EGFR mutations in lung, cancer: Correlation with clinical response to gefitinib therapy

J. Guillermo Paez; Pasi A. Jänne; Jeffrey C. Lee; Sean Tracy; Heidi Greulich; Stacey Gabriel; Paula Herman; Frederic J. Kaye; Neal Lindeman; Titus J. Boggon; Katsuhiko Naoki; Hidefumini Sasaki; Yoshitaka Fujii; Michael J. Eck; William R. Sellers; Bruce E. Johnson; Matthew Meyerson

doi:10.1126/science.1099314

EGFR mutations in lung, cancer: Correlation with clinical response to gefitinib therapy

J. Guillermo Paez, Pasi A. Jänne, Jeffrey C. Lee, Sean Tracy, Heidi Greulich, Stacey Gabriel, Paula Herman, Frederic J. Kaye, Neal Lindeman, Titus J. Boggon, Katsuhiko Naoki, Hidefumini Sasaki, Yoshitaka Fujii, Michael J. Eck, William R. Sellers, Bruce E. Johnson, Matthew Meyerson

Research output: Contribution to journal › Article › peer-review

8622 Citations (Scopus)

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 15 of 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.

Original language	English
Pages (from-to)	1497-1500
Number of pages	4
Journal	Science
Volume	304
Issue number	5676
DOIs	https://doi.org/10.1126/science.1099314
Publication status	Published - 2004 Jun 4
Externally published	Yes

ASJC Scopus subject areas

General

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

Access to Document

10.1126/science.1099314

Cite this

Paez, J. G., Jänne, P. A., Lee, J. C., Tracy, S., Greulich, H., Gabriel, S., Herman, P., Kaye, F. J., Lindeman, N., Boggon, T. J., Naoki, K., Sasaki, H., Fujii, Y., Eck, M. J., Sellers, W. R., Johnson, B. E., & Meyerson, M. (2004). EGFR mutations in lung, cancer: Correlation with clinical response to gefitinib therapy. Science, 304(5676), 1497-1500. https://doi.org/10.1126/science.1099314

Paez, JG, Jänne, PA, Lee, JC, Tracy, S, Greulich, H, Gabriel, S, Herman, P, Kaye, FJ, Lindeman, N, Boggon, TJ, Naoki, K, Sasaki, H, Fujii, Y, Eck, MJ, Sellers, WR, Johnson, BE & Meyerson, M 2004, 'EGFR mutations in lung, cancer: Correlation with clinical response to gefitinib therapy', Science, vol. 304, no. 5676, pp. 1497-1500. https://doi.org/10.1126/science.1099314

@article{f74dd0ff64cd46feab77f368221b33b3,

title = "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 15 of 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.",

author = "Paez, {J. Guillermo} and J{\"a}nne, {Pasi A.} and Lee, {Jeffrey C.} and Sean Tracy and Heidi Greulich and Stacey Gabriel and Paula Herman and Kaye, {Frederic J.} and Neal Lindeman and Boggon, {Titus J.} and Katsuhiko Naoki and Hidefumini Sasaki and Yoshitaka Fujii and Eck, {Michael J.} and Sellers, {William R.} and Johnson, {Bruce E.} and Matthew Meyerson",

year = "2004",

month = jun,

day = "4",

doi = "10.1126/science.1099314",

language = "English",

volume = "304",

pages = "1497--1500",

journal = "Science",

issn = "0036-8075",

publisher = "American Association for the Advancement of Science",

number = "5676",

}

TY - JOUR

T1 - EGFR mutations in lung, cancer

T2 - Correlation with clinical response to gefitinib therapy

AU - Paez, J. Guillermo

AU - Jänne, Pasi A.

AU - Lee, Jeffrey C.

AU - Tracy, Sean

AU - Greulich, Heidi

AU - Gabriel, Stacey

AU - Herman, Paula

AU - Kaye, Frederic J.

AU - Lindeman, Neal

AU - Boggon, Titus J.

AU - Naoki, Katsuhiko

AU - Sasaki, Hidefumini

AU - Fujii, Yoshitaka

AU - Eck, Michael J.

AU - Sellers, William R.

AU - Johnson, Bruce E.

AU - Meyerson, Matthew

PY - 2004/6/4

Y1 - 2004/6/4

N2 - 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 15 of 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.

AB - 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 15 of 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.

UR - http://www.scopus.com/inward/record.url?scp=2342624080&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=2342624080&partnerID=8YFLogxK

U2 - 10.1126/science.1099314

DO - 10.1126/science.1099314

M3 - Article

C2 - 15118125

AN - SCOPUS:2342624080

SN - 0036-8075

VL - 304

SP - 1497

EP - 1500

JO - Science

JF - Science

IS - 5676

ER -

EGFR mutations in lung, cancer: Correlation with clinical response to gefitinib therapy

Abstract

ASJC Scopus subject areas

UN SDGs

Access to Document

Other files and links

Fingerprint

Cite this