Abstract
Tyrosine kinase inhibitors (TKIs) are effective in EGFR mutant non-small cell lung cancer (NSCLC), but acquired resistance is virtually inevitable. Known resistance mechanisms include acquired EGFR mutations (e.g, 718V, c797x, 724s, 721s or T790M); copy number amplifications in MET, ERBB2, and PIK3CA; gene fusion events; and histological transformation. We herein present the prevalence of resistance mutations in the largest reported cohort of EGFR mutant NSCLC.
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