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Updated: Jul 19, 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

Basic science of hormonal therapy for prostate cancer

D M Peehl

    Reviews in Urology
    |September 21, 2006
    PubMed

    Insights

    Androgen receptor (AR) alterations, not loss, drive most recurrent prostate cancers after treatment. Understanding these molecular changes is key to developing new strategies for managing cancer recurrence.

    Area of Science:

    • Molecular and cellular biology
    • Prostate cancer research
    • Genetics and genomics

    Background:

    • Androgen deprivation therapy (ADT) is a standard treatment for recurrent prostate cancer.
    • Molecular mechanisms of androgen action in prostate cancer are complex and evolving.
    • Recurrent prostate cancer often exhibits resistance to ADT.

    Purpose of the Study:

    • To investigate the molecular mechanisms underlying recurrent prostate cancer after ADT.
    • To clarify the role of the androgen receptor (AR) in treatment-resistant prostate cancer.
    • To identify novel therapeutic targets for managing prostate cancer recurrence.

    Main Methods:

    • Molecular profiling of recurrent prostate cancer tissues.
    • Analysis of genetic alterations in the androgen receptor (AR) pathway.
    • Investigation of cell survival and proliferation mechanisms.

    Main Results:

    • Loss of the AR does not explain androgen-independent growth in most recurrent cancers.
    • Overexpression, mutation, and ligand-independent activation of the AR are common.
    • These AR alterations enhance sensitivity to androgens or other growth factors.

    Conclusions:

    • The term "androgen-independent" is often a misnomer for recurrent prostate cancer.
    • Altered AR signaling, rather than AR loss, drives treatment resistance.
    • This emerging understanding informs new strategies to prevent or slow cancer recurrence.

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