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. Author manuscript; available in PMC: 2016 Aug 17.
Published in final edited form as: Chem Res Toxicol. 2015 Jul 16;28(8):1584–1594. doi: 10.1021/acs.chemrestox.5b00157

Figure 1. Hypothesis: effect of botanicals on inflammation-stimulated estrogen chemical carcinogenesis.

Figure 1

Inflammation potentiates estrogen chemical carcinogenesis through activation of transcription factor NF-κB which up-regulates estrogen metabolizing enzyme P450 1B1 that is classically regulated by AhR (figure has been simplified for clarity). P450 1B1 increases the estrogen metabolite 4-OHE1 which redox cycles with the genotoxic estrogen quinone 4-OHE1-Q to form ROS. E2 (not shown for clarity) is similarly metabolized to genotoxic metabolites. The hypothesis is that, to prevent estrogen carcinogenesis, several steps in the inflammation-stimulated estrogen carcinogenesis pathway could be modulated by chemopreventive botanicals, as indicated with green arrows.