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The Main Types Of Lung Cancer

982 words - 4 pages

Lung cancer is a disease of uncontrolled cell growth in tissues of the lung. This growth may lead to metastasis to adjacent tissues and infiltration beyond the lungs. The majority of primary lung cancers are derived from epithelial cells. Lung cancer is the most common cause of cancer-related death in men and women, and is responsible for 1.3 million deaths worldwide annually, as of 2004 (37).

The main types of lung cancer are small cell lung carcinoma (SCLC) and non-small cell lung carcinoma (NSCLC). Depending on the type of lung cancer, the treatment varies: NSCLC is sometimes treated with surgery, while SCLC often responds better to chemotherapy and radiation (38). The most common ...view middle of the document...

Cigarette smoking causes 30% of all cancer mortality in developed countries (51).6.

4-(methylnitrosamino)-1-(30pyridyl)-1-butanone (NNK) is arguably one of the most important carcinogens in tobacco products. There is a considerable amount of evidence indicating that this tobacco-specific amine is one cause of lung cancer in smokers. NNK requires metabolic activation to form DNA adducts that are critical for its carcinogenicity (52). Moreover, polycyclic aromatic hydrocarbons (PAHs) are also widely regarded as important causes of lung cancer. In addition to the activation pathways, there are competing detoxification pathways which lead to harmless excretion of NNK and PAHs. Multiple cytochrome P450 (CYP) enzymes and phase II enzumes are involved in the metabolic activation and detoxification of NNK, its major metabolite 4-(Methylnitrosamino)-1-(3-Pyridyl)-1-Butanol (NNAL) and PAHs (52-54).
Most of the chemical carcinogens in the environment are chemically inert in themselves and require metabolic activation by CYP enzymes to more reactive metabolites in order to exhibit carcinogenicity in experimental animals and humans (55, 56). Of the 17 families of human CYPs identified to date, the CYP1, 2, and 3 family membes play major roles in the metabolic activation of a variety of environmental carcinogens. It has been implicated that CYP1A1 and CYP1B1 activate most PAHs to epoxide intermediates, which are then converted to more reactive diol-epoxides with the aid of epoxide hydrolase (55, 57). Both CYP1A1 and CYP1B1 are expressed mainly in extrahepatic organs and thus make a major contribution to the incidence of cancers in those organs, when PAHs and other carcinogens are ingested into animal‘s body (57). PAHs and polyhalogenated hydrocarbons such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) induce several xenobiotic-metabolizing enzymes, including CYP1A1 and CYP1B1, through the arylhydrocarbon receptor (AhR) and the increased synthesis of these enzymes, as well as genetic variations in CYP1A1 and CYP1B1 genes, may determine difference in susceptibility of individuals to carcinogenesis caused by PAHs and other carcinogens.
CYP1B1 metabolizes numerous PAHs,...

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