Therapeutic Targeting of the Receptor Tyrosine Kinase Met

摘要: There are different options to inhibit Met activation and these in part limited depending on the transforming phenotype. For example, inhibiting ligand/receptor interactions may be a useful approach when paracrine/autocrine mechanism but will show little effect gain-of-function mutation of Met. It still remains unknown as how much inhibition is required achieve clinically beneficial anti-tumor anti-metastatic results. The answer potentially upon whether ‘tumorigenic culprit’ lies with expression or mutations RTK. necessary further study optimize targeted approaches for clinical studies. Another intriguing area research, specific inhibitors available, would test drug efficaciesagainst mutant forms oncoprotein. possible that some cause resistance, conversely greater susceptibility, inhibitors. Among various strategies HGF/Met signaling, developing small molecule against have greatest potential molecularly anti-cancer therapy. However, lessons learned from Gleevec (imatinib mesylate) treatment chronic myelogenous leukemia demonstrate resistance real issu therapeutically. therefore furthercharacterize signaling mechanisms behind Met-mediated proliferation other biological effects identify additional molecules therapies.