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The hepatocyte growth factor (HGF) receptor MET is an oncogenic driver in a subpopulation of Non-small Lung Cancer Cells (NSCLC) at the primary tumor stage or in acquired resistance to treatment with tumor-targeting tyrosine kinase inhibitors (TKIs). This article summarizes the mechanisms leading to overexpression and activation of MET by amplification and mutations including exon 14 aberrations. Furthermore, the methods to detect and categorize MET as a tumor driver and the selective TKIs for patient treatment are discussed. Activating mutations and rearrangements of kinases in NSCLC are the target of successful therapeutic intervention. However, MET activation involves a number of complex alterations including gene amplification, prevention of degradation by METex14 exon skipping and a host of gene mutations. A high-level MET expression is the precondition for tumor responses to TKIs and the confirmation of MET-dependent tumor progression is difficult in primary lesions and in tumors exhibiting resistance to mutated EGFR-directed therapy in absence of standardized and concordant assays of MET amplification.

Met inhibitors in the treatment of lung cancer: the evidence to date