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Updated: Jun 22, 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

Development of androgen receptor antagonists with promising activity in castration-resistant prostate cancer

Howard C Shen1, Steven P Balk

  • 1Department of Medicine, Hematology-Oncology Division, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02115, USA.

Cancer Cell
|May 30, 2009
PubMed

Insights

A new drug prevents androgen receptor (AR) binding in prostate cancer cells, showing promise for treating relapsed cancers resistant to current therapies.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Androgen receptor (AR) signaling is crucial in prostate cancer development and progression.
  • Prostate cancers often relapse after androgen deprivation therapy (ADT), becoming resistant to existing AR antagonists.
  • Understanding AR's role in refractory tumors is critical for developing new treatments.

Purpose of the Study:

  • To identify and characterize a novel antagonist targeting the androgen receptor (AR).
  • To evaluate the efficacy of this new antagonist in preclinical models of relapsed prostate cancer.

Main Methods:

  • Utilized molecular biology techniques to develop and test a novel AR antagonist.
  • Assessed the antagonist's ability to inhibit AR recruitment to chromatin.
  • Evaluated the therapeutic efficacy in relevant prostate cancer models.

Main Results:

  • The novel antagonist effectively prevents AR recruitment to chromatin.
  • Demonstrated significant efficacy in treating prostate cancer models that have relapsed after ADT.
  • Indicated a potential mechanism for overcoming resistance to current therapies.

Conclusions:

  • A new AR antagonist shows therapeutic potential for refractory relapsed prostate cancer.
  • Inhibiting AR chromatin recruitment offers a viable strategy against treatment-resistant tumors.
  • Further research is warranted to translate these findings into clinical applications.

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