Targeting Met and VEGFR Axis in Metastatic Castration-Resistant Prostate Cancer: 'Game Over'?

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.

• Authors: Alessandra Modena, Francesco Massari, Chiara Ciccarese, Matteo Brunelli, Matteo Santoni, Rodolfo Montironi, Guido Martignoni, Giampaolo Tortora
• Journal: Targeted oncology (Target Oncol) Vol. 11 Issue 4 Pg. 431-46 (08 2016) ISSN: 1776-260X [Electronic] France
• PMID: 26846650 (Publication Type: Journal Article, Review, Research Support, Non-U.S. Gov't)

Chemical References

• Vascular Endothelial Growth Factor A
• MET protein, human
• Proto-Oncogene Proteins c-met

Topics

• Humans
• Male
• Neoplasm Metastasis
• Prostatic Neoplasms, Castration-Resistant (drug therapy, pathology)
• Proto-Oncogene Proteins c-met
• Vascular Endothelial Growth Factor A