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- W2801476327 endingPage "25" @default.
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- W2801476327 abstract "The standard paradigm providing a general mechanistic explanation for the association of cumulative, excessive estrogen exposure and breast cancer risk is that estrogen and perhaps progesterone affect the rate of cell division, and thus manifest their effect on the risk of breast cancer by causing proliferation of breast epithelial cells. Proliferating cells are susceptible to genetic errors during DNA replication which, if uncorrected, can ultimately lead to a malignant phenotype. This standard paradigm has recently been expanded to encompass emerging research data supporting a complementary genotoxic pathway mediated by the generation and redox cycling of reactive oxygen species through the metabolic effects of estrogens metabolites such 4 and 16a-hydroxy catechols. This paradigm shift is necessitated by evidence of estrogen induced carcinogenesis in several animal and human models following exposure to these estrogen metabolites. This review examines some of the available evidence relating these estrogen metabolites to animal and human breast carcinogenesis African Journal of Reproductive Health Vol. 10 (1) 2006: pp. 13-25" @default.
- W2801476327 created "2018-05-17" @default.
- W2801476327 creator A5019795255 @default.
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- W2801476327 date "2006-04-01" @default.
- W2801476327 modified "2023-09-28" @default.
- W2801476327 title "Estrogen metabolism and breast cancer risk--a review." @default.
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- W2801476327 doi "https://doi.org/10.4314/ajrh.v10i1.7872" @default.
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