Biology of castration-recurrent prostate cancer

Faris Azzouni; James Mohler

doi:10.1016/j.ucl.2012.07.002

Biology of castration-recurrent prostate cancer

Urol Clin North Am. 2012 Nov;39(4):435-52. doi: 10.1016/j.ucl.2012.07.002. Epub 2012 Aug 27.

Authors

Faris Azzouni¹, James Mohler

Affiliation

¹ Department of Urology, Roswell Park Cancer Institute, Buffalo, NY 14263, USA. faris.azzouni@roswellpark.org

PMID: 23084522
DOI: 10.1016/j.ucl.2012.07.002

Abstract

Although androgen-deprivation therapy is the standard therapy for advanced and metastatic prostate cancer, this treatment is only palliative. Prostate cancer recurs then grows despite low circulating testicular androgens, using several mechanisms that remain dependent on androgen-receptor signaling in most cases. This article reviews the diversity of mechanisms used for growth by castration-recurrent prostate cancer.

Publication types

Review

MeSH terms

Androgen Antagonists / therapeutic use
Antineoplastic Agents / pharmacology
Gene Amplification
Gene Expression Regulation, Neoplastic / physiology
Humans
Male
Neoplasm Recurrence, Local / pathology
Neoplasm Recurrence, Local / physiopathology*
Neoplasms, Hormone-Dependent / physiopathology*
Prostate / chemistry
Prostatic Neoplasms / drug therapy
Prostatic Neoplasms / genetics
Prostatic Neoplasms / metabolism
Prostatic Neoplasms / pathology
Prostatic Neoplasms / physiopathology*
Protein Isoforms / physiology
Receptors, Androgen / biosynthesis
Receptors, Androgen / drug effects
Receptors, Androgen / physiology*
Testosterone / biosynthesis
Transcriptional Activation / physiology

Substances

Androgen Antagonists
Antineoplastic Agents
Protein Isoforms
Receptors, Androgen
Testosterone