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Updated: May 17, 2026

A Bioluminescent and Fluorescent Orthotopic Syngeneic Murine Model of Androgen-dependent and Castration-resistant Prostate Cancer
Published on: March 6, 2018
Targeted therapies in metastatic castration-resistant prostate cancer: beyond the androgen receptor
Yohann Loriot1, Amina Zoubeidi, Martin E Gleave
1Vancouver Prostate Centre, University of British Columbia, Vancouver, British Columbia, Canada.
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.
Insights
Prostate cancer often progresses to castration-resistant prostate cancer (CRPC). This review explores novel therapeutic targets beyond androgen receptor signaling, including tubulin and DNA repair pathways, for CRPC treatment.
Area of Science:
- Oncology
- Molecular Biology
- Pharmacology
Background:
- Prostate cancer is a leading cause of cancer-related death in men.
- Androgen deprivation therapy is a common initial treatment for prostate cancer.
- Castration-resistant prostate cancer (CRPC) eventually develops, driven by androgen receptor signaling and other pathways.
Purpose of the Study:
- To review preclinical data and clinical trial status for novel therapeutic targets in CRPC.
- To explore targets beyond the androgen receptor signaling pathway.
Main Methods:
- Literature review of preclinical studies.
- Analysis of current clinical trial data.
- Focus on therapeutic targets including tubulin, DNA repair, molecular chaperones (CLU, Hsp27), and tyrosine kinases.
Main Results:
- Androgen receptor signaling is a key driver in CRPC.
- Emerging evidence indicates involvement of other pathways in CRPC progression.
- Multiple novel therapeutic targets are under investigation in clinical trials.
Conclusions:
- Targeting pathways beyond androgen receptor signaling holds promise for CRPC treatment.
- Further research and clinical trials are necessary to validate these novel therapeutic strategies.
- Developing new treatments for CRPC is crucial to improve patient outcomes.
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