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Preexistence and Clonal Selection of MET Amplification in EGFR Mutant NSCLC
Open accessAbstract
MET amplification activates ERBB3/PI3K/AKT signaling in EGFR mutant lung cancers and causes resistance to EGFR kinase inhibitors. We demonstrate that MET activation by its ligand, HGF, also induces drug resistance, but through GAB1 signaling. Using high-throughput FISH analyses in both cell lines and in patients with lung cancer, we identify subpopulations of cells with MET amplification prior to drug exposure. Surprisingly, HGF accelerates the development of MET amplification both in vitro and in vivo. EGFR kinase inhibitor resistance, due to either MET amplification or autocrine HGF production, was cured in vivo by combined EGFR and MET inhibition. These findings highlight the potential to prospectively identify treatment naive, patients with EGFR-mutant lung cancer who will benefit from initial combination therapy.
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“HGF-induced signaling through MET was shown to abrogate the action of trastuzumab (Shattuck et al., 2008; Turke et al., 2010).”
From ERBB Receptors: From Oncogene Discovery to Basic Science to Mechanism-Based Cancer Therapeutics (2014) · cites this paper as Turke et al., 2010
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“the (acquired) alterations identified in a single biopsy may not reflect all of the resistant clones in multiple metastatic sites in an individual patient (Bean et al., 2007; Engelman et al., 2007; Turke et al., 2010).”
From ERBB Receptors: From Oncogene Discovery to Basic Science to Mechanism-Based Cancer Therapeutics (2014) · cites this paper as Turke et al., 2010
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Metadata
- Authors
- Turke, A. B., Zejnullahu, K., Wu, Y.-L., Song, Y., Dias-Santagata, D., Lifshits, E., Toschi, L., Rogers, A., Mok, T., Sequist, L., Lindeman, N. I., Murphy, C., Akhavanfard, S., Yeap, B. Y., Xiao, Y., Capelletti, M., Iafrate, A. J., Lee, C., Christensen, J. G., Engelman, J. A., & Jänne, P. A.
- Affiliations
- Harvard University (US)
- Dana-Farber Cancer Institute (US)
- Guangdong General Hospital (CN)
- Massachusetts General Hospital (US)
- Chinese University of Hong Kong (HK)
- Brigham and Women's Hospital (US)
- Pfizer (United States) (US)
- Corresponding author
- Engelman, Jeffrey A.
- ORCID
- Venue
- Cancer Cell
- Publisher
- Elsevier BV
- Published
- 2010-01
- Volume
- 17
- Issue
- 1
- Pages
- 77-88
- ISSN
- 1535-6108 (ISSN-L)
- PMC
- PMC2980857
- OpenAlex
- W1985264867
- Cited by
- 1,059
- References
- 37
- Citations by year
- 2026: 22 · 2025: 31 · 2024: 36 · 2023: 58 · 2022: 41 · 2021: 55 · 2020: 41 · 2019: 56 · 2018: 66 · 2017: 73 · 2016: 93 · 2015: 84 · 2014: 88 · 2013: 94 · 2012: 106
- FWCI
- 83.75
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cancer Cell (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Guangdong Provincial Hospital of Traditional Chinese Medicine
- University of Hong Kong
- Chinese University of Hong Kong
- National Institutes of Health
- National Cancer Institute (P50CA127003, R01CA140594, R01CA114465, P50CA090578, R01CA135257, K08CA120060, R01CA137008)
- 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
- MET amplification, EGFR mutation, non-small cell lung cancer, hepatocyte growth factor, clonal selection, combination therapy
- MeSH terms
- Animals, Antineoplastic Agents, Carcinoma, Non-Small-Cell Lung, Gene Amplification, Humans, Lung Neoplasms, Mutation, Proto-Oncogene Proteins, Signal Transduction, Gene Expression, Polymerase Chain Reaction, Hepatocyte Growth Factor, In Situ Hybridization, Fluorescence, Receptors, Growth Factor, Drug Resistance, Neoplasm, Proto-Oncogene Proteins c-met, Xenograft Model Antitumor Assays, Cell Line, Tumor, Mice, Quinazolinones, ErbB Receptors
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