; Rowbotham, David; Yee, John; English, John C.; Buys, Timon P.H.; Selamat, Suhaida A.; Laird-Offringa, Ite A.; Liu, Pengyuan; Anderson, Marshall; You, Ming; Tsao, Ming-Sound; Brown, Carolyn J.; Bennewith, Kevin L.; MacAulay, Calum E.; Karsan, Aly; Gazdar, Adi F.; Lam, Stephen; Lam, Wan L.

    2015-01-01

    In an effort to identify novel biallelically inactivated tumor suppressor genes (TSG) in sporadic invasive and pre-invasive non-small cell lung cancer (NSCLC) genomes, we applied a comprehensive integrated multi-‘omics approach to investigate patient matched, paired NSCLC tumor and non-malignant parenchymal tissues. By surveying lung tumor genomes for genes concomitantly inactivated within individual tumors by multiple mechanisms, and by the frequency of disruption in tumors across multiple cohorts, we have identified a putative lung cancer TSG, Eyes Absent 4 (EYA4). EYA4 is frequently and concomitantly deleted, hypermethylated and underexpressed in multiple independent lung tumor data sets, in both major NSCLC subtypes, and in the earliest stages of lung cancer. We find not only that decreased EYA4 expression is associated with poor survival in sporadic lung cancers, but EYA4 SNPs are associated with increased familial cancer risk, consistent with EYA4’s proximity to the previously reported lung cancer susceptibility locus on 6q. Functionally, we find that EYA4 displays TSG-like properties with a role in modulating apoptosis and DNA repair. Cross examination of EYA4 expression across multiple tumor types suggests a cell type-specific tumorigenic role for EYA4, consistent with a tumor suppressor function in cancers of epithelial origin. This work shows a clear role for EYA4 as a putative TSG in NSCLC. PMID:24096489

  17. DIETARY AGENTS FOR PREVENTION AND TREATMENT OF LUNG CANCER

    PubMed Central

    Khan, Naghma; Mukhtar, Hasan

    2015-01-01

    Lung cancer is a prominent cause of cancer-associated mortality worldwide. The main reason for high mortality due to lung cancer is attributable to the fact that the diagnosis is generally made when it has spread beyond a curable stage and cannot be treated surgically or with radiation therapy. Therefore, new approaches like dietary modifications could be extremely useful in reducing lung cancer incidences. Several fruits and vegetables offer a variety of bioactive compounds to afford protection against several diseases, including lung cancer. A number of research studies involving dietary agents provide strong evidence for their role in the prevention and treatment of lung cancer, and have identified their molecular mechanisms of action and potential targets. In this review article, we summarize data from in-vitro and in-vivo studies and where available, in clinical trials, on the effects of some of the most promising dietary agents against lung cancer. PMID:25644088

  18. Recent developments in the epidemiology of lung cancer

    SciTech Connect

    Kabat, G.C. )

    1993-03-01

    Lung cancer is currently the leading cause of cancer death in the United States and also the most common tumor worldwide. Changes in the distribution of histologic types over the past two decades in the United States, as well as high rates of lung cancer in certain subpopulations, require explanation. While cigarette smoking and specific occupational exposures are firmly established as important risk factors for lung cancer, recent work provides evidence that other factors may play a role either as independent risk factors or as modifiers of the effect of smoking. This paper reviews the epidemiology of lung cancer, with an emphasis on developments in the past decade. 79 refs.

  19. Health-related quality of life questionnaires in lung cancer trials: a systematic literature review

    PubMed Central

    2013-01-01

    Background Lung cancer is one of the leading causes of cancer deaths. Treatment goals are the relief of symptoms and the increase of overall survival. With the rising number of treatment alternatives, the need for comparable assessments of health-related quality of life (HRQoL) parameters grows. The aim of this paper was to identify and describe measurement instruments applied in lung cancer patients under drug therapy. Methods We conducted a systematic literature review at the beginning of 2011 using the electronic database Pubmed. Results A total of 43 studies were included in the review. About 17 different measurement instruments were identified, including 5 generic, 5 cancer-specific, 4 lung cancer-specific and 3 symptom-specific questionnaires. In 29 studies at least 2 instruments were used. In most cases these were cancer and lung cancer-specific ones. The most frequently used instruments are the EORTC QLQ-C30 and its lung cancer modules LC13 or LC17. Only 5 studies combined (lung) cancer-specific questionnaires with generic instruments. Conclusions The EORTC-C30 and EORTC-LC13 are the most frequently used health-related quality of life measurement instruments in pharmacological lung cancer trials. PMID:23680096

  20. Ciprofloxacin mediates cancer stem cell phenotypes in lung cancer cells through caveolin-1-dependent mechanism.

    PubMed

    Phiboonchaiyanan, Preeyaporn Plaimee; Kiratipaiboon, Chayanin; Chanvorachote, Pithi

    2016-04-25

    Cancer stem cells (CSCs), a subpopulation of cancer cells with high aggressive behaviors, have been identified in many types of cancer including lung cancer as one of the key mediators driving cancer progression and metastasis. Here, we have reported for the first time that ciprofloxacin (CIP), a widely used anti-microbial drug, has a potentiating effect on CSC-like features in human non-small cell lung cancer (NSCLC) cells. CIP treatment promoted CSC-like phenotypes, including enhanced anchorage-independent growth and spheroid formation. The known lung CSC markers: CD133, CD44, ABCG2 and ALDH1A1 were found to be significantly increased, while the factors involving in epithelial to mesenchymal transition (EMT): Slug and Snail, were depleted. Also, self-renewal transcription factors Oct-4 and Nanog were found to be up-regulated in CIP-treated cells. The treatment of CIP on CSC-rich populations obtained from secondary spheroids resulted in the further increase of CSC markers. In addition, we have proven that the mechanistic insight of the CIP induced stemness is through Caveolin-1 (Cav-1)-dependent mechanism. The specific suppression of Cav-1 by stably transfected Cav-1 shRNA plasmid dramatically reduced the effect of CIP on CSC markers as well as the CIP-induced spheroid formation ability. Cav-1 was shown to activate protein kinase B (Akt) and extracellular signal-regulated kinase (ERK) pathways in CSC-rich population; however, such an effect was rarely found in the main lung cancer cells population. These findings reveal a novel effect of CIP in positively regulating CSCs in lung cancer cells via the activation of Cav-1, Akt and ERK, and may provoke the awareness of appropriate therapeutic strategy in cancer patients. PMID:26947806

