Lung cancer is the most commonly occurring noncutaneous cancer in men and women combined in the United States and is the leading cause of cancer deaths. In 2011 alone, it is estimated that there will be 221,130 new cases diagnosed, and 71,340 women and 85,600 men will die due to this disease. The lung cancer death rate rose rapidly over several decades in both sexes, with a persistent decline for males commencing in 1991. Death rates in men have been decreasing by 3% per year since 2005. Lung cancer death rates in women have been decreasing by 0.9% per year since 2003.
Standard Treatment Options for Stage II NSCLC
Standard treatment options for stage II NSCLC include the following:
Surgery is the treatment of choice for patients with stage II NSCLC. A lobectomy, pneumonectomy, or segmental resection, wedge resection, or sleeve resection may be performed as appropriate. Careful preoperative assessment of the patient's overall medical condition, especially...
The most important risk factor for lung cancer (and for many other cancers) is tobacco use.[2,3] Cigarette smoking has been definitively established by epidemiologic and preclinical animal experimental data as the primary cause of lungcancer. This causative link has been widely recognized since the 1960s, when national reports in Great Britain and the United States brought the cancer risk of smoking prominently to the public's attention. The percentages of lung cancers estimated to be caused by tobacco smoking in males and females are 90% and 78%, respectively.
Environmental or secondhand tobacco smoke is also implicated in causing lung cancer. Environmental tobacco smoke has the same components as inhaled mainstream smoke, although in lower absolute concentrations; between 1% and 10% depending on the constituent. Carcinogenic compounds in tobacco smoke include the polynuclear aromatic hydrocarbons (PAHs), including the classical carcinogen benzo[a]pyrene and the nicotine-derived tobacco-specific nitrosamine, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK). In rodents, total doses of both PAH and NNK that are similar to doses received by humans in a lifetime of smoking induce pulmonary tumors. Elevated biomarkers of tobacco exposure, including urinary cotinine, tobacco-related carcinogen metabolites, and carcinogen-protein adducts, are seen in passive or secondhand smokers.[6,7,8,9,10]
Lung cancer is considered to be the end stage of multistep carcinogenesis. Suggestive evidence of genetic damage is the association of cigarette smoking with the formation of the DNA adducts in human lung tissue. An unequivocal link between tobacco smoke and lung carcinogenesis has been established by molecular data.[11,12]
Many other exposures have been established as causally associated with lung cancer, but even the combined effect of these additional factors is very small compared with cigarette smoking. These additional causal factors are primarily related to occupational exposures to agents such as asbestos, arsenic, chromium, nickel, and radon. Radon, a naturally occurring gas, is of relevance to the general public because of the potential exposure in homes.
American Cancer Society.: Cancer Facts and Figures 2011. Atlanta, Ga: American Cancer Society, 2011. Also available online. Last accessed July 27, 2011.
U.S. Department of Health and Human Services.: The Health Consequences of Smoking: A Report of the Surgeon General. Atlanta, Ga: U.S. Department of Health and Human Services, CDC, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health. Available online. Last accessed July 28, 2011.
Smoking and Health: Report of the Advisory Committee to the Surgeon General of the Public Health Service. Washington, DC: US Department of Health, Education, and Welfare, 1965. PHS Publ No 1103.
Hackshaw AK, Law MR, Wald NJ: The accumulated evidence on lung cancer and environmental tobacco smoke. BMJ 315 (7114): 980-8, 1997.
Cinciripini PM, Hecht SS, Henningfield JE, et al.: Tobacco addiction: implications for treatment and cancer prevention. J Natl Cancer Inst 89 (24): 1852-67, 1997.
Hecht SS, Carmella SG, Murphy SE, et al.: A tobacco-specific lung carcinogen in the urine of men exposed to cigarette smoke. N Engl J Med 329 (21): 1543-6, 1993.
Finette BA, O'Neill JP, Vacek PM, et al.: Gene mutations with characteristic deletions in cord blood T lymphocytes associated with passive maternal exposure to tobacco smoke. Nat Med 4 (10): 1144-51, 1998.
Parsons WD, Carmella SG, Akerkar S, et al.: A metabolite of the tobacco-specific lung carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone in the urine of hospital workers exposed to environmental tobacco smoke. Cancer Epidemiol Biomarkers Prev 7 (3): 257-60, 1998.
Anderson KE, Carmella SG, Ye M, et al.: Metabolites of a tobacco-specific lung carcinogen in nonsmoking women exposed to environmental tobacco smoke. J Natl Cancer Inst 93 (5): 378-81, 2001.
Hecht SS: Human urinary carcinogen metabolites: biomarkers for investigating tobacco and cancer. Carcinogenesis 23 (6): 907-22, 2002.
Mao L, Lee JS, Kurie JM, et al.: Clonal genetic alterations in the lungs of current and former smokers. J Natl Cancer Inst 89 (12): 857-62, 1997.
Wistuba II, Lam S, Behrens C, et al.: Molecular damage in the bronchial epithelium of current and former smokers. J Natl Cancer Inst 89 (18): 1366-73, 1997.