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Science 304 (5676): 1497-1500

Copyright © 2004 by the American Association for the Advancement of Science

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

J. Guillermo Paez,1,2* Pasi A. Jänne,1,2* Jeffrey C. Lee,1,3* Sean Tracy,1 Heidi Greulich,1,2 Stacey Gabriel,4 Paula Herman,1 Frederic J. Kaye,5 Neal Lindeman,6 Titus J. Boggon,1,3 Katsuhiko Naoki,1 Hidefumi Sasaki,7 Yoshitaka Fujii,7 Michael J. Eck,1,3 William R. Sellers,1,2,4{dagger} Bruce E. Johnson,1,2{dagger} Matthew Meyerson1,3,4{dagger}

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 from U.S. patients who responded to gefitinib therapy and in a lung adenocarcinoma cell line that was hypersensitive to growth inhibition by gefitinib, but not in gefitinib-insensitive tumors or cell lines. These results suggest that EGFR mutations may predict sensitivity to gefitinib.

1 Departments of Medical Oncology and Cancer Biology, Dana-Farber Cancer Institute, Boston, MA 02115, USA.
2 Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA.
3 Departments of Pathology and Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, MA 02115, USA.
4 The Broad Institute at MIT and Harvard, Cambridge, MA 02142, USA.
5 Genetics Branch, National Cancer Institute, National Naval Medical Center, Bethesda, MD 20889, USA.
6 Department of Pathology, Brigham and Women's Hospital, Boston MA 02115, USA.
7 Department of Surgery 2, Nagoya City University Medical School, Nagoya 467-8601, Japan.

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Note added in proof: Similar results are being reported by T. J. Lynch et al. (28).

* These authors contributed equally to this work.

{dagger} To whom correspondence should be addressed. E-mail: William_Sellers{at}dfci.harvard.edu; Bruce_Johnson{at}dfci.harvard.edu; Matthew_Meyerson{at}dfci.harvard.edu

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S. Heon, B. Y. Yeap, N. I. Lindeman, V. A. Joshi, M. Butaney, G. J. Britt, D. B. Costa, M. S. Rabin, D. M. Jackman, and B. E. Johnson (2012)
Clin. Cancer Res. 18, 4406-4414
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Network-based drug discovery by integrating systems biology and computational technologies.
E. L. Leung, Z.-W. Cao, Z.-H. Jiang, H. Zhou, and L. Liu (2012)
Brief Bioinform
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Research Resource: Diagnostic and Therapeutic Potential of Nuclear Receptor Expression in Lung Cancer.
Y. Jeong, Y. Xie, W. Lee, A. L. Bookout, L. Girard, G. Raso, C. Behrens, I. I. Wistuba, A. F. Gadzar, J. D. Minna, et al. (2012)
Mol. Endocrinol. 26, 1443-1454
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Lung cancers with acquired resistance to EGFR inhibitors occasionally harbor BRAF gene mutations but lack mutations in KRAS, NRAS, or MEK1.
K. Ohashi, L. V. Sequist, M. E. Arcila, T. Moran, J. Chmielecki, Y.-L. Lin, Y. Pan, L. Wang, E. de Stanchina, K. Shien, et al. (2012)
PNAS 109, E2127-E2133
   Abstract »    Full Text »    PDF »
Oncogenic cooperation between SOCS family proteins and EGFR identified using a Drosophila epithelial transformation model.
H. Herranz, X. Hong, N. T. Hung, P. M. Voorhoeve, and S. M. Cohen (2012)
Genes & Dev. 26, 1602-1611
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Ultrasensitive Measurement of Hotspot Mutations in Tumor DNA in Blood Using Error-Suppressed Multiplexed Deep Sequencing.
A. Narayan, N. J. Carriero, S. N. Gettinger, J. Kluytenaar, K. R. Kozak, T. I. Yock, N. E. Muscato, P. Ugarelli, R. H. Decker, and A. A. Patel (2012)
Cancer Res. 72, 3492-3498
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EGFR and K-ras mutations in cytologic samples from fine-needle aspirates in NSCLC patients.
P. Ulivi, W. Zoli, E. Chiadini, L. Capelli, P. Candoli, D. Calistri, R. Silvestrini, and M. Puccetti (2012)
Eur. Respir. J. 40, 267-269
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Combining chemotherapy with epidermal growth factor receptor inhibition in advanced non-small cell lung cancer.
L. Leung, T. S. K. Mok, and H. Loong (2012)
Therapeutic Advances in Medical Oncology 4, 173-181
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Combined EGFR/MET or EGFR/HSP90 Inhibition Is Effective in the Treatment of Lung Cancers Codriven by Mutant EGFR Containing T790M and MET.
L. Xu, E. Kikuchi, C. Xu, H. Ebi, D. Ercan, K. A. Cheng, R. Padera, J. A. Engelman, P. A. Janne, G. I. Shapiro, et al. (2012)
Cancer Res. 72, 3302-3311
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Authors' response: 'Focusing on HER2 as a potential therapeutic target in primary ovarian mucinous carcinomas'.
B. Yan and G. S. D. Lim (2012)
J. Clin. Pathol. 65, 671-672
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Complex Role of Histone Deacetylase Inhibitors in the Treatment of Non-Small-Cell Lung Cancer.
J. W. Neal and L. V. Sequist (2012)
J. Clin. Oncol. 30, 2280-2282
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Clinical Outcomes in Non-Small Cell Lung Cancers Harboring Different Exon 19 Deletions in EGFR.
K.-P. Chung, S.-G. Wu, J.-Y. Wu, J. C.-H. Yang, C.-J. Yu, P.-F. Wei, J.-Y. Shih, and P.-C. Yang (2012)
Clin. Cancer Res. 18, 3470-3477
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Randomized Phase II Trial of Erlotinib Alone or With Carboplatin and Paclitaxel in Patients Who Were Never or Light Former Smokers With Advanced Lung Adenocarcinoma: CALGB 30406 Trial.
P. A. Janne, X. Wang, M. A. Socinski, J. Crawford, T. E. Stinchcombe, L. Gu, M. Capelletti, M. J. Edelman, M. A. Villalona-Calero, R. Kratzke, et al. (2012)
J. Clin. Oncol. 30, 2063-2069
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Pituitary Adenylate Cyclase-Activating Polypeptide Causes Tyrosine Phosphorylation of the Epidermal Growth Factor Receptor in Lung Cancer Cells.
T. W. Moody, N. Osefo, B. Nuche-Berenguer, L. Ridnour, D. Wink, and R. T. Jensen (2012)
J. Pharmacol. Exp. Ther. 341, 873-881
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Platelet-derived growth factor receptors differentially inform intertumoral and intratumoral heterogeneity.
Y. Kim, E. Kim, Q. Wu, O. Guryanova, M. Hitomi, J. D. Lathia, D. Serwanski, A. E. Sloan, R. J. Weil, J. Lee, et al. (2012)
Genes & Dev. 26, 1247-1262
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