  1. Effects of Cancer-Associated EPHA3 Mutations on Lung Cancer

    PubMed Central

    2012-01-01

    Background Cancer genome sequencing efforts recently identified EPHA3, which encodes the EPHA3 receptor tyrosine kinase, as one of the most frequently mutated genes in lung cancer. Although receptor tyrosine kinase mutations often drive oncogenic conversion and tumorigenesis, the oncogenic potential of the EPHA3 mutations in lung cancer remains unknown. Methods We used immunoprecipitation, western blotting, and kinase assays to determine the activity and signaling of mutant EPHA3 receptors. A mutation-associated gene signature was generated from one large dataset, mapped to another training dataset with survival information, and tested in a third independent dataset. EPHA3 expression levels were determined by quantitative reverse transcription-polymerase chain reaction in paired normal-tumor clinical specimens and by immunohistochemistry in human lung cancer tissue microarrays. We assessed tumor growth in vivo using A549 and H1299 human lung carcinoma cell xenografts in mice (n = 7–8 mice per group). Tumor cell proliferation was measured by bromodeoxyuridine incorporation and apoptosis by multiple assays. All P values are from two-sided tests. Results At least two cancer-associated EPHA3 somatic mutations functioned as dominant inhibitors of the normal (wild type) EPHA3 protein. An EPHA3 mutation–associated gene signature that was associated with poor patient survival was identified. Moreover, EPHA3 gene copy numbers and/or expression levels were decreased in tumors from large cohorts of patients with lung cancer (eg, the gene was deleted in 157 of 371 [42%] primary lung adenocarcinomas). Reexpression of wild-type EPHA3 in human lung cancer lines increased apoptosis by suppression of AKT activation in vitro and inhibited the growth of tumor xenografts (eg, for H1299 cells, mean tumor volume with wild-type EPHA3 = 437.4mm3 vs control = 774.7mm3, P < .001). Tumor-suppressive effects of wild-type EPHA3 could be overridden in trans by dominant negative EPHA3

  2. Lung Cancer Ablation: Technologies and Techniques

    PubMed Central

    Alexander, Erica S.; Dupuy, Damian E.

    2013-01-01

    The incidence of lung cancers in 2012 is estimated to reach 226,160 new cases, with only a third of patients suitable surgical candidates. Tumor ablation has emerged as an important and efficacious treatment option for nonsurgical lung cancer patients. This localized minimally invasive therapy is best suited for small oligonodular lesions or favorably located metastatic tumors. Radiofrequency ablation has been in use for over a decade, and newer modalities including microwave ablation, cryoablation, and irreversible electroporation have emerged as additional treatment options for patients. Ablation therapies can offer patients and clinicians a repeatable and effective therapy for palliation and, in some cases, cure of thoracic malignancies. This article discusses the available technologies and techniques available for tumor ablation of thoracic malignancies including patient selection, basic aspects of procedure technique, imaging follow-up, treatment outcomes, and comparisons between various therapies. PMID:24436530

  3. Spectral characteristic analysis of lung cancer serum

    NASA Astrophysics Data System (ADS)

    Li, Xiao Zhou; Jin, Huiqiang; Liu, Huasheng; Ding, Jianhua; Lin, Junxiu

    2001-10-01

    Spectral changes of lung cancer serum in the process of tumor evolution were investigated in this study. We kept close watch on the tumor progression of a group of patients, and measured their serum spectra using 488.0nm and 514.5nm excitation of an Ar-ion laser once a week. There was no apparent change observed in fluorescence spectrum in different period. However, the relative intensity of three Raman peaks (mode A, B and C) decreased every week later. For quantitative analysis of such changes, a parameter Ir (relative intensity of C Raman peak) was introduced and Ir-value was calculated. Calculation showed that Ir-value was degressive with tumor evolution, but (beta) (Ir5145 /Ir4880) varied irregularly. To the end, no Raman peak was observed. We assumed that three Raman peaks were derived from beta carotene. It indicated that the content of beta carotene decreased with the aggravation of lung cancer.

  4. Lung cancer-a fractal viewpoint.

    PubMed

    Lennon, Frances E; Cianci, Gianguido C; Cipriani, Nicole A; Hensing, Thomas A; Zhang, Hannah J; Chen, Chin-Tu; Murgu, Septimiu D; Vokes, Everett E; Vannier, Michael W; Salgia, Ravi

    2015-11-01

    Fractals are mathematical constructs that show self-similarity over a range of scales and non-integer (fractal) dimensions. Owing to these properties, fractal geometry can be used to efficiently estimate the geometrical complexity, and the irregularity of shapes and patterns observed in lung tumour growth (over space or time), whereas the use of traditional Euclidean geometry in such calculations is more challenging. The application of fractal analysis in biomedical imaging and time series has shown considerable promise for measuring processes as varied as heart and respiratory rates, neuronal cell characterization, and vascular development. Despite the advantages of fractal mathematics and numerous studies demonstrating its applicability to lung cancer research, many researchers and clinicians remain unaware of its potential. Therefore, this Review aims to introduce the fundamental basis of fractals and to illustrate how analysis of fractal dimension (FD) and associated measurements, such as lacunarity (texture) can be performed. We describe the fractal nature of the lung and explain why this organ is particularly suited to fractal analysis. Studies that have used fractal analyses to quantify changes in nuclear and chromatin FD in primary and metastatic tumour cells, and clinical imaging studies that correlated changes in the FD of tumours on CT and/or PET images with tumour growth and treatment responses are reviewed. Moreover, the potential use of these techniques in the diagnosis and therapeutic management of lung cancer are discussed. PMID:26169924

  5. Lung cancer in patients under the age of 40 years

    PubMed Central

    Kaczmarczyk, Grzegorz; Porębska, Irena; Szmygin-Milanowska, Katarzyna; Gołecki, Marcin

    2012-01-01

    Aim of the study In the paper clinical cases of individuals diagnosed with lung cancer below the age of 40 years have been analyzed. Material and methods The analysis included: sex, age, clinical symptoms found before and at the moment of diagnosis, character of changes visible in radiological imaging, time that passed from the first symptoms to reporting to a doctor and to establishing a diagnosis, type of diagnostic method used in establishing the final diagnosis, histopathologic type of cancer, degree of cancer progression. Results The results have been compared with a peer group who had been diagnosed 20 years earlier. Currently 7% of patients were diagnosed at the age of 25 or younger, whereas in the previous cohort patients in this age constituted 2%. The predominant pathological type was adenocarcinoma (currently 33%, previously 4%) in contrast to the earlier group in which 57% of patients had small cell lung cancer (57%). The incidence is equally distributed between both sexes, although there is an evident increase in female lung cancer cases. In the majority of patients the clinical presentation is a peripheral mass on chest X-ray. 20% of patients present pleural effusion on diagnosis. Patients reported the following complaints: breathlessness, chest pain, weight loss and fatigue. The majority of cases were diagnosed in advanced stages on the basis of a bronchoscopy acquired specimen. Time course from symptoms to diagnosis tends to be shorter than 20 years ago. PMID:23788919

  6. Black Smokers Less Likely to Get Lung Cancer Screening

    MedlinePlus

    ... nlm.nih.gov/medlineplus/news/fullstory_157850.html Black Smokers Less Likely to Get Lung Cancer Screening ... 2016 (HealthDay News) -- Differences in smoking habits between black and white Americans may lead to lower lung ...

  7. Discovery – Lung Cancer Screening Saves Lives: The NLST

    Cancer.gov

    NCI funded the National Lung Screening Trial, an eight-year study that used new technology to detect small, aggressive tumors early enough to surgically remove them. This approach reduced lung cancer deaths among participants by 20 percent.

  8. [Lung Cancer as an Occupational Disease].

