C-MET in non-small-cell lung cancer with acquired resistance to epidermal growth factor receptor tyrosine kinase inhibitors

In recent years epidermal growth factor receptor (EGFR) inhibitor is atreatment a major treatment of non-small cell lung cancer (NSCLC).But with the widespread clinical application of resistance as a new difficulty.Now researchers have discovered the main resistance mechanisms is C-MET oncogene amplification.C-MET is a proto oncogene,a protein product of hepatocyte growth factor/scatter factor (HGF/SF) receptor with tyrosine activity.The amplification of C-MET can activated Erb3-PI3K signaling pathway which result in NSCLC resistant to the EGFR-TKI.The patients who resist to EGFR-TKI for about 20％ were due to the amplification of C MET gene. Key words: C-MET;  Tyrosine Kinase Inhibitors;  Non-small cell lung cancer;  Epidermal growth factor receptor ;  Resistance ;  Hepatocyte growth factor