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Updated: Mar 26, 2026

A Bioluminescent and Fluorescent Orthotopic Syngeneic Murine Model of Androgen-dependent and Castration-resistant Prostate Cancer
Published on: March 6, 2018
Targeting Met and VEGFR Axis in Metastatic Castration-Resistant Prostate Cancer: 'Game Over'?
Alessandra Modena1, Francesco Massari2, Chiara Ciccarese1
1Medical Oncology, Azienda Ospedaliera Universitaria Integrata (AOUI), University of Verona, Piazzale L.A. Scuro 10, 37134, Verona, Italy.
Abstract:
Despite recent advances that have been made in the therapeutic landscape of metastatic castration-resistant prostate cancer (mCRPC), effective management of bone metastases remains a key goal not yet reached. The receptor tyrosine kinase MET and the vascular endothelial growth factor receptor (VEGFR) seem to play an important role in prostate cancer progression and pathological bone turnover, representing potential targets for improving clinical outcomes in mCRPC. Studies evaluating agents that target one or both these pathways have demonstrated modest activity but no improvement in overall survival. Nevertheless, this therapeutic strategy seems to still be a promising and engaging area of prostate cancer research and the interest in better understanding the MET/VEGFR axis and the mechanism of action of these inhibitors is growing. This review describes the rationale for targeting MET and VEGFR pathway in mCRPC and provides the clinical data available to date and an update on ongoing trials.
Insights
Targeting MET and VEGFR pathways shows promise for metastatic castration-resistant prostate cancer (mCRPC) bone metastases. While current agents offer modest benefits, further research into the MET/VEGFR axis is ongoing.
Area of Science:
- Oncology
- Molecular Biology
- Pharmacology
Background:
- Metastatic castration-resistant prostate cancer (mCRPC) management, particularly bone metastases, requires improved therapies.
- The MET receptor tyrosine kinase and vascular endothelial growth factor receptor (VEGFR) are implicated in prostate cancer progression and bone pathology.
Purpose of the Study:
- To review the rationale for targeting the MET and VEGFR pathways in mCRPC.
- To summarize available clinical data and ongoing trials for MET/VEGFR inhibitors.
Main Methods:
- Literature review of preclinical and clinical studies.
- Analysis of data from trials investigating MET and VEGFR inhibitors in mCRPC.
Main Results:
- Agents targeting MET and/or VEGFR pathways have shown modest activity in mCRPC.
- No significant improvement in overall survival has been observed with current agents.
- The MET/VEGFR axis remains an area of active research interest.
Conclusions:
- Targeting the MET/VEGFR axis is a promising strategy for mCRPC, especially for bone metastases.
- Further investigation is needed to optimize therapeutic approaches and improve patient outcomes.
- Understanding the mechanisms of MET/VEGFR inhibitors is crucial for future drug development.
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