General reviewEffects of various inducers on diethylstilbestrol metabolism, drug-metabolizing enzyme activities and the aromatic hydrocarbon (Ah) receptor in male syrian golden hamster liver☆
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The molecular etiology and prevention of estrogen-initiated cancers: Ockham's Razor: Pluralitas non est ponenda sine necessitate. Plurality should not be posited without necessity
2014, Molecular Aspects of MedicineCitation Excerpt :Oxidation of catechol estrogens to semiquinones and then to quinones is a pathway that can initiate cancer by natural estrogens, as well as synthetic estrogens such as the human carcinogen DES (Herbst et al., 1971) and its hydrogenated derivative HES. These compounds, similarly to the natural estrogens, are carcinogenic in the kidney of Syrian golden hamsters (Li et al., 1983; Liehr et al., 1985); the major metabolites are their catechols (Blaich et al., 1990; Haaf and Metzler, 1985; Liehr et al., 1985; Metzler and McLachlan, 1981). The catechols are easily oxidized to catechol quinones.
Catechol estrogen quinones as initiators of breast and other human cancers: Implications for biomarkers of susceptibility and cancer prevention
2006, Biochimica et Biophysica Acta - Reviews on CancerNovel spiro-quinone formation from 3′-hydroxydiethylstilbestrol after oxidation with silver oxide
2005, Tetrahedron Letters
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This paper was presented at the 2nd Turku Symposium on Environmental Estrogens on June 9 1987, and is dedicated to Professor D. Henschler on the occasion of his 65th birthday.