Yap, T. A., Carden, C. P., Attard, G., de Bono, J. S. (2008) Targeting CYP17: established and novel approaches in prostate cancer. CURRENT OPINION IN PHARMACOLOGY, 8 (4). pp. 449-457. ISSN 1471-4892

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Abstract

There is a growing body of evidence that although medical or surgical castration blocks the generation of gonadal testosterone in prostate cancer, androgens originating from other sources may continue to drive androgen receptor (AR) signaling. Recent studies have demonstrated high intratumoral levels of androgens and continued AR signaling in castration-resistant prostate cancer (CRPC), suggesting that androgens may also be synthesized de novo. Inhibiting the systemic biosynthesis of androgens in CRPC by targeting CYP17 may thus represent a rational therapeutic approach since this enzyme catalyses two key steroid reactions involving 17 alpha-hydroxylase and C-17,C-20-lyase in the androgen biosynthesis pathway. This review will discuss the rationale for and implications of targeting CYP17 in CRPC and focus on established and novel CYP17 inhibitors, including ketoconazole, abiraterone acetate, and VN/124-1, which are agents currently at different stages of development.

Item Type:	Review Article
Authors (ICR Faculty only):	De-Bono, Johann
All Authors:	Yap, T. A., Carden, C. P., Attard, G., de Bono, J. S.
Uncontrolled Keywords:	HUMAN CYTOCHROME P450(17-ALPHA); LEUKEMIA GROUP-B; ANDROGEN-RECEPTOR; STEROIDAL INHIBITORS; PHASE-II; ANTIANDROGEN WITHDRAWAL; STEROIDOGENIC ENZYMES; DOSE KETOCONAZOLE; IN-VITRO; PROGRESSION
Research teams:	ICR divisions > Cancer Therapeutics > Cancer Biomarkers ICR divisions > Clinical Studies > Cancer Biomarkers ICR divisions > Clinical Studies > Prostate Cancer Targeted Therapy Group
Depositing User:	Users 10 not found.
Date Deposited:	30 Oct 2008 12:10
Last Modified:	11 Jul 2017 10:31
URI:	http://publications.icr.ac.uk/id/eprint/7127

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