Cited by 679Lung Cancer Treatments and MutationsHER2/EGFR in Cancer ResearchCancer Genomics and Diagnostics

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Oncogenic Transformation by Inhibitor-Sensitive and -Resistant EGFR Mutants

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Greulich, Heidi, Chen, Tzu-Hsiu, Feng, Whei, Jänne, Pasi A, Alvarez, James V, Zappaterra, Mauro, Bulmer, Sara E, Frank, David A, Hahn, William C, Sellers, William R, Meyerson, Matthew·2005·PLoS Medicine

DOI 10.1371/journal.pmed.0020313PMC PMC1240052

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Abstract

BACKGROUND: Somatic mutations in the kinase domain of the epidermal growth factor receptor tyrosine kinase gene EGFR are common in lung adenocarcinoma. The presence of mutations correlates with tumor sensitivity to the EGFR inhibitors erlotinib and gefitinib, but the transforming potential of specific mutations and their relationship to drug sensitivity have not been described. METHODS AND FINDINGS: Here, we demonstrate that EGFR active site mutants are oncogenic. Mutant EGFR can transform both fibroblasts and lung epithelial cells in the absence of exogenous epidermal growth factor, as evidenced by anchorage-independent growth, focus formation, and tumor formation in immunocompromised mice. Transformation is associated with constitutive autophosphorylation of EGFR, Shc phosphorylation, and STAT pathway activation. Whereas transformation by most EGFR mutants confers on cells sensitivity to erlotinib and gefitinib, transformation by an exon 20 insertion makes cells resistant to these inhibitors but more sensitive to the irreversible inhibitor CL-387,785. CONCLUSION: Oncogenic transformation of cells by different EGFR mutants causes differential sensitivity to gefitinib and erlotinib. Treatment of lung cancers harboring EGFR exon 20 insertions may therefore require the development of alternative kinase inhibition strategies.

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Self-citation
EGF receptor gene mutations are common in lung cancers from “never smokers” and are associated with sensitivity of tumors to gefitinib and erlotinib
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Acquired Resistance of Lung Adenocarcinomas to Gefitinib or Erlotinib Is Associated with a Second Mutation in the EGFR Kinase Domain
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“Patients who responded to gefitinib and subsequently relapsed were found to have T790M secondary mutations, also in exon 20 [19,20].”
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Authors: Greulich, H., Chen, T.-H., Feng, W., Jänne, P. A., Alvarez, J. V., Zappaterra, M., Bulmer, S. E., Frank, D. A., Hahn, W. C., Sellers, W. R., & Meyerson, M.
Affiliations: Broad Institute (US)
Brigham and Women's Hospital (US)
Dana-Farber Cancer Institute (US)
Corresponding author: Greulich, Heidi
Sellers, William R
Meyerson, Matthew
ORCID: Greulich, Heidi
Alvarez, James V
Frank, David A
Hahn, William C
Sellers, William R
Meyerson, Matthew
Venue: PLoS Medicine
Publisher: Public Library of Science (PLoS)
Published: 2005-10-04
Volume: 2
Issue: 11
Pages: e313
ISSN: 1549-1277 (ISSN-L)
1549-1676
DOI: 10.1371/journal.pmed.0020313
PMC: PMC1240052
OpenAlex: W2037873277
Cited by: 677
References: 35
Citations by year: 2026: 9 · 2025: 10 · 2024: 10 · 2023: 22 · 2022: 23 · 2021: 23 · 2020: 16 · 2019: 29 · 2018: 20 · 2017: 27 · 2016: 26 · 2015: 47 · 2014: 27 · 2013: 54 · 2012: 46
FWCI: 45.72
Type: journal article
Language: en
Update notices: correction (2024-09-16)
Open access: gold
doi.org
Licence: cc-by
creativecommons.org/licenses/by/4.0/ (unspecified)
Locations: PLoS Medicine (publishedVersion, cc-by)
Europe PMC (PubMed Central) (publishedVersion, cc-by)
PubMed Central (publishedVersion, cc-by)
PubMed (publishedVersion)
Digital Access to Scholarship at Harvard (DASH) (Harvard University) (submittedVersion, cc-by)
DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders: American Cancer Society
Doris Duke Charitable Foundation
Flight Attendant Medical Research Institute
Barr Foundation
National Institutes of Health
National Cancer Institute
Topics: Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Lung Cancer Treatments and Mutations
Health Sciences › Medicine › Oncology › HER2/EGFR in Cancer Research
Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer Genomics and Diagnostics
Keywords: EGFR mutation, oncogenic transformation, lung adenocarcinoma, erlotinib, gefitinib, EGFR inhibitors, exon 20 insertion, autophosphorylation, Shc phosphorylation, STAT pathway, drug resistance, kinase inhibitors
MeSH terms: Erlotinib Hydrochloride, Src Homology 2 Domain-Containing, Transforming Protein 1, Gefitinib, Animals, Antineoplastic Agents, Cell Transformation, Neoplastic, Exons, Humans, Mice, Nude, Mutation, Neoplasms, Experimental, Quinazolines, Transfection, Tumor Stem Cell Assay, Genetic Therapy, Drug Resistance, Neoplasm, NIH 3T3 Cells, Protein Kinase Inhibitors, Adaptor Proteins, Signal Transducing, STAT3 Transcription Factor, Proto-Oncogene Proteins c-akt, Mice, Shc Signaling Adaptor Proteins, ErbB Receptors

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Oncogenic Transformation by Inhibitor-Sensitive and -Resistant EGFR Mutants

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