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• W135674329 endingPage "500" @default.
• W135674329 startingPage "477" @default.
• W135674329 abstract "While there is excellent concordance between the results of animal and human studies on known human carcinogens, the data are much less consistent for known animal carcinogens, There could be many reasons for this, First, there may have been inadequate study or length and magnitude of human exposure to demonstrate human susceptibility. A second major factor is the difference in the proportion of genotoxic and nongenotoxic agents among known human and animal carcinogens: the vast majority of known human carcinogens are genotoxic. Arecent survey by Shelby (1988) showed that 20 of23 known human carcinogens were genotoxic. A similar proportion of the expanded IARC list of human carcinogens (IARC, 1987) is genotoxic (Shelby & Zeiger, 1990). In contrast, roughly half of the much larger number ofrodent carcinogens are nongenotoxic (Ashby & Tenant, 1991). It is difficult to imagine that for only a few or none of these chemicals has there been adequate human exposure or epidemiological investigation to demonstrate human carcinogenicity. Unlike their genotoxic counterparts, the nongenotoxic agents usually induce neoplasia in rodents at maximum tolerated doses and rarely at doses one order of magnitude lower. Exceptions, such as tumour promotion by 2,3,7,8-tetrachlorodibenzo-para-dioxin, have been shown to work through a receptor-based mechanism. A principal mechanism for several nongenotoxic carcinogens is increased cell proliferation. While it has long been recognized that cell proliferation is required for both mutagenesis and carcinogenesis, its role is beginning to be better understood. Cell proliferation is required to 'fix' DNA damage into mutations, whether that damage is chemically induced by a genotoxic agent or spontaneous. Such spontaneous DNA damage is common, with 50000 to 250 000 such events occurring per cell per day (Loeb, 1989; US National Research Council, 1989). Most of these events are rapidly and efficiently repaired; when cell proliferation is increased, however, there is less time available for repair prior to DNA replication. Cell proliferation is also required for donal expansion of initiated ceIls, a mechanism that enhances the probability of additional genetic events taking place. These" @default.
• W135674329 created "2016-06-24" @default.
• W135674329 creator A5015944099 @default.
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• W135674329 date "1992-01-01" @default.
• W135674329 modified "2023-09-23" @default.
• W135674329 title "Species-specific mechanisms of carcinogenesis." @default.
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