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• W2085698963 startingPage "370" @default.
• W2085698963 abstract "Recent clinical trials suggest that tamoxifen (TAM) is a preventive agent for breast cancer, however, the mechanism is unknown. Previously, we found that both 17beta-estradiol (E2) and estrone (E1) could be activated by epoxidation resulting in their ability to bind to DNA, forming DNA adducts both in vitro and in vivo, and to inhibit nuclear DNA-dependent RNA synthesis. Since epoxidation is required for the activation of many well-known chemical carcinogens including benzo(a)pyrene, 7,12-dimethylbenz(a)anthracene, aflatoxins, etc., we proposed that estrogen epoxidation is the underlying mechanism for the initiation of breast cancer (Carcinogenesis 17 (1996) 1957). Here, we report that TAM is able to dramatically inhibit the formation of E2 and E1 epoxides as measured by both the loss of their ability to inhibit nuclear DNA-dependent RNA synthesis and to bind to nuclear DNA. These findings suggest that the breast cancer preventive effect of TAM may be through a competitive epoxidation inhibition mechanism that prevents the formation of E2 and E1 epoxides and consequently, the initiation of breast cancer." @default.
• W2085698963 created "2016-06-24" @default.
• W2085698963 creator A5055174558 @default.
• W2085698963 creator A5035287609 @default.
• W2085698963 date "2002-11-01" @default.
• W2085698963 modified "2023-09-30" @default.
• W2085698963 title "A proposed mechanism of tamoxifen in breast cancer prevention" @default.
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• W2085698963 doi "https://doi.org/10.1016/s0361-090x(02)00124-1" @default.
• W2085698963 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/12518867" @default.
• W2085698963 hasPublicationYear "2002" @default.
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