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• W1988030425 abstract "Epidemiological studies strongly suggest associations between chronic exposure to endogenous oestrogens and the development of breast and gynaecological tumours. Two mechanisms by which 17 beta-oestradiol (E2) may enhance tumorigenesis are: (i) enhancement of cell proliferation and (ii) the production of reactive, genotoxic metabolites. Here we suggest an additional mechanism, inhibition of DNA repair. The removal of UV-induced thymine dimers from human keratinocytes, reflective of nucleotide excision repair, was significantly attenuated by treatment of cells with E2. In contrast, treatment with 17 alpha-oestradiol had no effect. Mechanisms are proposed for this effect of E2, which may contribute to its carcinogenic potential." @default.
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• W1988030425 date "2003-01-10" @default.
• W1988030425 modified "2023-10-10" @default.
• W1988030425 title "17β-Oestradiol attenuates nucleotide excision repair" @default.
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• W1988030425 doi "https://doi.org/10.1016/s0014-5793(02)03898-x" @default.
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