Molecular pathogenesis and progression of prostate cancer

Semin Oncol. 2013 Jun;40(3):244-58. doi: 10.1053/j.seminoncol.2013.04.001.


Prostate cancer (PCa) is the most commonly diagnosed noncutaneous malignancy and second leading cause of cancer-related deaths in US males. Clinically, locally confined disease is treated surgically and/or with radiation therapy. Invasive disease, however, must be treated with pharmacological inhibitors of androgen receptor (AR) activity, since disease progression is fundamentally reliant on AR activation. However, despite initially effective treatment options, recurrent castration-resistant PCa (CRPC) often occurs due to aberrant reactivation of AR. Additionally, it is appreciated that many other signaling molecules, such as transcription factors, oncogenes, and tumor suppressors, are often perturbed and significantly contribute to PCa initiation and progression to incurable disease. Understanding the interplay between AR signaling and other signaling networks altered in PCa will advance therapeutic approaches. Overall, comprehension of the molecular composition promoting neoplastic growth and formation of CRPC is paramount for developing durable treatment options.

Publication types

  • Review

MeSH terms

  • Androgen Antagonists / pharmacology
  • Androgen Antagonists / therapeutic use
  • Androgens / biosynthesis
  • Animals
  • Antineoplastic Agents, Hormonal / pharmacology
  • Antineoplastic Agents, Hormonal / therapeutic use
  • Gene Amplification
  • Humans
  • Male
  • Mutation
  • Prostate / growth & development
  • Prostate / metabolism
  • Prostate / pathology
  • Prostatic Hyperplasia / genetics
  • Prostatic Hyperplasia / metabolism
  • Prostatic Hyperplasia / pathology*
  • Prostatic Neoplasms / drug therapy
  • Prostatic Neoplasms / genetics
  • Prostatic Neoplasms / metabolism
  • Prostatic Neoplasms / pathology*
  • Protein Processing, Post-Translational
  • Receptors, Androgen / genetics
  • Receptors, Androgen / metabolism
  • Signal Transduction


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