    PubMed

    Baur, X; Woitowitz, H-J

    2016-08-01

    Lung cancer is one of the most frequently encountered cancer types. According to the latest WHO data, about 10 % of this disease are due to occupational exposure to cancerogens. Asbestos is still the number one carcinogen. Further frequent causes include quarz and ionizing radiation (uranium mining). Probable causes of the disease can be identified only with the help of detailed occupational history taken by a medical specialist and qualified exposure assessment. Without clarifying the cause of the disease, there is neither a correct insurance procedure nor compensation for the victim, and furthermore, required preventive measures cannot be initiated. PMID:27512930

  9. Murine Lung Cancer Induces Generalized T Cell Exhaustion

    PubMed Central

    Mittal, Rohit; Chen, Ching-Wen; Lyons, John D; Margoles, Lindsay M; Liang, Zhe; Coopersmith, Craig M; Ford, Mandy L

    2015-01-01

    Background Cancer is known to modulate tumor-specific immune responses by establishing a micro-environment that leads to the upregulation of T cell inhibitory receptors, resulting in the progressive loss of function and eventual death of tumor-specific T cells. However, the ability of cancer to impact the functionality of the immune system on a systemic level is much less well characterized. Because cancer is known to predispose patients to infectious complications including sepsis, we hypothesized that the presence of cancer alters pathogen-directed immune responses on a systemic level. Materials and Methods We assessed systemic T cell coinhibitory receptor expression, cytokine production, and apoptosis in mice with established subcutaneous lung cancer tumors and in unmanipulated mice without cancer. Results Results indicated that the frequencies of PD-1+, BTLA+, and 2B4+ cells in both the CD4+ and CD8+ T cell compartments were increased in mice with localized cancer relative to non-cancer controls, and the frequencies of both CD4+ and CD8+ T cells expressing multiple different inhibitory receptors was increased in cancer animals relative to non-cancer controls. Additionally, 2B4+CD8+ T cells in cancer mice exhibited reduced IL-2 and IFN-γ, while BTLA+CD8+ T cells in cancer mice exhibited reduced IL-2 and TNF. Conversely, CD4+ T cells in cancer animals demonstrated an increase in the frequency of Annexin V+ apoptotic cells. Conclusion Taken together, these data suggest that the presence of cancer induces systemic T cell exhaustion and generalized immune suppression. PMID:25748104

  10. IGFBP7 is a p53 target gene inactivated in human lung cancer by DNA hypermethylation.

    PubMed

    Chen, Yuan; Cui, Tiantian; Knösel, Thomas; Yang, Linlin; Zöller, Kristin; Petersen, Iver

    2011-07-01

    Insulin-like growth factor binding protein 7 (IGFBP7) was considered a tumor suppressor gene in lung cancer. However, the mechanism responsible for the downregulation of this gene has not yet been fully understood. In this study, we analyzed the epigenetic inactivation of IGFBP7 expression in human lung cancer. We found that 14 out of 16 lung cancer cell lines showed decreased expression of IGFBP7 compared to control cells by real-time RT-PCR, and 42 out of 90 patients (46.7%) with primary lung tumor exhibited negative staining of IGFBP7 by immunohistochemistry analysis. The IGFBP7 expression could be restored by demethylation agent 5-aza-2'-deoxycytidine (DAC) in 7 cancer cell lines. Methylation status of IGFBP7 was further evaluated by bisulfite sequencing (BS) and methylation-specific-PCR (MSP). It turned out that low expression of IGFBP7 was associated with DNA methylation in lung cancer cell lines and in primary lung tumors (P=0.019). To explore the regulatory role of p53 on IGFBP7, we transfected a wild type p53 expression vector into lung cancer cell lines H1299, H2228, and H82. Forced expression of p53 increased IGFBP7 expression only in H82 harboring no IGFBP7 methylation, while transfection in combination with DAC induced the expression of IGFBP7 in H1299 and H2228, in which IGFBP7 was methylated. Additionally, treatment with p53 inducer adriamycin (ADR) alone or in combination with DAC increased the expression of IGFBP7 in the 3 cell lines. Our data suggest that IGFBP7 is inactivated in lung cancer by DNA hypermethylation in both lung cancer cell lines and primary lung tumors, and IGFBP7 might be regulated by p53 in lung cancer cells. PMID:21095038

  11. The National Lung Screening Trial (NLST) | Division of Cancer Prevention

    Cancer.gov

    The National Lung Screening Trial (NLST) compared two ways of detecting lung cancer: low-dose helical computed tomography (CT) and standard chest X-ray. Both chest X-rays and low-dose helical CT scans have been used to find lung cancer early, but the effects of these screening techniques on lung cancer mortality rates had not been determined. NLST enrolled 53,454 current or former heavy smokers from 33 sites and coordinating centers across the United States. | The National Lung Screening Trial (NLST) compared two ways of detecting lung cancer: participants who received low-dose helical CT scans had a 20% lower risk of dying from lung cancer than participants who received standard chest X-rays.

  12. Pemetrexed (Alimta) in small cell lung cancer.

    PubMed

    Socinski, Mark A

    2005-04-01

    Small cell lung cancer (SCLC) comprises approximately 13% of all lung cancers. In limited stage (LS)-SCLC, combined-modality therapy represents the standard of care. Therapy should be approached curatively in fit patients with a good performance status because 5-year survival rates approach 26% in aggressively treated patients. In contrast, cure is not possible in extensive stage (ES)-SCLC with median 2-year survival rates with current therapy remaining at less than 10%. Pemetrexed (Alimta; Eli Lilly and Co, Indianapolis, IN) is a novel, multi-targeted antifolate that inhibits several folate-dependent enzymes involved in purine and pyrimidine synthesis, and is active as a single-agent or in combination with a platinum in both non-small cell lung cancer and malignant pleural mesothelioma. Pemetrexed/platinum combinations appear active in ES-SCLC based on objective response rates observed in a randomized phase II trial. However, no survival data is yet available from this trial. The toxicity profile of both cisplatin and carboplatin in combination with pemetrexed was extremely favorable, as was the ability to deliver full doses of each of the component drugs. Given the limited options available for patients in the relapsed setting, the activity of single-agent pemetrexed is interesting. Also, preliminary data indicates that full doses of carboplatin/pemetrexed can be administered with thoracic radiation therapy, supporting a future clinical trial initiative in LS-SCLC. PMID:15818532

  13. Lung Cancer Ablation: What Is the Evidence?

    PubMed Central

    de Baere, Thierry; Farouil, Geoffroy; Deschamps, Frederic

    2013-01-01

    Percutaneous ablation of small non-small cell lung cancer (NSCLC) has been demonstrated to be both feasible and safe in nonsurgical candidates. Radiofrequency ablation (RFA), the most commonly used technique for ablation, has a reported rate of complete ablation of ~90%, with best results obtained in tumors <2 to 3 cm in diameter. The best reported 1-, 3-, and 5-year overall survival rates after RFA of NSCLC are 97.7%, 72.9%, and 55.7%, respectively. It is noteworthy that in most studies, cancer-specific survival is greater than overall survival due to severe comorbidities in patients treated with RFA for NSCLC. Aside from tumor size and tumor stage, these comorbidities are predictive of survival. Other ablation techniques such as microwave and irreversible electroporation may in the future prove to overcome some of the limitations of RFA, namely for large tumors or tumors close to large vessels. Stereotactic body radiation therapy has also been demonstrated to be highly efficacious in treating small lung tumors and will need to be compared with percutaneous ablation. This article reviews the current evidence regarding RFA for lung cancer. PMID:24436531

  14. Hyperspectral imaging of skin and lung cancers

    NASA Astrophysics Data System (ADS)

    Zherdeva, Larisa A.; Bratchenko, Ivan A.; Alonova, Marina V.; Myakinin, Oleg O.; Artemyev, Dmitry N.; Moryatov, Alexander A.; Kozlov, Sergey V.; Zakharov, Valery P.

