Preexistence and clonal selection of MET amplification in EGFR mutant NSCLC

Turke, Alexa B.; Zejnullahu, Kreshnik; Wu, Yi-Long; Song, Youngchul; Dias-Santagata, Dora; Lifshits, Eugene; Toschi, Luca; Rogers, Andrew; Mok, Tony; Sequist, Lecia; Lindeman, Neal I.; Murphy, Carly; Akhavanfard, Sara; Yeap, Beow Y.; Xiao, Yun; Capelletti, Marzia; Iafrate, A. John; Lee, Charles; Christensen, James G.; Engelman, Jeffrey A.; Jänne, Pasi A.

doi:10.1016/j.ccr.2009.11.022

Cited by 1,059Lung Cancer Treatments and MutationsHER2/EGFR in Cancer ResearchCancer Genomics and Diagnostics

Preexistence and clonal selection of MET amplification in EGFR mutant NSCLC

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Turke, Alexa B., Zejnullahu, Kreshnik, Wu, Yi-Long, Song, Youngchul, Dias-Santagata, Dora, Lifshits, Eugene, Toschi, Luca, Rogers, Andrew +13 more·2010·Cancer Cell

DOI 10.1016/j.ccr.2009.11.022PMC PMC2980857

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Abstract

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 abrogates the action of trastuzumab.
“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
Acquired alterations identified in a single biopsy may not reflect all resistant clones in multiple metastatic sites in an individual patient.
“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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Mok T Wu Y Thongprasert S Phase III, randomized, open label, first-line study of gefitinib vs. carboplatin/paclitaxel in clinically selected patients with advanced non-small cell lung cancer (IPASS) Annals of Oncology 2008 19

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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: Wu, Yi-Long
Song, Youngchul
Dias-Santagata, Dora
Toschi, Luca
Mok, Tony
Sequist, Lecia
Lindeman, Neal I.
Akhavanfard, Sara
Yeap, Beow Y.
Capelletti, Marzia
Iafrate, A. John
Lee, Charles
Christensen, James G.
Engelman, Jeffrey A.
Venue: Cancer Cell
Publisher: Elsevier BV
Published: 2010-01
Volume: 17
Issue: 1
Pages: 77-88
ISSN: 1535-6108 (ISSN-L)
DOI: 10.1016/j.ccr.2009.11.022
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: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/open-access/userlicense/1.0/ (vor, 1293 d)
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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Preexistence and clonal selection of MET amplification in EGFR mutant NSCLC

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