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Updated: Jun 16, 2026

A Bioluminescent and Fluorescent Orthotopic Syngeneic Murine Model of Androgen-dependent and Castration-resistant Prostate Cancer
07:25

A Bioluminescent and Fluorescent Orthotopic Syngeneic Murine Model of Androgen-dependent and Castration-resistant Prostate Cancer

Published on: March 6, 2018

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

Karen E Knudsen1, Trevor M Penning

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

Trends in Endocrinology and Metabolism: TEM
|February 9, 2010
PubMed

Insights

Prostate cancer treatment faces challenges with advanced disease. This study explores how androgen receptor (AR) deregulation and altered androgen synthesis drive castration-resistant prostate cancer progression.

Area of Science:

  • Oncology
  • Endocrinology
  • Molecular Biology

Background:

  • Prostate cancer is a major cause of cancer mortality, with limited treatment options for advanced stages.
  • Current treatments target androgen receptor (AR) activity, but castration-resistant tumors eventually emerge.
  • Emerging evidence suggests that altered androgen synthesis pathways contribute to treatment resistance.

Purpose of the Study:

  • To discuss the mechanisms linking AR deregulation and aberrant androgen synthesis in prostate cancer.
  • To elucidate how these factors contribute to the progression of castration-resistant prostate cancer.
  • To provide insights into potential therapeutic targets for advanced prostate cancer.

Main Methods:

  • Review of current literature on prostate cancer progression.
  • Analysis of molecular mechanisms underlying AR activity and androgen synthesis.
  • Discussion of the interplay between AR signaling and androgen production pathways.

Main Results:

  • AR deregulation is a known driver of therapy resistance in prostate cancer.
  • Aberrant androgen synthesis pathways unexpectedly support AR activity in castration-resistant tumors.
  • The combination of AR deregulation and altered androgen synthesis promotes lethal prostate cancer progression.

Conclusions:

  • Understanding the dual role of AR deregulation and androgen synthesis is crucial for treating advanced prostate cancer.
  • Targeting both AR signaling and androgen production pathways may offer new therapeutic strategies.
  • Further research into these mechanisms is needed to develop durable treatments for prostate cancer.

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