Bisphenol A facilitates bypass of androgen ablation therapy in prostate cancer.

Bisphenol A facilitates bypass of androgen ablation therapy in prostate cancer. Research Abstract Details 

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Bisphenol A facilitates bypass of androgen ablation therapy in prostate cancer. Abstract Text:

Yelena B Wetherill,Janet K Hess-Wilson,Clay E S Comstock,Supriya A Shah,C Ralph Buncher,Larry Sallans,Patrick A Limbach,Sandy Schwemberger,George F Babcock,Karen E Knudsen,Yelena B Wetherill,Janet K Hess-Wilson,Clay E S Comstock,Supriya A Shah,C Ralph Buncher,Larry Sallans,Patrick A Limbach,Sandy Schwemberger,George F Babcock,Karen E Knudsen,

Prostatic adenocarcinomas depend on androgen for growth and survival. First line treatment of disseminated disease exploits this dependence by specifically targeting androgen receptor function. Clinical evidence has shown that androgen receptor is reactivated in recurrent tumors despite the continuance of androgen deprivation therapy. Several factors have been shown to restore androgen receptor activity under these conditions, including somatic mutation of the androgen receptor ligand-binding domain. We have shown previously that select tumor-derived mutants of the androgen receptor are receptive to activation by bisphenol A (BPA), an endocrine-disrupting compound that is leached from polycarbonate plastics and epoxy resins into the human food supply. Moreover, we have shown that BPA can promote cell cycle progression in cultured prostate cancer cells under conditions of androgen deprivation. Here, we challenged the effect of BPA on the therapeutic response in a xenograft model system of prostate cancer containing the endogenous BPA-responsive AR-T877A mutant protein. We show that after androgen deprivation, BPA enhanced both cellular proliferation rates and tumor growth. These effects were mediated, at least in part, through androgen receptor activity, as prostate-specific antigen levels rose with accelerated kinetics in BPA-exposed animals. Thus, at levels relevant to human exposure, BPA can modulate tumor cell growth and advance biochemical recurrence in tumors expressing the AR-T877A mutation.

Bisphenol A facilitates bypass of androgen ablation therapy in prostate cancer. Publishing Authors By Initials

YB Wetherill,JK Hess-Wilson,CE Comstock,SA Shah,CR Buncher,L Sallans,PA Limbach,S Schwemberger,GF Babcock,KE Knudsen,YB Wetherill,JK Hess-Wilson,CE Comstock,SA Shah,CR Buncher,L Sallans,PA Limbach,S Schwemberger,GF Babcock,KE Knudsen,

For similar xenograft model antitumor assays research abstracts see: xenograft model antitumor assays research

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Bisphenol A facilitates bypass of androgen ablation therapy in prostate cancer. Journal Published:

PUBLICATION TYPE: Research Support, N.I.H., Extr

Journal: Molecular cancer therapeutics

VOLUME: 5

Page Numbers: 3181-90

Journal Abbreviation: Mol. Cancer Ther.

ISSN: 1535-7163

DAY: 3

MONTH: Dec

YEAR: 2006

Bisphenol A facilitates bypass of androgen ablation therapy in prostate cancer. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 101132535

Bisphenol A facilitates bypass of androgen ablation therapy in prostate cancer. Keywords Mesh Terms:

KEYWORDS: Xenograft Model Antitumor Assays

MESH TERMS: antagonists & inhibitors

Chemical & Substance for Abstract: Bisphenol A facilitates bypass of androgen ablation therapy in prostate cancer. Information

Substance Name: bisphenol A

Registry Number: 80-05-7

Grant and Affiliation Information for Bisphenol A facilitates bypass of androgen ablation therapy in prostate cancer.

AFFILIATION: Department of Cell and Cancer Biology, Vontz Center for Molecular Studies, University of Cincinnati College of Medicine, 3125 Eden Avenue, ML 0521, Cincinnati, OH 45267-0521, USA.

Country: United States

AGENCY: United States NCRR

GRANT: RR019900

ACRONYM: RR

MEDLINETA: Mol Cancer Ther

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