Abstract
Background c-MET is a receptor tyrosine kinase receptor (RTK) for the hepatocyte growth factor (HGF). The binding of HGF to c-MET regulates several cellular functions: differentiation, proliferation, epithelial cell motility, angiogenesis, and epithelial-mesenchymal transition (EMT). Moreover, it is known to be involved in carcinogenesis. Comprehension of HGF-c-MET signaling pathway might have important clinical consequences allowing to predict prognosis, response to treatment, and survival rates based on its expression and dysregulation. Discussion. c-MET represents a useful molecular target for novel engineered drugs. Several clinical trials are underway for various solid tumors and the development of new specific monoclonal antibodies depends on the recent knowledge about the definite c-MET role in each different malignance. Recent clinical trials based on c-MET molecular targets result in good safety profile and represent a promising therapeutic strategy for solid cancers, in monotherapy or in combination with other target drugs. Conclusion The list of cell surface receptors crosslinking with the c-MET signaling is constantly growing, highlighting the importance of this pathway for personalized target therapy. Research on the combination of c-MET inhibitors with other drugs will hopefully lead to discovery of new effective treatment options.
Highlights
MET (Mesenchymal-Epithelial Transition) is a N-methylN′-nitro-N-nitrosoguanidine gene aberrantly overexpressed in human osteosarcoma, located in the 7q21-31 loci of chromosome 7
Many achievements have been made in our understanding of clinical importance and biological mechanisms of c-MET/ Hepatocyte Growth Factor (HGF) pathway
Aberrant HGF/ MET pathway plays as an oncogenic driver, since dysregulation of c-MET and HGF has been implicated in cancer pathogenesis as it is involved in the mechanisms of cell proliferation and survival, invasion, and metastasis
Summary
MET (Mesenchymal-Epithelial Transition) is a N-methylN′-nitro-N-nitrosoguanidine gene aberrantly overexpressed in human osteosarcoma, located in the 7q21-31 loci of chromosome 7. In SAVANNAH, a multicentre phase Ib single arm study, the investigators are exploring the efficacy of 28-day continuative combined therapy with osimertinib (80 mg oral OD) and savolitinib, a c-MET selective inhibitor (300 mg oral OD or 300 mg oral BID or 600 mg oral OD), in patients with EGFR mutationpositive locally advanced or metastatic NSCLC with METdriven resistance to osimertinib.
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