Abstract
Arsenic is a carcinogen to which alarmingly large numbers of people are chronically exposed (Tseng et al., 1968; US Environmental Protection Agency, 1980; Smith et al., 1992). Human exposure to arsenic has been documented in large ecological and epidemiologic studies, and there is little question that such exposure is associated with elevated numbers of cancers (Tseng et al., 1968; Enterline et al., 1995). Most disheartening, though, is the fact that a unified and cogent hypothesis for the mechanism of action of arsenic as a carcinogen has not been advanced, and the factors that govern individual susceptibility to arsenic carcinogenesis are not known. Further, although we have comprehended how arsenic acts as a poison for many years (Fowler, 1991), whether or not this mode of action is related to its carcinogenicity is unknown, and cannot be directly tested given the fact that an animal model for arsenic carcinogenesis that is relevant to human exposure scenarios has not been thoroughly validated.
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Mass, M.J., Wang, L. (1997). Alterations of methylation of the tumor suppressor gene p53: insights into potential mechanisms of arsenic carcinogenesis. In: Abernathy, C.O., Calderon, R.L., Chappell, W.R. (eds) Arsenic. Springer, Dordrecht. https://doi.org/10.1007/978-94-011-5864-0_27
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DOI: https://doi.org/10.1007/978-94-011-5864-0_27
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