Arl-Hydrocarbon Receptor Based Antiestrogenicity of Diindolylmethane Analogs
Annual summary 1 Aug 1999-31 Jul 2002
TEXAS A AND M RESEARCH FOUNDATION COLLEGE STATION
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Research in our laboratory has been focused on the mechanism of inhibitory aryl hydrocarbon Ah receptor-estrogen receptor a ER alpha crosstalk in breast cancer cells, and results indicate that Ah receptor agonists inhibit estrogen E2-induced gene expression and cell proliferation 1,2. Moreover, 2,3,7,8-tetrachlorodibenzo-p-dioxin TCDD, a high affinity ligand for the Ah receptor, inhibits age-dependent and carcinogen-induced mammary tumor formation and growth in female Sprague-Dawley rats, and a recent study reported that women accidentally exposed to TCDD in Seveso, Italy, over 20 years ago exhibit lower incidence rates of breast and endometrial cancer 3. Studies on various structural classes of AhR agonists have identified alternate substituted 1 ,3,6,8- or 2,4,6,8- alkyl polychlorinated dibenzofurans PCDFs and substituted diindolylmethanes DlMs as selective Ah receptor modulators SAhRMs that are relative nontoxic but inhibit mammary tumor growth in rodent models 4. With financial support from this grant, I have been investigating the indirect antiestrogenic activity of substituted DIMs and applications of these compounds for treating mammary cancer 5-7.
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