    2016-04-01

    The problem of cancer control requires design of new approaches for instrumental diagnostics, as the accuracy of cancer detection on the first step of diagnostics in clinics is slightly more than 50%. In this study, we present a method of visualization and diagnostics of skin and lung tumours based on registration and processing of tissues hyperspectral images. In a series of experiments registration of hyperspectral images of skin and lung tissue samples is carried out. Melanoma, basal cell carcinoma, nevi and benign tumours are studied in skin ex vivo and in vivo experiments; adenocarcinomas and squamous cell carcinomas are studied in ex vivo lung experiments. In a series of experiments the typical features of diffuse reflection spectra for pathological and normal tissues were found. Changes in tissues morphology during the tumour growth lead to the changes of blood and pigments concentration, such as melanin in skin. That is why tumours and normal tissues maybe differentiated with information about spectral response in 500-600 nm and 600 - 670 nm areas. Thus, hyperspectral imaging in the visible region may be a useful tool for cancer detection as it helps to estimate spectral properties of tissues and determine malignant regions for precise resection of tumours.

  15. A combinatorial strategy for treating KRAS-mutant lung cancer.

    PubMed

    Manchado, Eusebio; Weissmueller, Susann; Morris, John P; Chen, Chi-Chao; Wullenkord, Ramona; Lujambio, Amaia; de Stanchina, Elisa; Poirier, John T; Gainor, Justin F; Corcoran, Ryan B; Engelman, Jeffrey A; Rudin, Charles M; Rosen, Neal; Lowe, Scott W

    2016-06-30

    Therapeutic targeting of KRAS-mutant lung adenocarcinoma represents a major goal of clinical oncology. KRAS itself has proved difficult to inhibit, and the effectiveness of agents that target key KRAS effectors has been thwarted by activation of compensatory or parallel pathways that limit their efficacy as single agents. Here we take a systematic approach towards identifying combination targets for trametinib, a MEK inhibitor approved by the US Food and Drug Administration, which acts downstream of KRAS to suppress signalling through the mitogen-activated protein kinase (MAPK) cascade. Informed by a short-hairpin RNA screen, we show that trametinib provokes a compensatory response involving the fibroblast growth factor receptor 1 (FGFR1) that leads to signalling rebound and adaptive drug resistance. As a consequence, genetic or pharmacological inhibition of FGFR1 in combination with trametinib enhances tumour cell death in vitro and in vivo. This compensatory response shows distinct specificities: it is dominated by FGFR1 in KRAS-mutant lung and pancreatic cancer cells, but is not activated or involves other mechanisms in KRAS wild-type lung and KRAS-mutant colon cancer cells. Importantly, KRAS-mutant lung cancer cells and patients’ tumours treated with trametinib show an increase in FRS2 phosphorylation, a biomarker of FGFR activation; this increase is abolished by FGFR1 inhibition and correlates with sensitivity to trametinib and FGFR inhibitor combinations. These results demonstrate that FGFR1 can mediate adaptive resistance to trametinib and validate a combinatorial approach for treating KRAS-mutant lung cancer. PMID:27338794

  16. Photodynamic therapy for lung cancer and malignant pleural mesothelioma.

    PubMed

    Simone, Charles B; Cengel, Keith A

    2014-12-01

    Photodynamic therapy (PDT) is a form of non-ionizing radiation therapy that uses a drug, called a photosensitizer, combined with light to produce singlet oxygen ((1)O2) that can exert anti-cancer activity through apoptotic, necrotic, or autophagic tumor cell death. PDT is increasingly being used to treat thoracic malignancies. For early-stage non-small cell lung cancer (NSCLC), PDT is primarily employed as an endobronchial therapy to definitively treat endobronchial or roentgenographically occult tumors. Similarly, patients with multiple primary lung cancers may be definitively treated with PDT. For advanced or metastatic NSCLC and small cell lung cancer (SCLC), PDT is primarily employed to palliate symptoms from obstructing endobronchial lesions causing airway compromise or hemoptysis. PDT can be used in advanced NSCLC to attempt to increase operability or to reduce the extent of operation intervention required, and selectively to treat pleural dissemination intraoperatively following macroscopically complete surgical resection. Intraoperative PDT can be safely combined with macroscopically complete surgical resection and other treatment modalities for malignant pleural mesothelioma (MPM) to improve local control and prolong survival. This report reviews the mechanism of and rationale for using PDT to treat thoracic malignancies, details prospective and major retrospectives studies of PDT to treat NSCLC, SCLC, and MPM, and describes improvements in and future roles and directions of PDT. PMID:25499640

  17. Death Concerns among Individuals Newly Diagnosed with Lung Cancer

    ERIC Educational Resources Information Center

    Lehto, Rebecca; Therrien, Barbara

    2010-01-01

    Confronting the reality of death is an important challenge for individuals facing life-threatening illness such as lung cancer, the leading cause of cancer death. Few studies, however, document the nature of death-related concerns in individuals newly diagnosed with lung cancer. The aims of this exploratory study were to examine unsolicited…

  18. Randomization to Screening for Prostate, Lung, Colorectal and Ovarian Cancers and Thyroid Cancer Incidence in Two Large Cancer Screening Trials

    PubMed Central

    O'Grady, Thomas J.; Kitahara, Cari M.; DiRienzo, A. Gregory; Boscoe, Francis P.; Gates, Margaret A.

    2014-01-01

    Background Thyroid cancer incidence has increased significantly over the past three decades due, in part, to incidental detection. We examined the association between randomization to screening for lung, prostate, colorectal and/or ovarian cancers and thyroid cancer incidence in two large prospective randomized screening trials. Methods We assessed the association between randomization to low-dose helical CT scan versus chest x-ray for lung cancer screening and risk of thyroid cancer in the National Lung Screening Trial (NLST). In the Prostate Lung Colorectal and Ovarian Cancer Screening Trial (PLCO), we assessed the association between randomization to regular screening for said cancers versus usual medical care and thyroid cancer risk. Over a median 6 and 11 years of follow-up in NLST and PLCO, respectively, we identified 60 incident and 234 incident thyroid cancer cases. Cox proportional hazards regression was used to calculate the cause specific hazard ratios (HR) and 95% confidence intervals (CI) for thyroid cancer. Results In NLST, randomization to lung CT scan was associated with a non-significant increase in thyroid cancer risk (HR  = 1.61; 95% CI: 0.96–2.71). This association was stronger during the first 3 years of follow-up, during which participants were actively screened (HR  = 2.19; 95% CI: 1.07–4.47), but not subsequently (HR  = 1.08; 95% CI: 0.49–2.37). In PLCO, randomization to cancer screening compared with usual care was associated with a significant decrease in thyroid cancer risk for men (HR  = 0.61; 95% CI: 0.49–0.95) but not women (HR  = 0.91; 95% CI: 0.66–1.26). Similar results were observed when restricting to papillary thyroid cancer in both NLST and PLCO. Conclusion Our study suggests that certain medical encounters, such as those using low-dose helical CT scan for lung cancer screening, may increase the detection of incidental thyroid cancer. PMID:25192282

  19. Influence of Pulmonary Rehabilitation on Lung Function Changes After the Lung Resection for Primary Lung Cancer in Patients with Chronic Obstructive Pulmonary Disease.

