Abstract
Globally, lung cancer is the leading cause of cancer death accounting for nearly one million deaths each year (1). In the United States, lung cancer accounts for approx 13% of all incident cases and 28% of all cancer deaths (2). It has been estimated that 90% of male lung cancer deaths and over 75% of female lung cancer deaths in the U.S. are caused by cigarette smoking (3,4). Thus, elucidating the mechanisms of tobacco-induced lung cancer could lead to new strategies for decreasing lung cancer risk, for identifying susceptible individuals, and for developing innovative techniques for early detection (4). One such mechanism that has been intensively investigated is the structure, function, and end-point effects of genetic polymorphisms in human metabolic genes.
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Wu, X., Schabath, M.B., Spitz, M.R. (2003). Myeloperoxidase Promoter Region Polymorphism and Lung Cancer Risk. In: Driscoll, B. (eds) Lung Cancer. Methods in Molecular Medicineā¢, vol 75. Humana Press, Totowa, NJ. https://doi.org/10.1385/1-59259-324-0:121
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DOI: https://doi.org/10.1385/1-59259-324-0:121
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