Abstract
Nowadays, EGFR tyrosine kinase inhibitors (EGFR-TKIs) have become the first-line treatment for non-small cell lung cancer (NSCLC) patients with EGFR-sensitive mutations. However, acquired drug resistance remains an unavoidable bottleneck in clinical application. Herein, the mechanisms of acquired drug resistance were reviewed first, including secondary mutation of EGFR, amplification of MET gene, IGF1R and amplification of HER2. Then, therapeutic
Abstract
Nowadays, EGFR tyrosine kinase inhibitors (EGFR-TKIs) have become the first-line treatment for non-small cell lung cancer (NSCLC) patients with EGFR-sensitive mutations. However, acquired drug resistance remains an unavoidable bottleneck in clinical application. Herein, the mechanisms of acquired drug resistance were reviewed first, including secondary mutation of EGFR, amplification of MET gene, IGF1R and amplification of HER2. Then, therapeutic