Small cell lung cancer (SCLC) accounts for approximately 15% of bronchogenic carcinomas.
At the time of diagnosis, approximately 30% of patients with SCLC will have tumors confined to the hemithorax of origin, the mediastinum, or the supraclavicular lymph nodes. These patients are designated as having limited-stage disease (LD). Patients with tumors that have spread beyond the supraclavicular areas are said to have extensive-stage disease (ED).
SCLC is more responsive to chemotherapy and radiation...
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 2014 alone, it is estimated that there will be 224,210 new cases diagnosed, and 72,330 women and 86,930 men will die from this disease. The lung cancer death rate rose rapidly over several decades in both sexes, with a persistent decline for men commencing in 1991. From 2006 to 2010, death rates decreased by 2.9% per year in men and by 1.4% per year in women.
The most important risk factor for lung cancer (as 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 lung cancer. 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]
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.