2004
DOI: 10.1126/science.1099314
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EGFR Mutations in Lung Cancer: Correlation with Clinical Response to Gefitinib Therapy

Abstract: Receptor tyrosine kinase genes were sequenced in non–small cell lung cancer (NSCLC) and matched normal tissue. Somatic mutations of the epidermal growth factor receptor gene EGFR were found in 15of 58 unselected tumors from Japan and 1 of 61 from the United States. Treatment with the EGFR kinase inhibitor gefitinib (Iressa) causes tumor regression in some patients with NSCLC, more frequently in Japan. EGFR mutations were found in additional lung cancer samples fr… Show more

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Cited by 8,835 publications
(6,659 citation statements)
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“…4 In recent years, attention has been paid to the role that 'driver mutations,' such as epidermal growth factor receptor (EGFR) and anaplastic lymphoma kinase (ALK), have in the tumorigenesis of adenocarcinomas, and their potential use as targets for therapy. [5][6][7][8][9] Recent data suggest EGFR may also serve as a prognostic factor, in addition to its role as a predictive factor, as patients-bearing EGFR mutations have shown favorable clinical outcomes even with conventional chemotherapy. [10][11][12][13] EGFR and members of its family have an important role in carcinogenesis through their involvement in the modulation of cell proliferation, apoptosis, cell motility, and neovascularization.…”
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confidence: 99%
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“…4 In recent years, attention has been paid to the role that 'driver mutations,' such as epidermal growth factor receptor (EGFR) and anaplastic lymphoma kinase (ALK), have in the tumorigenesis of adenocarcinomas, and their potential use as targets for therapy. [5][6][7][8][9] Recent data suggest EGFR may also serve as a prognostic factor, in addition to its role as a predictive factor, as patients-bearing EGFR mutations have shown favorable clinical outcomes even with conventional chemotherapy. [10][11][12][13] EGFR and members of its family have an important role in carcinogenesis through their involvement in the modulation of cell proliferation, apoptosis, cell motility, and neovascularization.…”
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confidence: 99%
“…The results of the clinical trials indicated that many of the tumors harboring mutant EGFR are highly sensitive to EGFR TKIs, with up to 70% demonstrating a significant clinical response. 5,28,29,[37][38][39] Recent studies have provided more compelling evidence of the clinical benefits of anti-EGFR treatment in the appropriate setting. 13,15,22,38,[40][41][42][43][44][45][46][47][48] Evidence from the large phase III randomized Iressa Pan-Asia Study trial and other phase III trials have prompted the American Society of Clinical Oncology to issue a provisional clinical opinion recommending the testing of EGFR mutational status in patients being considered for first line EGFR TKI therapy owing to their demonstrated benefit on progression-free survival.…”
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confidence: 99%
“…The other is a point mutation in exon 21 (2573T>G) that results in substitution of leucine by arginine at codon 858 (L858R). [4][5][6][7][8][9][10] Other much less common mutations have also been described in exons 18, 20, and 21.…”
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confidence: 99%
“…For example, mutated forms of the EGFR found in some NSCLCs can be inhibited by EGFR kinase inhibitors at concentrations approximately 100-fold lower than those required to inhibit wild-type EGFRs. 42 Such marked genetic variations in drug sensitivity can complicate the establishment of dose-response relationships in phase I studies.…”
Section: Measuring Target Inhibitionmentioning
confidence: 99%