Cited by 1,598Lung Cancer Treatments and MutationsHER2/EGFR in Cancer ResearchCancer Genomics and Diagnostics

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MET amplification occurs with or without T790M mutations in EGFR mutant lung tumors with acquired resistance to gefitinib or erlotinib

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Bean, James, Brennan, Cameron, Shih, Jin-Yuan, Riely, Gregory, Viale, Agnes, Wang, Lu, Chitale, Dhananjay, Motoi, Noriko, Szoke, Janos, Broderick, Stephen, Balak, Marissa, Chang, Wen-Cheng, Yu, Chong-Jen, Gazdar, Adi, Pass, Harvey, Rusch, Valerie, Gerald, William, Huang, Shiu-Feng, Yang, Pan-Chyr, Miller, Vincent, Ladanyi, Marc, Yang, Chih-Hsin, Pao, William·2007·Proceedings of the National Academy of Sciences

DOI 10.1073/pnas.0710370104PMC PMC2409244

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Abstract

In human lung adenocarcinomas harboring EGFR mutations, a second-site point mutation that substitutes methionine for threonine at position 790 (T790M) is associated with approximately half of cases of acquired resistance to the EGFR kinase inhibitors, gefitinib and erlotinib. To identify other potential mechanisms that contribute to disease progression, we used array-based comparative genomic hybridization (aCGH) to compare genomic profiles of EGFR mutant tumors from untreated patients with those from patients with acquired resistance. Among three loci demonstrating recurrent copy number alterations (CNAs) specific to the acquired resistance set, one contained the MET proto-oncogene. Collectively, analysis of tumor samples from multiple independent patient cohorts revealed that MET was amplified in tumors from 9 of 43 (21%) patients with acquired resistance but in only two tumors from 62 untreated patients (3%) (P = 0.007, Fisher's Exact test). Among 10 resistant tumors from the nine patients with MET amplification, 4 also harbored the EGFR(T790M) mutation. We also found that an existing EGFR mutant lung adenocarcinoma cell line, NCI-H820, harbors MET amplification in addition to a drug-sensitive EGFR mutation and the T790M change. Growth inhibition studies demonstrate that these cells are resistant to both erlotinib and an irreversible EGFR inhibitor (CL-387,785) but sensitive to a multikinase inhibitor (XL880) with potent activity against MET. Taken together, these data suggest that MET amplification occurs independently of EGFR(T790M) mutations and that MET may be a clinically relevant therapeutic target for some patients with acquired resistance to gefitinib or erlotinib.

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Authors: Bean, J., Brennan, C., Shih, J.-Y., Riely, G., Viale, A., Wang, L., Chitale, D., Motoi, N., Szoke, J., Broderick, S., Balak, M., Chang, W.-C., Yu, C.-J., Gazdar, A., Pass, H., Rusch, V., Gerald, W., Huang, S.-F., Yang, P.-C., Miller, V., Ladanyi, M., Yang, C.-H., & Pao, W.
Affiliations: Memorial Sloan Kettering Cancer Center (US)
National Taiwan University (TW)
Department of Pathology, Memorial Sloan–Kettering Cancer Center, New York, NY 10021;
Chang Gung Memorial Hospital (TW)
The University of Texas Southwestern Medical Center (US)
NYU Langone Health (US)
National Health Research Institutes (TW)
National Taiwan University Hospital (TW)
ORCID: Bean, James
Brennan, Cameron
Shih, Jin-Yuan
Riely, Gregory
Viale, Agnes
Wang, Lu
Chitale, Dhananjay
Motoi, Noriko
Broderick, Stephen
Yu, Chong-Jen
Gazdar, Adi
Pass, Harvey
Rusch, Valerie
Huang, Shiu-Feng
Yang, Pan-Chyr
Miller, Vincent
Ladanyi, Marc
Pao, William
Venue: Proceedings of the National Academy of Sciences
Publisher: National Academy of Sciences
Published: 2007-12-26
Volume: 104
Issue: 52
Pages: 20932-20937
ISSN: 0027-8424 (ISSN-L)
1091-6490
DOI: 10.1073/pnas.0710370104
PMC: PMC2409244
OpenAlex: W2093613683
Cited by: 1,598
References: 37
Citations by year: 2026: 17 · 2025: 19 · 2024: 33 · 2023: 42 · 2022: 59 · 2021: 54 · 2020: 78 · 2019: 78 · 2018: 100 · 2017: 89 · 2016: 116 · 2015: 135 · 2014: 124 · 2013: 148 · 2012: 126
FWCI: 71.72
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Locations: Proceedings of the National Academy of Sciences (publishedVersion)
Europe PMC (PubMed Central) (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Funders: Conquer Cancer Foundation
Memorial Sloan-Kettering Cancer Center
Exelixis
National Cancer Institute (U01 CA 84999, P50CA75907, R01CA121210, U01CA084999, K08CA097980, R21CA115051)
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, T790M mutation, EGFR mutation, lung adenocarcinoma, acquired drug resistance, gefitinib, erlotinib, EGFR tyrosine kinase inhibitors, copy number alterations, multikinase inhibitor, therapeutic target
MeSH terms: Erlotinib Hydrochloride, Gefitinib, Proto-Oncogene Mas, Adenocarcinoma, Antineoplastic Agents, Chromosomes, Human, Pair 7, DNA Mutational Analysis, Humans, Lung Neoplasms, Mutation, Quinazolines, Cohort Studies, Gene Expression Regulation, Neoplastic, In Situ Hybridization, Fluorescence, Drug Resistance, Neoplasm, Proto-Oncogene Proteins c-met, Protein Kinase Inhibitors, ErbB Receptors

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MET amplification occurs with or without T790M mutations in EGFR mutant lung tumors with acquired resistance to gefitinib or erlotinib

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