Lung adenocarcinomas induced in mice by mutant EGF receptors foundin human lung cancers respondto a tyrosine kinase inhibitor orto down-regulation of the receptors

Politi, Katerina; Zakowski, Maureen F.; Fan, Pang-Dian; Schonfeld, Emily A.; Pao, William; Varmus, Harold E.

doi:10.1101/gad.1417406

PreprintCited by 478Lung Cancer Treatments and MutationsHER2/EGFR in Cancer ResearchLung Cancer Research Studies

Lung adenocarcinomas induced in mice by mutant EGF receptors foundin human lung cancers respondto a tyrosine kinase inhibitor orto down-regulation of the receptors

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Politi, Katerina, Zakowski, Maureen F., Fan, Pang-Dian, Schonfeld, Emily A., Pao, William, Varmus, Harold E.·2006·Genes & Development

DOI 10.1101/gad.1417406

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Abstract

Somatic mutations in exons encoding the tyrosine kinase domain of the epidermal growth factor receptor ( EGFR ) gene are found in human lung adenocarcinomas and are associated with sensitivity to the tyrosine kinase inhibitors gefitinib and erlotinib. Nearly 90% of the EGFR mutations are either short, in-frame deletions in exon 19 or point mutations that result in substitution of arginine for leucine at amino acid 858 (L858R). To study further the role of these mutations in the initiation and maintenance of lung cancer, we have developed transgenic mice that express an exon 19 deletion mutant ( EGFR Δ L747–S752 ) or the L858R mutant ( EGFR L858R ) in type II pneumocytes under the control of doxycycline. Expression of either EGFR mutant leads to the development of lung adenocarcinomas. Two weeks after induction with doxycycline, mice that express the EGFR L858R allele show diffuse lung cancer highly reminiscent of human bronchioloalveolar carcinoma and later develop interspersed multifocal adenocarcinomas. In contrast, mice expressing EGFR Δ L747–S752 develop multifocal tumors embedded in normal lung parenchyma with a longer latency. With mice carrying either EGFR allele, withdrawal of doxycycline (to reduce expression of the transgene) or treatment with erlotinib (to inhibit kinase activity) causes rapid tumor regression, as assessed by magnetic resonance imaging and histopathology, demonstrating that mutant EGFR is required for tumor maintenance. These models may be useful for developing improved therapies for patients with lung cancers bearing EGFR mutations.

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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 [9]
Cell culture and transgenic mouse model studies have shown that mutant EGFR has transforming activity.
“Cell culture and transgenic mouse model studies have shown that mutant EGFR has transforming activity (Greulich et al., 2005; Ji et al., 2006; Politi et al., 2006).”
From ERBB Receptors: From Oncogene Discovery to Basic Science to Mechanism-Based Cancer Therapeutics (2014) · cites this paper as Politi et al., 2006

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Abstract 725: In vivo imaging and quantitative proteomics to study responsiveness to EGFR targeted therapy.
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Authors: Politi, K., Zakowski, M. F., Fan, P.-D., Schonfeld, E. A., Pao, W., & Varmus, H. E.
Affiliations: Memorial Sloan Kettering Cancer Center (US)
ORCID: Politi, Katerina
Zakowski, Maureen F.
Fan, Pang-Dian
Schonfeld, Emily A.
Pao, William
Varmus, Harold E.
Venue: Genes & Development
Publisher: Cold Spring Harbor Laboratory
Published: 2006-05-16
Volume: 20
Issue: 11
Pages: 1496-1510
ISSN: 0890-9369 (ISSN-L)
1549-5477
DOI: 10.1101/gad.1417406
OpenAlex: W2126181231
Cited by: 478
References: 50
Citations by year: 2026: 10 · 2025: 14 · 2024: 18 · 2023: 23 · 2022: 15 · 2021: 17 · 2020: 15 · 2019: 9 · 2018: 24 · 2017: 11 · 2016: 23 · 2015: 38 · 2014: 25 · 2013: 19 · 2012: 27
Type: posted content
Language: en
Open access: bronze
doi.org
Locations: Genes & Development (publishedVersion)
Europe PMC (PubMed Central) (publishedVersion)
PubMed (publishedVersion)
Funders: Memorial Sloan-Kettering Cancer Center
Dana-Farber Cancer Institute
University of Cincinnati
National Institutes of Health (R24 CA83084)
Genentech
National Cancer Institute (K08CA097980, R24CA083084)
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, epidermal growth factor receptor, EGFR mutation, exon 19 deletion, L858R mutation, tyrosine kinase inhibitors, erlotinib, gefitinib, transgenic mouse model, alveolar type II cells, tumor regression, tumor maintenance, doxycycline-inducible expression, bronchioloalveolar carcinoma
MeSH terms: Adenocarcinoma, Animals, Base Sequence, Humans, Lung Neoplasms, Magnetic Resonance Imaging, Phosphorylation, Protein-Tyrosine Kinases, Down-Regulation, DNA Primers, Mice, ErbB Receptors

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Lung adenocarcinomas induced in mice by mutant EGF receptors foundin human lung cancers respondto a tyrosine kinase inhibitor orto down-regulation of the receptors

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