Epidemiological studies strongly suggest associations between chronic exposure to endogenous oestrogens and the development of breast and gynaecological tumours. Two mechanisms by which 17L L-oestradiol (E 2 ) 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, re£ec-tive of nucleotide excision repair, was signi¢cantly attenuated by treatment of cells with E 2 . In contrast, treatment with 17K Koestradiol had no e¡ect. Mechanisms are proposed for this effect of E 2 , which may contribute to its carcinogenic potential.
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