Concomitant driver mutations in advanced <i>EGFR</i>-mutated non-small-cell lung cancer and their impact on erlotinib treatment

Abstract

Co-mutations in other cancer-driver genes (oncogenes or tumor suppressor genes) were frequent in <i>EGFR</i>-mutated NSCLCs and few cases harbored concomitant activating and resistance <i>EGFR</i>-mutations before TKI-treatment. Most co-mutations did not impact the response to first-line erlotinib-treatment, but may represent potential additional therapeutic targets.