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Trends Endocrinol Metab. 2010 May;21(5):315-24. doi: 10.1016/j.tem.2010.01.002. Epub 2010 Feb 6.

Partners in crime: deregulation of AR activity and androgen synthesis in prostate cancer.

Author information

1
Kimmel Cancer Center, Department of Cancer Biology and Department of Urology, Thomas Jefferson University, Philadelphia, PA 19107, USA. karen.knudsen@kimmelcancercenter.org

Abstract

Prostate cancer remains a leading cause of cancer death, as there are no durable means to treat advanced disease. Treatment of non-organ-confined prostate cancer hinges on its androgen dependence. First-line therapeutic strategies suppress androgen receptor (AR) activity, via androgen ablation and direct AR antagonists, whereas initially effective, incurable, 'castration-resistant' tumors arise as a result of resurgent AR activity. Alterations of AR and/or associated regulatory networks are known to restore receptor activity and support resultant therapy-resistant tumor progression. However, recent evidence also reveals an unexpected contribution of the AR ligand, indicating that alterations in pathways controlling androgen synthesis support castration-resistant AR activity. In this report, the mechanisms underlying the lethal pairing of AR deregulation and aberrant androgen synthesis in prostate cancer progression will be discussed.

PMID:
20138542
PMCID:
PMC2862880
DOI:
10.1016/j.tem.2010.01.002
[Indexed for MEDLINE]
Free PMC Article

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