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Updated: Jun 4, 2026

A New Technique for Treating Low-risk Prostate Cancer—Super Active Surveillance
Published on: November 7, 2025
Castration-resistant prostate cancer: targeted therapies and individualized treatment
Rahul Aggarwal1, Charles J Ryan
1Department of Medicine, University of California, San Francisco, CA 94143-1270, USA. Rahul.Aggarwal@ucsf.edu
Abstract:
Various molecular mechanisms have been implicated in the progression from hormone-sensitive to castration-resistant prostate cancer (CRPC). Novel targeted agents to treat CRPC have been developed that inhibit either androgen receptor (AR)-mediated signaling (AR antagonists and inhibitors of androgen synthesis) or non-AR-mediated signaling (inhibitors of Src, mammalian target of rapamycin, chaperone proteins, insulin-like growth factor-1 receptor, vascular endothelial growth factor, and endothelin-A receptor) pathways. However, variable efficacy has been observed in clinical trials, most likely because of the biologic heterogeneity of CRPC. To account for potential differences in disease biology, a more individualized approach to treatment, based on genomic and/or proteomic analyses of individual tumors, is being investigated. By identifying tumors with a characteristic molecular subtype and assigning treatment accordingly, it is hoped that a higher proportion of patients will benefit from targeted therapy. Additionally, lessons learned through the application of these technologies to prostate cancer may subsequently influence therapeutic development in other solid tumors.
Insights
Castration-resistant prostate cancer (CRPC) treatment faces challenges due to tumor heterogeneity. Personalized medicine using genomic and proteomic analyses aims to improve targeted therapy efficacy for CRPC patients.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Hormone-sensitive prostate cancer progresses to castration-resistant prostate cancer (CRPC) through various molecular mechanisms.
- Novel targeted agents for CRPC inhibit androgen receptor (AR)-mediated signaling or non-AR pathways.
- Variable efficacy of current CRPC treatments is attributed to the biologic heterogeneity of the disease.
Purpose of the Study:
- To investigate an individualized treatment approach for CRPC based on molecular profiling.
- To determine if matching treatments to specific molecular subtypes of CRPC can improve patient outcomes.
- To explore the potential of genomic and proteomic analyses in guiding CRPC therapy.
Main Methods:
- Review of molecular mechanisms driving CRPC progression.
- Analysis of targeted agents inhibiting AR-mediated and non-AR-mediated signaling pathways.
- Investigation of genomic and proteomic analyses for tumor subtyping.
Main Results:
- CRPC exhibits significant biologic heterogeneity, impacting treatment efficacy.
- Targeted agents show variable efficacy, necessitating refined treatment strategies.
- Individualized treatment based on molecular subtypes is under investigation.
Conclusions:
- Personalized medicine approaches, utilizing genomic and proteomic data, hold promise for improving CRPC treatment.
- Identifying molecular subtypes can lead to more effective targeted therapy selection.
- Insights from CRPC research may inform therapeutic development for other solid tumors.
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