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This article has been peer reviewed. It is the authors' final version prior to publication in Acta Cytologica

November-December 2012;Volume 56, Issue, 6, pp.587–589

The published version is available at DOI: 10.1159/000345183. Copyright © Karger


In 2004, three groups working independently [1–3] , almost simultaneously, reported remarkable findings: that activating mutations in the epidermal growth factor receptor (EGFR) were common in certain lung carcinomas and that these mutations correlated with the response of those lung tumors to therapy with gefitinib and erlotinib, both EGFR tyrosine kinase inhibitors (TKIs). This was the first time driver mutations in lung cancer that responded to targeted therapy had been identified, marking the beginning of a new era of personalized medicine in lung cancer. Prior to the discovery of these mutations, patients had been treated with EGFR TKIs but predicting who would respond and who would not was only imperfectly correlated with the histologic appearance of the tumor and the clinical profile of the patient.

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