作者: N T Telang , M Katdare , H L Bradlow , M P Osborne
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摘要: The natural estrogen 17beta-estradiol (E2) has a profound influence on proliferation and neoplastic transformation of mammary epithelium. role cellular metabolism E2 in carcinogenesis, however, remains to be elucidated. Explant culture cell models developed from noncancerous human tissue were used examine modulation response treatment with prototype rodent carcinogens the ability naturally occurring phytochemical indole-3-carbinol (13C) regulate aberrant proliferation. In two models, chemical 7,12-dimethylbenz[a]anthracene benzo[a]pyrene altered as determined radiometric (tritium release) gas chromatography-mass spectrometry (GC-MS) assays. This alteration was accompanied by abrogation apoptosis extent replicative DNA synthesis, S-phase fraction Sub G0 (apoptotic) peak. Exposure carcinogen-initiated cultures 13C resulted induction C2-hydroxylation downregulation hyperproliferation. Determination initiators modulators carcinogenesis evaluation cycle related markers for may provide mechanism-oriented approach validate an endocrine biomarker prevention carcinogenesis.