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During the past several years, treatment of patients with non–small-cell lung cancer (NSCLC) has evolved beyond use of conventional cytotoxic chemotherapeutic agents to include molecularly directed therapy. One such approach involves using epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors, including gefitinib (Iressa) and erlotinib (Tarceva). Patients with tumor-associated activating mutations in the EGFR gene have a dramatic response to these agents. But drug resistance develops in most of these individuals (J Clin Oncol 2007; 25:587), likely from secondary EGFR mutations at T790M that emerge during therapy and hinder binding of the tyrosine kinase inhibitors (PLoS Med 2005; 2:e73).
Molecular characterization of the EGFR ge…