Two are better than one on progression through MET mechanism for EGFR+ NSCLC patients

Recent years have borne witness to the development of numerous acquired resistances to epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitors (TKIs) treatment for patients with EGFR-mutated non-small cell lung cancer (NSCLC). Mechanism of resistant includes EGFR T790M, MET gene amplification (1,2), transformation to small cell lung cancer and others. Approximately 5 to 26 percent of these acquired modifications occur due to dysregulation of the mesenchymal-epithelial transition factor (MET) either by amplification or overexpression patterns. Previous studies have failed to show efficacy of adding MET inhibitors to EGFR-TKI therapies upon progression (3).