Targeted therapies in metastatic castration-resistant prostate cancer: beyond the androgen receptor

Urol Clin North Am. 2012 Nov;39(4):517-31. doi: 10.1016/j.ucl.2012.07.008. Epub 2012 Sep 1.

Abstract

Prostate cancer is the most common male cancer and one of the top causes of male cancer-related death in Western countries. Most patients with prostate cancer respond to initial androgen deprivation therapy but eventually progress to castration-resistant prostate cancer (CRPC). Although androgen receptor signaling remains the main driver in CRPC, a growing body of evidence suggests that other pathways are involved in this progression. This article reviews the preclinical data and current status of clinical trials therapeutically targeting tubulin, DNA repair, molecular chaperones such as CLU and Hsp27, tyrosine kinases, and DNA repair.

Publication types

  • Review

MeSH terms

  • Bone Neoplasms / drug therapy*
  • Cell Proliferation / drug effects
  • Cell Survival / drug effects
  • Cell Survival / physiology
  • DNA Repair / physiology
  • Dasatinib
  • Disease Progression
  • Epothilones / pharmacology
  • Epothilones / therapeutic use
  • Gene Fusion
  • Humans
  • Male
  • Neoplasm Invasiveness
  • Prostatic Neoplasms / drug therapy*
  • Prostatic Neoplasms / physiopathology
  • Prostatic Neoplasms / secondary*
  • Proto-Oncogene Proteins c-met / physiology
  • Pyrimidines / pharmacology
  • Pyrimidines / therapeutic use
  • Receptors, Androgen / physiology
  • Taxoids / pharmacology
  • Thiazoles / pharmacology
  • Thiazoles / therapeutic use

Substances

  • Epothilones
  • Pyrimidines
  • Receptors, Androgen
  • Taxoids
  • Thiazoles
  • cabazitaxel
  • MET protein, human
  • Proto-Oncogene Proteins c-met
  • ixabepilone
  • Dasatinib