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Mutations in the epidermal growth factor receptor (EGFR), most commonly deletions in exon 19 affecting the amino acid motif LREA (delE746-750) or substitution of arginine for leucine at position 858 (L858R) in exon 21, are present in approximately 17% of tumors in patients with pulmonary adenocarcinoma and lead to constitutive activation of the EGFR tyrosine kinase.1 These activating EGFR mutations are associated with high response rates to EGFR tyrosine kinase inhibitor (TKI) therapy, with combined results from 21 studies from 2004 to 2006 showing responses in 210 of 268 patients (78%).2 These response rates observed in patients with EGFR-mutant tumors receiving TKIs were much higher than what had been described in patients treated with standard platinum-doublet chemotherapy. Follow-up studies directly comparing the 2 treatment strategies in patients with advanced-stage non–small-cell lung cancer harboring activating EGFR mutations confirmed the superiority of EGFR TKI therapy to chemotherapy in this patient population as described herein.
Morgensztern D, Politi K, Herbst RS. EGFR Mutations in Non–Small-Cell Lung Cancer: Find, Divide, and Conquer. JAMA Oncol. 2015;1(2):146–148. doi:10.1001/jamaoncol.2014.278
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