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Originally published in Science Express on 29 April 2004
Science 4 June 2004:
Vol. 304. no. 5676, pp. 1497 - 1500
DOI: 10.1126/science.1099314
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Reports

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}

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.


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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