Somatic mutations in certain tyrosine kinases have emerged as central 'drivers' of specific cancers and these mutant proteins are proving to be excellent substrates for targeted therapies. This is the case for mutant EGFR-dependent lung adenocarcinomas, where EGFR mutation testing is already being used to help guide treatment decisions. Here, we provide an overview of the biology of EGFR-targeted therapies and the clinical experience to date, the positive and negative predictors of response, pathologic correlates of EGFR-mutant status, testing methods to establish patient eligibility for these agents, and the basis for primary and secondary resistance.
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