EGFR Mutations in Lung Cancer: Correlation with Clinical Response to Gefitinib Therapy

By J. Paez, P. Jänne, Jeffrey C. Lee, Sean I Tracy, H. Greulich, Stacey Gabriel, P. Herman, F. Kaye, N. Lindeman, T. Boggon and 7 more. Science, 2004

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An epithelial-mesenchymal transition (EMT) gene signature predicts resistance to EGFR and PI3K inhibitors and identifies Axl as a therapeutic target for overcoming EGFR inhibitor resistance (2012, neutral): “Analysis was limited to the EGFR wild-type/KRASwild-type patients, as there are no validated markers of response to EGFR inhibitors in that group [whereas EGFR mutation is associated with response and KRAS mutation with resistance (3, 4, 43)].”
Mutations in the EGFR kinase domain mediate STAT3 activation via IL-6 production in human lung adenocarcinomas. (2007, background): “Somatic-activating mutations in the tyrosine kinase domains of the EGFR are found in approximately 10% of lung adenocarcinomas (3, 4, 7).”
Multi-platform analysis of 12 cancer types reveals molecular classification within and across tissues-of-origin (2014, background): “(Lynch et al., 2004; Paez et al., 2004) and ERBB2 amplifications among all breast cancers (The_Cancer_Genome_Atlas_Network, 2012c).”
Somatic mutations of the HER2 kinase domain in lung adenocarcinomas. (2005, background): “Because mutations in the EGFR gene target adenocarcinoma histology, female gender, never smoking status, and Oriental ethnicity (6, 7, 23), we Requests for reprints: Adi F.”