The impact of human EGFR kinase domain mutations on lung tumorigenesis and in vivo sensitivity to EGFR-targeted therapies

Ji, Hongbin; Li, Danan; Chen, Liang; Shimamura, Takeshi; Kobayashi, Susumu; McNamara, Kate; Mahmood, Umar; Mitchell, Albert; Sun, Yangping; Al-Hashem, Ruqayyah; Chirieac, Lucian R.; Padera, Robert; Bronson, Roderick T.; Kim, William; Jänne, Pasi A.; Shapiro, Geoffrey I.; Tenen, Daniel; Johnson, Bruce E.; Weissleder, Ralph; Sharpless, Norman E.; Wong, Kwok-Kin

doi:10.1016/j.ccr.2006.04.022

Cited by 462Lung Cancer Treatments and MutationsHER2/EGFR in Cancer ResearchLung Cancer Research Studies

The impact of human EGFR kinase domain mutations on lung tumorigenesis and in vivo sensitivity to EGFR-targeted therapies

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Ji, Hongbin, Li, Danan, Chen, Liang, Shimamura, Takeshi, Kobayashi, Susumu, McNamara, Kate, Mahmood, Umar, Mitchell, Albert +13 more·2006·Cancer Cell

DOI 10.1016/j.ccr.2006.04.022

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Abstract

To understand the role of human epidermal growth factor receptor (hEGFR) kinase domain mutations in lung tumorigenesis and response to EGFR-targeted therapies, we generated bitransgenic mice with inducible expression in type II pneumocytes of two common hEGFR mutants seen in human lung cancer. Both bitransgenic lines developed lung adenocarcinoma after sustained hEGFR mutant expression, confirming their oncogenic potential. Maintenance of these lung tumors was dependent on continued expression of the EGFR mutants. Treatment with small molecule inhibitors (erlotinib or HKI-272) as well as prolonged treatment with a humanized anti-hEGFR antibody (cetuximab) led to dramatic tumor regression. These data suggest that persistent EGFR signaling is required for tumor maintenance in human lung adenocarcinomas expressing EGFR mutants.

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Exon 19 deletions and L858R are oncogenic in cell lines and mouse models.
“These EGFR mutations are oncogenic in both cell lines and mouse models 9,10.”
From Structural, Biochemical, and Clinical Characterization of Epidermal Growth Factor Receptor (EGFR) Exon 20 Insertion Mutations in Lung Cancer (2013) · cites this paper as [10]

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Tsien, C. I., Nyati, M. K., Ahsan, A., Ramanand, S. G., Chepeha, D. B., Worden, F. P., Helman, J. I., D’Silva, N. J., Bradford, C. R., Wolf, G. T., et al. (2012) · Head & Neck · doi:10.1002/hed.23128 · Cited by 30 · see citing works
Development and evaluation of a cetuximab-based imaging probe to target EGFR and EGFRvIII
Aerts, H. J. W. L., Dubois, L. J., Hackeng, T. M., et al. (2007) · Radiotherapy and Oncology · doi:10.1016/j.radonc.2007.04.030 · Cited by 36 · see citing works

Authors: Ji, H., Li, D., Chen, L., Shimamura, T., Kobayashi, S., McNamara, K., Mahmood, U., Mitchell, A., Sun, Y., Al-Hashem, R., Chirieac, L. R., Padera, R., Bronson, R. T., Kim, W., Jänne, P. A., Shapiro, G. I., Tenen, D., Johnson, B. E., Weissleder, R., Sharpless, N. E., & Wong, K.-K.
Affiliations: Dana-Farber Cancer Institute (US)
Beth Israel Deaconess Medical Center (US)
Harvard University (US)
Brigham and Women's Hospital (US)
University of North Carolina at Chapel Hill (US)
Corresponding author: Wong, Kwok-Kin
ORCID: Ji, Hongbin
Chen, Liang
Shimamura, Takeshi
Kobayashi, Susumu
Mahmood, Umar
Chirieac, Lucian R.
Padera, Robert
Bronson, Roderick T.
Kim, William
Shapiro, Geoffrey I.
Tenen, Daniel
Johnson, Bruce E.
Weissleder, Ralph
Sharpless, Norman E.
Wong, Kwok-Kin
Venue: Cancer Cell
Publisher: Elsevier BV
Published: 2006-06
Volume: 9
Issue: 6
Pages: 485-495
ISSN: 1535-6108 (ISSN-L)
DOI: 10.1016/j.ccr.2006.04.022
OpenAlex: W2070011883
Cited by: 462
References: 46
Citations by year: 2026: 2 · 2025: 8 · 2024: 10 · 2023: 17 · 2022: 13 · 2021: 13 · 2020: 17 · 2019: 10 · 2018: 22 · 2017: 13 · 2016: 20 · 2015: 27 · 2014: 26 · 2013: 22 · 2012: 22
FWCI: 43.28
Type: journal article
Language: en
Open access: bronze
doi.org
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/open-access/userlicense/1.0/ (vor, 2639 d)
Locations: Cancer Cell (publishedVersion)
PubMed (publishedVersion)
Carolina Digital Repository (University of North Carolina at Chapel Hill) (submittedVersion)
Digital Access to Scholarship at Harvard (DASH) (Harvard University) (submittedVersion, cc-by)
The Mouseion at the JAXlibrary (Jackson Laboratory) (submittedVersion)
UNC Libraries
Funders: Flight Attendant Medical Research Institute
Sidney Kimmel Foundation for Cancer Research
Memorial Sloan-Kettering Cancer Center
National Institutes of Health (5r01ag024379-15, AG024379)
National Institute on Aging (AG024379, AG2400401)
National Cancer Institute (K08CA090679, CA90679)
Topics: Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Lung Cancer Treatments and Mutations
Health Sciences › Medicine › Oncology › HER2/EGFR in Cancer Research
Health Sciences › Medicine › Oncology › Lung Cancer Research Studies
Keywords: lung adenocarcinoma, lung carcinogenesis, anti-EGFR therapy, erlotinib, cetuximab, bitransgenic mice, alveolar type II cells, oncogenicity, tumor maintenance, EGFR signaling
MeSH terms: Cetuximab, Erlotinib Hydrochloride, Adenocarcinoma, Animals, Antibodies, Monoclonal, Antineoplastic Agents, Adenocarcinoma, Bronchiolo-Alveolar, Enzyme Activation, Exons, Humans, Lung, Lung Neoplasms, Mice, Transgenic, Mutation, Quinazolines, Quinolines, Protein Structure, Tertiary, Mice, Antibodies, Monoclonal, Humanized, ErbB Receptors

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The impact of human EGFR kinase domain mutations on lung tumorigenesis and in vivo sensitivity to EGFR-targeted therapies

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