Understanding themolecular profile of non–small-cell lung can-cer (NSCLC) is becoming ever more relevant to patient care and treatment decisionmaking. The development ofmolecularly targeted therapies against the epidermal growth factor receptor (EGFR) ty-rosine kinase has led to the discovery ofmutations and other genomic alterations that affect the efficacy of these agents. A set of activating mutations inEGFR, primarilyoverlappingdeletionmutations in exon 19and the singleL858Rpointmutation inexon21, are associatedwith increased response and survival after tyrosine kinase inhibitor (TKI) therapy,whereas theT790Mpointmutationor insertionmutations in exon 20 of EGFR, amplification ofMET, and mutations in K-ras are associated with failure to respond.1-11 As a result, the field is moving toward acceptance of molecular testing as an integral component of clinical care. However, several practical obstacles to this paradigm shift re-
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Sequist et al. (2009) studied this question.
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