    PubMed

    Mujovic, Natasa; Mujovic, Nebojsa; Subotic, Dragan; Ercegovac, Maja; Milovanovic, Andjela; Nikcevic, Ljubica; Zugic, Vladimir; Nikolic, Dejan

    2015-11-01

    Influence of physiotherapy on the outcome of the lung resection is still controversial. Study aim was to assess the influence of physiotherapy program on postoperative lung function and effort tolerance in lung cancer patients with chronic obstructive pulmonary disease (COPD) that are undergoing lobectomy or pneumonectomy. The prospective study included 56 COPD patients who underwent lung resection for primary non small-cell lung cancer after previous physiotherapy (Group A) and 47 COPD patients (Group B) without physiotherapy before lung cancer surgery. In Group A, lung function and effort tolerance on admission were compared with the same parameters after preoperative physiotherapy. Both groups were compared in relation to lung function, effort tolerance and symptoms change after resection. In patients with tumors requiring a lobectomy, after preoperative physiotherapy, a highly significant increase in FEV1, VC, FEF50 and FEF25 of 20%, 17%, 18% and 16% respectively was registered with respect to baseline values. After physiotherapy, a significant improvement in 6-minute walking distance was achieved. After lung resection, the significant loss of FEV1 and VC occurred, together with significant worsening of the small airways function, effort tolerance and symptomatic status. After the surgery, a clear tendency existed towards smaller FEV1 loss in patients with moderate to severe, when compared to patients with mild baseline lung function impairment. A better FEV1 improvement was associated with more significant loss in FEV1. Physiotherapy represents an important part of preoperative and postoperative treatment in COPD patients undergoing a lung resection for primary lung cancer. PMID:26618048

  20. Lung cancer stem cells: The root of resistance.

    PubMed

    MacDonagh, Lauren; Gray, Steven G; Breen, Eamon; Cuffe, Sinead; Finn, Stephen P; O'Byrne, Kenneth J; Barr, Martin P

    2016-03-28

    In the absence of specific treatable mutations, platinum-based chemotherapy remains the gold standard of treatment for lung cancer patients. However, 5-year survival rates remain poor due to the development of resistance and eventual relapse. Resistance to conventional cytotoxic therapies presents a significant clinical challenge in the treatment of this disease. The cancer stem cell (CSC) hypothesis suggests that tumors are arranged in a hierarchical structure, with the presence of a small subset of stem-like cells that are responsible for tumor initiation and growth. This CSC population has a number of key properties such as the ability to asymmetrically divide, differentiate and self-renew, in addition to having increased intrinsic resistance to therapy. While cytotoxic chemotherapy kills the bulk of tumor cells, CSCs are spared and have the ability to recapitulate the heterogenic tumor mass. The identification of lung CSCs and their role in tumor biology and treatment resistance may lead to innovative targeted therapies that may ultimately improve clinical outcomes in lung cancer patients. This review will focus on lung CSC markers, their role in resistance and their relevance as targets for future therapies. PMID:26797015

  1. Digital tomosynthesis in lung cancer: state of the art

    PubMed Central

    Viti, Andrea; Terzi, Alberto

    2015-01-01

    Chest digital tomosynthesis (CDT) is a limited angle image tomography, which improves the visibility of anatomy compared with radiographic imaging. Due to the limited acquisition angle of CDT, it has the potential to significantly increase the temporal resolution of patient surveillance at the cost of reduced resolution in one direction. CDT is 3 times more effective in identifying pulmonary nodules compared to conventional radiography and at lower doses and cost compared with routine chest computed tomography (CT) examinations. There is only one report in which CDT was used in a single-arm observational study for lung cancer detection in at-risk population while a few studies suggested that CDT sensitivity is superior to radiography but inferior to CT in detecting lung nodules, other studies on the accuracy of CDT suggest that the specificity is much closer to CT than radiography. Therefore, large-scale randomized controlled trial would be needed to confirm benefits of CDT and identify where it is best used in the clinical setting. CDT seems to be a cost-effectiveness first-line lung cancer screening tool to detect potential lung cancer nodule. PMID:26207232

  2. Smoky coal, tobacco smoking, and lung cancer risk in Xuanwei, China

    PubMed Central

    Kim, Christopher; Chapman, Robert S.; Hu, Wei; He, Xingzhou; Hosgood, H. Dean; Liu, Larry Z.; Lai, Hong; Chen, Wei; Silverman, Debra T.; Vermeulen, Roel; Tian, Linwei; Bassig, Bryan; Shen, Min; Zhang, Yawei; Ma, Shuangge; Rothman, Nathaniel; Lan, Qing

    2014-01-01

    Objectives Lung cancer rates in Xuanwei are the highest in China. In-home use of smoky coal was associated with lung cancer risk, and the association of smoking and lung cancer risk strengthens after stove improvement. Here, we explored the differential association of tobacco use and lung cancer risk by the intensity, duration, and type of coal used. Materials and Methods We conducted a population-based case–control study of 260 male lung cancer cases and 260 age-matched male controls. Odds ratios (OR) and 95% confidence interval (CI) for tobacco use was calculated by conditional logistic regression. Results Use of smoky coal was significantly associated with an increased risk of lung cancer risk, and tobacco use was weakly and non-significantly associated with lung cancer risk. When the association was assessed by coal use, the cigarette-lung cancer risk association was null in hazardous coal users and elevated in less hazardous smoky coal users and non-smoky coal users. The risk of lung cancer per cigarette per day decreased as annual use of coal increased (>0-3 tons: OR: 1.09; 95% CI: 1.03-1.17; >3 tons: OR: 0.99; 95% CI: 0.95-1.03). Among more hazardous coal users, attenuation occurs at even low levels of usage (>0-3 tons: OR: 1.02; 95% CI: 0.91-1.14; >3 tons: OR: 0.94; 95% CI: 0.97-1.03). Conclusion We found evidence that smoky coal attenuated the tobacco and lung cancer risk association in males that lived in Xuanwei, particularly among users of hazardous coal where even low levels of smoky coal attenuated the association. Our results suggest that the adverse effects of tobacco may become more apparent as China's population continues to switch to using cleaner fuels for the home, underscoring the urgent need for smoking cessation in China and elsewhere. PMID:24506909

  3. Potentially estrogenic polychlorinated biphenyls congeners serum levels and its relation with lung cancer.

    PubMed

    Recio-Vega, Rogelio; Mendez-Henandez, Alejandra; Gabriel, Antonio Padua Y; Jacobo-Avila, Antonio; Portales-Castanedo, Arnulfo; Hernandez-Gonzalez, Sandra; Gallegos-Arreola, Martha Patricia; Ocampo-Gomez, Guadalupe

