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Activating Mutations in the Epidermal Growth Factor Receptor Underlying Responsiveness of Non–Small-Cell Lung Cancer to Gefitinib

New England Journal of Medicine · 2004 · Vol. 350(21) · pp. 2129–2139

Thomas J. Lynch✉(Massachusetts General Hospital)Daphne W. Bell(Harvard University)Raffaella Sordella(Harvard University)Sarada Gurubhagavatula(Massachusetts General Hospital)Ross A. Okimoto(Harvard University)Brian W. Brannigan(Massachusetts General Hospital)Patricia L. Harris(Massachusetts General Hospital)Sara M. Haserlat(Massachusetts General Hospital)Jeffrey G. Supko(Massachusetts General Hospital)Frank G. Haluska(Harvard University)David N. Louis(Harvard University)David C. Christiani(Harvard University)Jeff Settleman(Massachusetts General Hospital)Daniel A. Haber(Harvard University)

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Abstract

A subgroup of patients with non-small-cell lung cancer have specific mutations in the EGFR gene, which correlate with clinical responsiveness to the tyrosine kinase inhibitor gefitinib. These mutations lead to increased growth factor signaling and confer susceptibility to the inhibitor. Screening for such mutations in lung cancers may identify patients who will have a response to gefitinib.

Lung Cancer Treatments and Mutations Colorectal Cancer Treatments and Studies HER2/EGFR in Cancer ResearchGefitinibEpidermal growth factor receptorLung cancerCancer researchTyrosine kinaseMedicineEpidermal growth factorTyrosine-kinase inhibitorMutationBiology

MeSH terms

HeterozygoteHumansFemaleGefitinibAdenocarcinomaAdultAgedAged, 80 and overAmino Acid SequenceAntineoplastic AgentsBase SequenceCarcinoma, Non-Small-Cell LungDNA Mutational AnalysisEpidermal Growth FactorLung Neoplasms

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EGF receptor gene mutations are common in lung cancers from “never smokers” and are associated with sensitivity of tumors to gefitinib and erlotinib