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Steroid Sulfatase Stimulates Intracrine Androgen Synthesis and is a Therapeutic Target for Advanced Prostate Cancer
Author(s) -
Cameron M. Armstrong,
Chengfei Liu,
Joy C. Yang,
Wei Lou,
Renliang Zhao,
Shu Ning,
Alan P. Lombard,
Jinge Zhao,
Leandro S. D’Abronzo,
Christopher P. Evans,
Pui-Kai Li,
Allen C. Gao
Publication year - 2020
Publication title -
clinical cancer research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.427
H-Index - 324
eISSN - 1557-3265
pISSN - 1078-0432
DOI - 10.1158/1078-0432.ccr-20-1682
Subject(s) - enzalutamide , intracrine , prostate cancer , androgen receptor , cancer research , androgen , cancer , antiandrogen , lncap , medicine , biology , endocrinology , receptor , hormone , paracrine signalling
Most patients with prostate cancer receiving enzalutamide or abiraterone develop resistance. Clinical evidence indicates that serum levels of dehydroepiandrosterone sulfate (DHEAS) and biologically active DHEA remain in the high range despite antiandrogen treatment. The conversion of DHEAS into DHEA by steroid sulfatase (STS) may contribute to sustained intracrine androgen synthesis. Here, we determine the contribution of STS to treatment resistance and explore the potential of targeting STS to overcome resistance in prostate cancer.

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