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ORIGINAL ARTICLE EGFR-Mutant Lung Adenocarcinomas Treated First-Line with the Novel EGFR Inhibitor, XL647, Can Subsequently Retain Moderate Sensitivity to Erlotinib Juliann Chmielecki, PhD,* M. Catherine Pietanza, MD,† Dana Aftab, PhD,‡ Ronglai Shen, PhD,§ Zhiguo Zhao, MS, Xi Chen, PhD, Katherine Hutchinson, BS,¶ Agnes Viale, PhD,# Mark G. Kris, MD,† Thomas Stout, PhD,‡ Vincent Miller, MD,† Naiyer Rizvi, MD,† and William Pao, MD, PhD¶ assays. Crystal structure analyses of XL647/EGFR T790M did not Introduction: EGFR-mutant lung cancers are sensitive to EGFR reveal a different binding mode from that of erlotinib. tyrosine kinase inhibitors (TKIs). Unfortunately, they develop resis- Conclusions: The findings of this exploratory study suggest that tance, often due to acquisition of a second-site mutation (T790M). different EGFR TKIs may select for distinct mechanisms of resistance. Current EGFR TKIs select for T790M in preclinical models of These results raise the possibility that different EGFR TKIs could be acquired resistance. We explored whether all EGFR TKIs similarly sequentially used to improve outcomes in patients with EGFR-mutant select for the T790M mutation using data from early clinical trials lung cancer. Further work investigating this hypothesis is warranted. and established in vitro models of acquired resistance. Methods: We analyzed the clinical characteristics
Journal of Thoracic Oncology – Wolters Kluwer Health
Published: Feb 1, 2012
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