    2013-09-01

    Lung cancer is the most common cancer in the world. The main cause of lung cancer is cigarette smoke; however, other important genetic and environmental risk factors play a significant role in the development of lung cancer. Among these factors, occupational and accidental exposure to polychlorinated biphenyls (PCBs) has been associated with an increased risk in lung cancer, suggesting that PCBs could be potent carcinogens. The aim of the present study was to investigate the association between PCB exposure levels, CYP1A1 polymorphisms and the risk of lung cancer. This study enrolled newly diagnosed lung cancer patients. Environmental and occupational information related to the patients studied was collected. Blood samples were taken for the measurement of serum levels of 20 PCB congeners and for CYP1A1 polymorphism analysis. The serum levels of two PCB congeners with potential estrogenic activity were higher in lung cancer patients. The risk of lung cancer was found to correlate with age, gender, smoking history and with agricultural workers, as well as with congener 18. No differences were found in the frequency of CYP1A1 polymorphisms. Furthermore, we did not find a correlation between CYP1A1 polymorphisms and PCB serum levels. The high levels of PCB with estrogenic activity found in our cases, could promote lung cancer inducing cell proliferation in non-neoplastic and neoplastic lung cells via ERβ; inducing the formation of DNA adducts, producing oxidative stress with the subsequent DNA damage and increasing the endogenous catechol levels by catechol-O-methyl transferase (COMT) inhibition. PMID:22729568

  4. An ecological analysis of PM2.5 concentrations and lung cancer mortality rates in China

    PubMed Central

    Fu, Jingying; Jiang, Dong; Lin, Gang; Liu, Kun; Wang, Qiao

    2015-01-01

    Objective To explore the association between Particulate Matter (PM)2.5 (particles with an aerodynamic diameter less than 2.5 µm) and lung cancer mortality rates and to estimate the potential risk of lung cancer mortality related to exposure to high PM2.5 concentrations. Design Geographically weighted regression was performed to evaluate the relation between PM2.5 concentrations and lung cancer mortality for males, females and for both sexes combined, in 2008, based on newly available long-term data. Lung cancer fatalities from long-term exposure to PM2.5 were calculated according to studies by Pope III et al and the WHO air quality guidelines (AQGs). Setting 31 provinces in China. Results PM2.5 was associated with the lung cancer mortality of males, females and both sexes combined, in China, although there were exceptions in several regions, for males and females. The number of lung cancer fatalities calculated by the WHO AQGs ranged from 531 036 to 532 004, whereas the number calculated by the American Cancer Society (ACS) reached 614 860 after long-term (approximately 3–4 years) exposure to PM2.5 concentrations since 2008. Conclusions There is a positive correlation between PM2.5 and lung cancer mortality rate, and the relationship between them varies across the entire country of China. The number of lung cancer fatalities estimated by ACS was closer to the actual data than those of the WHO AQGs. Therefore, the ACS estimate of increased risk of lung cancer mortality from long-term exposure to PM2.5 might be more applicable for evaluating lung cancer fatalities in China than the WHO estimate. PMID:26603253

  5. Diversity in the association between occupation and lung cancer among black and white men.

    PubMed

    Swanson, G M; Lin, C S; Burns, P B

    1993-01-01

    A population-based case comparison study of incident lung cancer and occupational risk factors was conducted in the tricounty Detroit metropolitan area. Nearly 6000 lung cancer cases and a comparison group of 3600 colon cancer cases were interviewed. This report includes 3792 white and black male lung cancer cases and 1966 black and white colon cancer referents. Cigarette smoking, age at diagnosis, and lifetime work history were assessed to determine the relationship between length of employment in specific occupations and industries and lung cancer. Diverse patterns of association between work history and lung cancer were observed for black and white men. Significant associations were seen between lung cancer and increasing length of employment in the following occupations: for white men, concrete and terrazzo finishers, grinding machine operators, heat treating machine operators, miscellaneous machine operators, truck drivers, driver sales, and laborers; for black men, farm workers, automobile mechanics, painting machine operators, furnace operators, and garbage collectors; for both black and white men, farmers, slicing and cutting machine operators, and garbage collectors. Distinct patterns for black and white men also were observed for length of employment by industry. This study clearly demonstrates the need to include black men in studies of occupational cancer etiology and to evaluate black and white men separately. It also indicates the necessity for cigarette smoking history to accurately assess workplace cancer risks. We propose guidelines for incorporating the use of biomarkers into further studies of occupational cancer epidemiology. PMID:8348054

  6. Increased isoprostane levels in oleic acid-induced lung injury

    SciTech Connect

    Ono, Koichi; Koizumi, Tomonobu; Tsushima, Kenji; Yoshikawa, Sumiko; Yokoyama, Toshiki; Nakagawa, Rikimaru; Obata, Toru

    2009-10-16

    The present study was performed to examine a role of oxidative stress in oleic acid-induced lung injury model. Fifteen anesthetized sheep were ventilated and instrumented with a lung lymph fistula and vascular catheters for blood gas analysis and measurement of isoprostanes (8-epi prostaglandin F2{alpha}). Following stable baseline measurements, oleic acid (0.08 ml/kg) was administered and observed 4 h. Isoprostane was measured by gas chromatography mass spectrometry with the isotope dilution method. Isoprostane levels in plasma and lung lymph were significantly increased 2 h after oleic acid administration and then decreased at 4 h. The percent increases in isoprostane levels in plasma and lung lymph at 2 h were significantly correlated with deteriorated oxygenation at the same time point, respectively. These findings suggest that oxidative stress is involved in the pathogenesis of the pulmonary fat embolism-induced acute lung injury model in sheep and that the increase relates with the deteriorated oxygenation.

  7. Perspectives of African Americans on Lung Cancer: A Qualitative Analysis

    PubMed Central

    Waldman, Laura Tesler; Browning, Emily; Gagne, Joshua; Emmons, Karen

    2015-01-01

    Background. Disparities in incidence and mortality for lung cancer in African Americans are well documented; however, the extent to which disparities reflect differences in patient perceptions of tobacco and lung cancer treatment is unclear. The objective of this study was to explore African Americans’ knowledge of lung cancer, perceived risk, interest in smoking cessation, attitudes toward lung cancer treatment, and lung cancer diagnosis and treatment experiences. Patients and Methods. The cohort comprised 32 African-American current and former smokers without a cancer diagnosis who participated in focus groups and 10 African Americans with lung cancer who participated in in-depth interviews. Transcripts were analyzed using a modified grounded theory approach. Results. Participants without a cancer diagnosis were aware of the link between smoking and lung cancer, the common symptoms of the disease, and its poor prognosis. They desired specific, personalized smoking-cessation information. If diagnosed, the majority reported, they would seek medical care. Most believed that insurance and socioeconomic factors were more likely to affect treatment access than racial discrimination. Participants with a cancer diagnosis were also aware of the relationship between smoking and lung cancer. They felt their treatment plans were appropriate and trusted their physicians. Most did not believe that race affected their care. Conclusion. This qualitative study suggests that African-American smokers are aware of the relationship between smoking and lung cancer and are interested in smoking-cessation treatment. These data also indicate that lung cancer disparities are unlikely to be associated with differential willingness to receive care but that African Americans may perceive financial and insurance barriers to lung cancer treatment. PMID:25795634

  8. Smoking, air pollution, and the high rates of lung cancer in Shenyang, China

    SciTech Connect

    Xu, Z.Y.; Blot, W.J.; Xiao, H.P.; Wu, A.; Feng, Y.P.; Stone, B.J.; Sun, J.; Ershow, A.G.; Henderson, B.E.; Fraumeni, J.F. Jr. )

    1989-12-06

    A case-control study involving interviews with 1,249 patients with lung cancer and 1,345 population-based controls was conducted in Shenyang, an industrial city in northeastern China, where mortality rates are high among men and women. Cigarette smoking was found to be the principal cause of lung cancer in this population, accounting for 55% of the lung cancers in males and 37% in females. The attributable risk percentage among females is high compared to elsewhere in China, largely because of a higher prevalence of smoking among women. After adjustment for smoking, there were also significant increases in lung cancer risk associated with several measures of exposure to air pollutants. Risks were twice as high among those who reported smoky outdoor environments, and increased in proportion to years of sleeping on beds heated by coal-burning stoves (kang), and to an overall index of indoor air pollution. Threefold increases in lung cancer risk were found among men who worked in the nonferrous smelting industry, where heavy exposures to inorganic arsenic have been reported. The associations with both smoking and indoor air pollution were stronger for squamous cell and small cell carcinomas than for adenocarcinoma of the lung. Risks due to smoking or air pollution were not greatly altered by adjustment for consumption of fresh vegetables or sources of beta carotene or retinol, prior chronic lung diseases, or education level. The findings suggest that smoking and environmental pollution combine to account for the elevated rates of lung cancer mortality in Shenyang.

