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Journals The FASEB Journal Volume 23 Issue 5

Regarding “Prostatic hormonal carcinogenesis is mediated by in situ estrogen production and estrogen receptor alpha signaling” A. Edward Friedman 1 Department of Mathematics, University of Chicago, Chicago, Illinois, USA 1 Correspondence: Department of Mathematics, University of Chicago, 5734 S. University Ave., Chicago, IL 60637, USA. E-mail: ed@math.uchicago.edu Ricke et al. (1) ⇓ presented elegant evidence that the presence of estrogen receptor-α is essential for hormonal carcinogenesis in prostate cancer. This is consistent with my model (2) ⇓ for prostate cancer, which concluded that hormonal carcinogenesis in vivo might be initiated by the binding of estradiol (E 2 ) to estrogen receptor-α homodimers as well as by the binding of E 2 to estrogen receptor-αβ heterodimers. If high local levels of E 2 can initiate prostate cancer, then aromatase activity must be involved, as aromatase converts testosterone to E 2 . Although aromatase activity is not present in normal prostate epithelial cells, it is present in prostate cancer cell lines (3) ⇓ and in almost all prostate cancer tumors (4) ⇓ . If aromatase is not present in normal prostate cells as a result of methylation of the DNA comprising the aromatase gene, then this might explain why prostate

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Regarding “Prostatic hormonal carcinogenesis is mediated by in situ estrogen production and estrogen receptor alpha signaling”

Friedman, A. Edward
The FASEB Journal , Volume 23 (5): 1285
Fed of American Socs for Experimental Biology – May 1, 2009

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