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Mutation in the tyrosine kinase domain of epidermal growth factor receptor is a predictive and prognostic factor for gefitinib treatment in patients with non-small cell lung cancer



Mutation in the tyrosine kinase domain of epidermal growth factor receptor is a predictive and prognostic factor for gefitinib treatment in patients with non-small cell lung cancer



Journal of Clinical Oncology 23(16_Suppl): 7086-7086



NlmCategory="UNASSIGNED">7086 Background: It has been reported that mutations in epidermal growth factor receptor (EGFR) play a critical role in predicting tumor response in patients receiving gefitinib for non-small cell lung cancer (NSCLC). We investigated the associations of EGFR mutations to tumor response and survival in gefitinib-treated NSCLC patients. We examined EGFR gene mutations in exons 18, 19 and 21 by DNA sequencing in paraffin-embedded tumor tissues of NSCLC patients who have received gefitinib. The results were correlated with the clinical parameters. Mutations in the tyrosine kinase domain of EGFR were found in 29 of 54 cases (53.7%). Of them, twelve cases had a deletion in exon 19 and seventeen cases had a substitution in exon 18 and/or 21. Mutation was an independent predictor for disease control (P< 0.001) and tumor response (P= 0.020); the positive predictive values were 93% and 75% and negative predictive values were 60% and 65%, respectively. Compared with patients whose tumor bearing non-mutant EGFR, patients with EGFR mutations showed better progression-free survival (median 7.9 m vs. 1.8 m, P< 0.001) and overall survival (median 12 m vs. 4.7 m, P= 0.029). Moreover, in the gefitinib responders, patients with mutations had a longer response duration than patients without mutations (median 9.1 m vs. 2.9 m, P= 0.033). It was unlikely that patients with EGFR mutations in different exons have variable response or survival to gefitinib treatment. EGFR mutations can be used as a predictive and prognostic indicator in patients receiving gefitinib for NSCLC No significant financial relationships to disclose.

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Accession: 058366128

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PMID: 27944542


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