  9. Familial aggregation of lung cancer in a high incidence area in China

    PubMed Central

    Jin, Y T; Xu, Y C; Yang, R D; Huang, C F; Xu, C W; He, X Z

    2005-01-01

    To investigate whether lung cancer clusters in families in a high incidence county of China, an analysis was conducted using data on domestic fuel history and tobacco use for family members of 740 deceased lung cancer probands and 740 controls (probands' spouses). Lung cancer prevalence was compared among first-degree relatives of probands and of controls, taking into account various factors using logistic regression and generalised estimating equations. First-degree relatives of probands, compared with those of controls, showed an excess risk of lung cancer (odds ratio (OR)=2.05, 95% confidence interval (CI): 1.68–2.53). Overall, female relatives of probands had a greater risk than did their male counterparts, and the risk was 2.90-fold for parents of probands as compared with parents of spouses. Female relatives of probands had 2.67-fold greater risk than female controls. Lung cancer risk was particularly marked among mothers (OR=3.78, 95% CI: 2.03–7.12). Having two or more affected relatives was associated with a 2.69–5.40-fold risk increase. The risk elevation was also found for other cancers overall. Results confirm previous findings of a genetic predisposition to lung cancer, and also imply that lung cancer may share a genetic background with other cancers. PMID:15756270

  10. Cordyceps militaris (L.) Link Fruiting Body Reduces the Growth of a Non-Small Cell Lung Cancer Cell Line by Increasing Cellular Levels of p53 and p21.

    PubMed

    Bizarro, Ana; Ferreira, Isabel C F R; Soković, Marina; van Griensven, Leo J L D; Sousa, Diana; Vasconcelos, M Helena; Lima, Raquel T

    2015-01-01

    Cordyceps militaris (L.) Link, an edible entomopathogenic fungus widely used in traditional Chinese medicine, has numerous potential medicinal properties including antitumor activity. The methanolic extract of C. militaris fruiting body was recently shown to have tumor cell growth inhibitory activity in several human tumor cell lines. Nonetheless, the mechanism of action involved is still not known. This work aimed at further studying the effect of the methanolic extract of C. militaris regarding its antitumor mechanism of action, using the non-small cell lung cancer cell line (NCI-H460) as a model. Results showed that treatment with the extract decreased cellular proliferation, induced cell cycle arrest at G0/G1 and increased apoptosis. In addition, the extract increased the levels of p53 and p21. Moreover, an increase in p-H2A.X and 53BP1 levels, together with an increase in the number of 53BP1 foci/cell (all indicative of DNA damage), were also observed after treatment with the extract. This work suggests that this extract affected NCI-H460 cellular viability through a mechanism involving DNA damage and p53 activation. This further supports the potential of this extract as a source of bioactive compounds, which may be used in anticancer strategies. PMID:26263965

  11. Lung cancer biomarkers, targeted therapies and clinical assays

    PubMed Central

    Ersek, Jennifer L.; Kim, Edward S.

    2015-01-01

    Until recently, the majority of genomic cancer research has been in discovery and validation; however, as our knowledge of tumor molecular profiling improves, the idea of genomic application in the clinic becomes increasingly tangible, paralleled with the drug development of newer targeted therapies. A number of profiling methodologies exist to identify biomarkers found within the patient (germ-line DNA) and tumor (somatic DNA). Subsequently, commercially available clinical assays to test for both germ-line and somatic alterations that are prognostic and/or predictive of disease outcome, toxicity or treatment response have significantly increased. This review aims to summarize clinically relevant cancer biomarkers that serve as targets for therapy and their potential relationship to lung cancer. In order to realize the full potential of genomic cancer medicine, it is imperative that clinicians understand these intricate molecular pathways, the therapeutic implication of mutations within these pathways, and the availability of clinical assays to identify such biomarkers. PMID:26629419

  12. AKAP4 is a circulating biomarker for non-small cell lung cancer

    PubMed Central

    Gumireddy, Kiranmai; Li, Anping; Chang, David H.; Liu, Qin; Kossenkov, Andrew V.; Yan, Jinchun; Korst, Robert J.; Nam, Brian T.; Xu, Hua; Zhang, Lin; Ganepola, Ganepola A.P.; Showe, Louise C.; Huang, Qihong

    2015-01-01

    Cancer testis antigens (CTAs) are widely expressed in tumor tissues, circulating tumor cells (CTCs) and in cancer derived exosomes that are frequently engulfed by lymphoid cells. To determine whether tumor derived CTA mRNAs could be detected in RNA from purified peripheral blood mononuclear cells (PBMC) of non-small cell lung cancer (NSCLC) patients, we assayed for the expression of 116 CTAs in PBMC RNA in a discovery set and identified AKAP4 as a potential NSCLC biomarker. We validated AKAP4 as a highly accurate biomarker in a cohort of 264 NSCLCs and 135 controls from 2 different sites including a subset of controls with high risk lung nodules. When all (264) lung cancers were compared with all (135) controls the area under the ROC curve (AUC) was 0.9714. When 136 stage I NSCLC lung cancers are compared with all controls the AUC is 0.9795 and when all lung cancer patients were compared to 27 controls with histologically confirmed benign lung nodules, a comparison of significant clinical importance, the AUC was 0.9825. AKAP4 expression increases significantly with tumor stage, but independent of age, gender, smoking history or cancer subtype. Follow-up studies in a small number of resected NSCLC patients revealed a decrease of AKAP4 expression post-surgical resection that remained low in patients in remission and increased with tumor recurrence. AKAP4 is a highly accurate biomarker for the detection of early stage lung cancer. PMID:26160834

  13. Exposure to low levels of ionizing radiation and lung cancer risk in Florida

    SciTech Connect

    Stockwell, H.G.; Lyman, G.H.; Waltz, J.

