Abstract: |
Background: Estrogens are potent mammary tumor promoters influencing post-initiational events via epigenetic mechanisms. The upregulation (i.e., induction) of the C16α-hydroxylation pathway during 17β-estradiol (E2) biotransformation has been associated with mammary cell transformation. The action of E2 metabolites on tumorigenic transformation, however, is poorly understood. Purpose: The newly established mammary epithelial cell line C57/MG, derived from the C57BL mouse strain, was used to examine whether E2 or its metabolites, 16-hydroxyestrone (16α-OHE1) and estriol (E3), function as initiators of mammary cell transformation. Methods: DNA repair (hydroxyurea-insensitive thymidine uptake), estrogen metabolism (3H exchange to form 3H20), hyperproliferation (increased cell number), and acquisition of anchorage-independent © 1992 Oxford University Press. |
Keywords: |
controlled study; nonhuman; dna synthesis; animal cell; mouse; animal; mice; cell division; dna repair; cell growth; estrogen; tumor cells, cultured; mice, inbred c57bl; cell transformation, neoplastic; dimethyl sulfoxide; cell transformation; carcinogenicity; breast epithelium; estrogen receptor; estradiol; genotoxicity; mammary neoplasms, experimental; hydroxylation; estrogen metabolism; female; priority journal; article; support, non-u.s. gov't; support, u.s. gov't, p.h.s.; dimethylbenz[a]anthracene; 16alpha hydroxyestrone; estriol; hydroxyestrones
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