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Updated: Jul 19, 2026
A Bioluminescent and Fluorescent Orthotopic Syngeneic Murine Model of Androgen-dependent and Castration-resistant Prostate Cancer
Published on: March 6, 2018
Improving the outcome of patients with castration-resistant prostate cancer through rational drug development
1Cancer Research UK Centre for Cancer Therapeutics, Institute of Cancer Research, Royal Marsden Hospital, Sutton, Surrey SM2 5PT, UK.
Abstract:
Castration-resistant prostate cancer (CRPC) is now the second most common cause of male cancer-related mortality. Although docetaxel has recently been shown to extend the survival of patients with CRPC in two large randomised phase III studies, subsequent treatment options remain limited for these patients. A greater understanding of the molecular causes of castration resistance is allowing a more rational approach to the development of new drugs and many new agents are now in clinical development. Therapeutic targets include the adrenal steroid synthesis pathway, androgen receptor signalling, the epidermal growth factor receptor family, insulin growth factor-1 receptor, histone deacetylase, heat shock protein 90 and the tumour vasculature. Drugs against these targets are giving an insight into the molecular pathogenesis of this disease and promise to improve patient quality of life and survival. Finally, the recent discovery of chromosomal translocations resulting in the upregulation of one of at least 3 ETS genes (ERG, ETV1, ETV4) may lead to novel agents for the treatment of this disease.
Insights
Castration-resistant prostate cancer (CRPC) is a leading cause of cancer death in men. New drugs targeting molecular pathways and ETS gene alterations offer improved treatment options and survival for CRPC patients.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Castration-resistant prostate cancer (CRPC) is the second leading cause of male cancer-related mortality.
- Docetaxel improves survival in CRPC, but subsequent treatment options are limited.
- Understanding CRPC's molecular drivers is crucial for developing new therapies.
Purpose of the Study:
- To review current and emerging therapeutic strategies for castration-resistant prostate cancer.
- To highlight novel molecular targets and their potential clinical applications.
- To discuss the role of genetic alterations in CRPC pathogenesis and treatment.
Main Methods:
- Review of recent clinical studies and research on CRPC.
- Analysis of molecular pathways implicated in castration resistance.
- Examination of novel therapeutic targets and drug development.
Main Results:
- Several therapeutic targets are under investigation, including adrenal steroid synthesis, androgen receptor signaling, and growth factor pathways.
- New agents targeting these pathways are in clinical development.
- Chromosomal translocations leading to ETS gene (ERG, ETV1, ETV4) upregulation represent a novel therapeutic avenue.
Conclusions:
- Advances in understanding CRPC's molecular pathogenesis are enabling a rational drug development approach.
- Targeted therapies hold promise for improving patient quality of life and survival.
- Novel agents targeting ETS gene alterations may offer new treatment strategies for CRPC.
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