New hormonal therapies for castration-resistant prostate cancer

Endocrinol Metab Clin North Am. 2011 Sep;40(3):625-42, x. doi: 10.1016/j.ecl.2011.05.013. Epub 2011 Jul 14.

Abstract

Continued activation of the androgen receptor (AR) axis despite castration remains a critical force in the development of castration-resistant prostate cancer (CRPC). Therapeutic strategies designed to more effectively ablate tumoral androgen activity are required to improve clinical efficacy and prevent disease progression. Tumor-based alterations in expression and activity of the AR and in steroidogenic pathways mediating ligand generation facilitate the development of CRPC. This article reviews AR and ligand-dependent mechanisms underlying CRPC progression and the status of novel hormonal therapies targeting the AR axis that are currently in clinical and preclinical development.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.
  • Review

MeSH terms

  • Adenocarcinoma / drug therapy*
  • Adenocarcinoma / genetics
  • Adenocarcinoma / surgery
  • Androgen Antagonists / therapeutic use*
  • Animals
  • Antineoplastic Agents, Hormonal / therapeutic use*
  • Gene Expression Regulation, Neoplastic / drug effects
  • Humans
  • Male
  • Models, Biological
  • Orchiectomy
  • Prostatic Neoplasms / drug therapy*
  • Prostatic Neoplasms / genetics
  • Prostatic Neoplasms / surgery
  • Receptors, Androgen / genetics
  • Receptors, Androgen / metabolism
  • Treatment Failure

Substances

  • Androgen Antagonists
  • Antineoplastic Agents, Hormonal
  • Receptors, Androgen