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Pharmacogenetics of Lung Cancer

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Lung Cancer

Part of the book series: Current Clinical Oncology ((CCO))

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Abstract

Lung cancer is the most commonly diagnosed cancer and the leading cause of cancer-related death in the United States and around the world. Smoking is the predominant cause of lung cancer and also affects treatment response and survival of lung cancer patients. There is compelling evidence supporting a genetic susceptibility to lung cancer. A family history of lung cancer increases the relative risk of lung cancer by approximately 1.8-fold. The associations between common genetic polymorphisms and the risk of lung cancer have been firmly established through candidate gene studies and genome-wide association studies. Genetic polymorphisms may not only directly affect lung cancer susceptibility through their functional impact on genes involved in processes of tobacco-induced carcinogenesis, including carcinogen metabolism and DNA damage response, but also indirectly influence lung cancer risk through their effect on nicotine addiction and other risk behavior. The same genes that are implicated in lung cancer risk may also be involved in the modulation of clinical outcome. For example, tobacco carcinogen metabolism genes may affect cancer risk and clinical outcome due to the dual role of smoking in lung cancer etiology and outcome, and genes involved in repairing DNA-carcinogen adducts are also responsible for removing DNA-cisplatin complex and therefore can impact chemotherapy response. This chapter summarizes current knowledge of genetic susceptibility to lung cancer and genetic determinants of lung cancer clinical outcomes, focusing on pharmacogenetics of platinum-based chemotherapy and genetic predictors of radiotherapy response and toxicity.

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Wu, X., Gu, J. (2010). Pharmacogenetics of Lung Cancer. In: Stewart, D. (eds) Lung Cancer. Current Clinical Oncology. Humana Press, Totowa, NJ. https://doi.org/10.1007/978-1-60761-524-8_4

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