| Literature DB >> 26846650 |
Alessandra Modena1, Francesco Massari2, Chiara Ciccarese1, Matteo Brunelli3, Matteo Santoni4, Rodolfo Montironi5, Guido Martignoni3, Giampaolo Tortora1.
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.Entities:
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Year: 2016 PMID： 26846650 DOI： 10.1007/s11523-015-0412-7
Source DB: PubMed Journal: Target Oncol ISSN： 1776-2596 Impact factor: 4.493