Targeting MET in EGFR-MMutated NSCLC

MET alterations, mainly gene amplification and protein overexpression, represent a major mechanism of primary and acquired resistance to epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) in EGFR-mutated (EGFRm) non-small cell lung cancer (NSCLC). Both de novo and acquired MET dysregulation can activate downstream oncogenic signaling, providing a strong rationale for dual inhibition of EGFR and MET.This review summarizes the data for targeting MET alterations in EGFRm NSCLC, with emphasis on the clinical relevance of distinguishing MET amplification from c-MET overexpression.