    1986-09-01

    The phosphate deposits of central Florida contain levels of uranium and its daughter products 30-60 times greater than average soils. A case-control study was conducted to assess the risk of lung cancer associated with living on these phosphateic soils. Using the records of the state-wide Florida Cancer Data System to address this issue, all cases of lung cancer among Florida residents in 1981 were identified (n = 7049). Information was obtained regarding residence, age, sex, race, and smoking habits. Controls consisted of 6643 individuals with cancers of the colon or rectum. Residents of the central Florida phosphate region experienced a significant increase in lung cancer risk compared to other Florida residents (odds ratio (OR) = 1.4). Excess risks appeared concentrated among squamous cell cancer (OR = 1.6) and small cell cancer (OR = 1.6). When smoking habits as well as residential area was considered, no significant excess risk, associated with residence, was observed among nonsmokers or light smokers. Area residents smoking a pack or more per day experienced a 70% increase in lung cancer risk compared to individuals smoking a similar amount but living elsewhere. Highest risks were observed among persons with squamous cell cancer (OR = 2.1) and small cell cancer (OR = 2.5) who smoked more than 40 cigarettes a day. Results suggest exposure to low levels of ionizing radiation increases the lung cancer risk of residents of this area.

  14. Mediastinal Staging in Non-Small Cell Lung Cancer.

    PubMed

    Gamliel, Ziv

    2016-07-01

    In the absence of distant metastases, lung cancer treatment is determined by the results of mediastinal lymph node staging. Occult mediastinal lymph node metastases can be missed by radiologic and needle-based staging methods. Aggressive staging of mediastinal lymph nodes improves staging accuracy. Improved accuracy of mediastinal lymph node staging results in more appropriate lung cancer treatment. Improved accuracy of mediastinal lymph node staging can improve stage-specific survival from lung cancer. PMID:27261911

  15. Antitumor effect of traditional Chinese herbal medicines against lung cancer.

    PubMed

    Chen, Yuezhou; Zhu, Jianping; Zhang, Wenpeng

    2014-10-01

    Traditional Chinese herbal medicine (TCHM) is used widely alone or in combination with chemotherapy to treat lung cancer in China. Meta-analysis of clinical trials of TCHM against lung cancer suggested the potential, but not confirmed therapeutic effect. To gain detailed insight into the antilung cancer effects of TCHM, we searched for preclinical studies of TCHM against lung cancer published from 1995 to 2012 and systematically analyzed published articles focusing on the antitumor effect of individual TCHM in lung cancer cell lines or animal models. Among 93 herbal components isolated from 73 Chinese herbs, we found 10 herbal compounds that showed the strongest cytotoxicity in lung cancer cell lines through apoptosis or cell cycle arrest, and agents isolated from seven Chinese herbs that inhibited the primary tumor growth more than 35% in A549 xenografted mice models. In addition, three herbal components suppressed lung cancer cell migration in vitro at the concentration without cytotoxicity. Polyphyllin I, tanshinone IIA, isochaihulactone, 25-OCH3-PPD, and andrographolide were the five TCHM compounds that showed strong antilung cancer effects both in cells and in animal models, and studies of their analogs showed their structure-activity relationships. This review summarizes and analyzes contemporary studies on the antitumor effect of individual TCHM against lung cancer and animal models, providing perspectives to better understand the TCHM effect in lung cancer treatment and develop new antilung cancer drugs from TCHM. PMID:24892722

  16. Lung cancer in HIV-infected patients in the combination antiretroviral treatment era

    PubMed Central

    Moltó, José; Sirera, Guillem; Clotet, Bonaventura

    2015-01-01

    The advent of combination antiretroviral treatment (cART) has been followed by a decrease in HIV-associated morbidity and mortality, but also by an apparent increase in the incidence of non-AIDS-defining cancers (NADCs). The risk of lung cancer is substantially higher in HIV-infected patients than in the general population, in part due to aging and tobacco use, and it is the most frequent NADC. The management of lung cancer in HIV-infected patients has some peculiarities that need to be taken into account. This review focuses on the epidemiology, risk factors, and clinical management of lung cancer in HIV-infected patients. In addition, screening tools and future perspectives are also discussed. Keywords Lung cancer; non-AIDS-defining cancers (NADCs); HIV infection; antiretroviral treatment PMID:26798577

  17. A case control study on the lung cancer risk factors in north of Iran.

    PubMed

    Karimzadeh, Laleh; Koohdani, Fariba; Siassi, Fereydoon; Mahmoudi, Mahmoud; Moslemi, Dariush; Shokrzadeh, Mohammad; Safari, Farid

    2011-01-01

    In this case control study, the risk factors of lung cancer was assessed in the north of Iran. Two groups were matched for gender and age (+/- 5 years). Data were collected from 40 cases and 40 controls attending to hospitals. A public information questionnaire was used for data collection. Incidence odds ratios (OR) and corresponding 95% confidence intervals calculated using logistic regression analyses. Results showed that in adjusted odd ratio positive family history of cancer (OR = 0/19, 95% CI: 0/04-0/8) was associated with a reduction, and consumption of baked bread in traditional oven (OR = 22/6, 95% CI: 1/9-270), was associated with increase in lung cancer risk. Based on the results, smoking was not correlated with lung cancer. In conclusion, the data offers consumption of traditional oven-baked bread may enhance the risk of lung cancer but positive family history of cancer may reduce it. PMID:21699022

  18. Asbestos-related lung cancer and malignant mesothelioma of the pleura: selected current issues.

    PubMed

    Markowitz, Steven

    2015-06-01

    Asbestos-related diseases persist, because millions of workers have had prior exposure and many industrializing countries continue to use asbestos. Globally, an estimated 107,000 people die annually from lung cancer, malignant mesothelioma, and asbestosis due to occupational asbestos exposure. Malignant mesothelioma and lung cancer are caused by all major types of asbestos. Asbestos causes more lung cancer deaths than malignant mesothelioma of the pleura; most cases of the latter are due to asbestos exposure. The cancer risk increases with cumulative asbestos exposure, with increased risk even at low levels of exposure to asbestos. Based on empirical studies, an estimated cumulative occupational exposure to asbestos of 1 fiber/mL-year substantially raises malignant mesothelioma risk. No safe threshold for asbestos exposure has been established for lung cancer and mesothelioma. The validity of fiber-type risk assessments depends critically on the quality of exposure assessments, which vary considerably, leading to a high degree of uncertainty. Asbestos exposure without asbestosis and smoking increases the risk of lung cancer. The joint effect of asbestos and smoking is supra-additive, which may depend in part on the presence of asbestosis. Asbestos workers who cease smoking experience a dramatic drop in lung cancer risk, which approaches that of nonsmokers after 30 years. Studies to date show that longer, thinner fibers have a stronger association with lung cancer than shorter, less thin fibers, but the latter nonetheless also show an association with lung cancer and mesothelioma. Low-dose chest computed tomographic scanning offers an unprecedented opportunity to detect early-stage lung cancers in asbestos-exposed workers. PMID:26024342

  19. Invasive thymoma associated with lung cancer: report of a case.

    PubMed

    Shimada, T; Terashima, H; Shimizu, T; Hirayama, K

    2001-01-01

    We report herein a case of invasive thymoma simultaneously associated with lung cancer. A 64-year-old man presented with a cough and anterior chest pain, and preoperative examinations revealed an anterior mediastinal tumor as well as lung cancer. The patient underwent a total thymectomy, partial resection of the right lung, left lower lobectomy, and mediastinal lymph node dissection, followed by radiotherapy. Although it is well known that thymomas may be accompanied by nonthymic cancers, invasive thymomas occurring coincidentally with lung cancer are rarely reported in Japan. This case is very interesting in its relation to the oncogenesis of thymomas. PMID:11428602