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

The DOI matches its Crossref record; 37 of the 37 references it cites were found in a registry or an index.

Preexistence and Clonal Selection of MET Amplification in EGFR Mutant NSCLC

Open access

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.·2010·Cancer Cell

DOI 10.1016/j.ccr.2009.11.022PMC PMC2980857

Open this paper in CoChat — free account Open PDF

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.

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

Integrity signals

Registry

Crossref · 10.1016/j.ccr.2009.11.022

Cites

37 of 37 references verified0 citation errors · 0 not checkable

Statistics

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Gefitinib or Carboplatin–Paclitaxel in Pulmonary Adenocarcinoma
Mok, T. S., Wu, Y.-L., Thongprasert, S., Yang, C.-H., Chu, D.-T., Saijo, N., Sunpaweravong, P., Han, B., Margono, B., Ichinose, Y., et al. (2009) · New England Journal of Medicine · doi:10.1056/nejmoa0810699 · Cited by 8,261
Self-citation
MET Amplification Leads to Gefitinib Resistance in Lung Cancer by Activating ERBB3 Signaling
Engelman, J. A., Zejnullahu, K., Mitsudomi, T., Song, Y., Hyland, C., Park, J. O., Lindeman, N., Gale, C.-M., Zhao, X., Christensen, J., et al. (2007) · Science · doi:10.1126/science.1141478 · Cited by 4,496
Self-citation
Efficacy and safety of imatinib mesylate in advanced gastrointestinal stromal tumors
Demetri, G. D., von Mehren, M., Blanke, C. D., Van den Abbeele, A. D., Eisenberg, B., Roberts, P. J., Heinrich, M. C., Tuveson, D. A., Singer, S., Janicek, M., et al. (2002) · New England Journal of Medicine · doi:10.1056/nejmoa020461 · Cited by 4,389
EGFR Mutation and Resistance of Non–Small-Cell Lung Cancer to Gefitinib
Kobayashi, S., Boggon, T. J., Dayaram, T., Jänne, P. A., Kocher, O., Meyerson, M., Johnson, B. E., Eck, M. J., Tenen, D. G., & Halmos, B. (2005) · New England Journal of Medicine · doi:10.1056/nejmoa044238 · Cited by 3,964
Acquired Resistance of Lung Adenocarcinomas to Gefitinib or Erlotinib Is Associated with a Second Mutation in the EGFR Kinase Domain
Pao, W., Miller, V. A., Politi, K. A., Riely, G. J., Somwar, R., Zakowski, M. F., Kris, M. G., & Varmus, H. (2005) · PLoS Medicine · doi:10.1371/journal.pmed.0020073 · Cited by 3,527 · cited 2×
“Secondary mutations in EGFR itself, including the EGFR T790M ‘‘gatekeeper’’ mutation is observed in 50% of resistance cases, and amplification of the MET oncogene is observed in 20% of resistance cases (Balak et al., 2006; Bean et al., 2007; Engelman et al., 2007b; Kobayashi et al., 2005; Kosaka et al., 2006; Pao et a…”
Background
Clinical Resistance to STI-571 Cancer Therapy Caused by BCR-ABL Gene Mutation or Amplification
Gorre, M. E., Mohammed, M., Ellwood, K., Hsu, N., Paquette, R., Rao, P. N., & Sawyers, C. L. (2001) · Science · doi:10.1126/science.1062538 · Cited by 3,104
Activity of a Specific Inhibitor of the BCR-ABL Tyrosine Kinase in the Blast Crisis of Chronic Myeloid Leukemia and Acute Lymphoblastic Leukemia with the Philadelphia Chromosome
Druker, B. J., Sawyers, C. L., Kantarjian, H., Resta, D. J., Reese, S. F., Ford, J. M., Capdeville, R., & Talpaz, M. (2001) · New England Journal of Medicine · doi:10.1056/nejm200104053441402 · Cited by 2,713
Screening for Epidermal Growth Factor Receptor Mutations in Lung Cancer
Rosell, R., Moran, T., Queralt, C., Porta, R., Cardenal, F., Camps, C., Majem, M., Lopez-Vivanco, G., Isla, D., Provencio, M., et al. (2009) · New England Journal of Medicine · doi:10.1056/nejmoa0904554 · Cited by 2,373
The T790M mutation in EGFR kinase causes drug resistance by increasing the affinity for ATP
Yun, C.-H., Mengwasser, K. E., Toms, A. V., Woo, M. S., Greulich, H., Wong, K.-K., Meyerson, M., & Eck, M. J. (2008) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0709662105 · Cited by 2,118 · cited 2×
“To date, resistance mechanisms have predominately involved secondary genomic alterations in the target kinase that alter either the physical (such as steric hindrance) or biochemical (change in ATP affinity) properties of the receptor and result in drug resistance (Gorre et al., 2001; Shah et al., 2002; Yun et al., 20…”
Background
Detection of Mutations in EGFR in Circulating Lung-Cancer Cells
Maheswaran, S., Sequist, L. V., Nagrath, S., Ulkus, L., Brannigan, B., Collura, C. V., Inserra, E., Diederichs, S., Iafrate, A. J., Bell, D. W., et al. (2008) · New England Journal of Medicine · doi:10.1056/nejmoa0800668 · Cited by 1,617
Self-citation
Multiple BCR-ABL kinase domain mutations confer polyclonal resistance to the tyrosine kinase inhibitor imatinib (STI571) in chronic phase and blast crisis chronic myeloid leukemia
Shah, N. P., Nicoll, J. M., Nagar, B., Gorre, M. E., PAQUETTE, R. L., Kuriyan, J., & Sawyers, C. L. (2002) · Cancer Cell · doi:10.1016/s1535-6108(02)00096-x · Cited by 1,614
MET amplification occurs with or without T790M mutations in EGFR mutant lung tumors with acquired resistance to gefitinib or erlotinib
Bean, J., Brennan, C., Shih, J.-Y., Riely, G., Viale, A., Wang, L., Chitale, D., Motoi, N., Szoke, J., Broderick, S., et al. (2007) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0710370104 · Cited by 1,598
Biomarker Analyses and Final Overall Survival Results From a Phase III, Randomized, Open-Label, First-Line Study of Gefitinib Versus Carboplatin/Paclitaxel in Clinically Selected Patients With Advanced Non–Small-Cell Lung Cancer in Asia (IPASS)
Fukuoka, M., Wu, Y.-L., Thongprasert, S., Sunpaweravong, P., Leong, S.-S., Sriuranpong, V., Chao, T.-Y., Nakagawa, K., Chu, D.-T., Saijo, N., et al. (2011) · Journal of Clinical Oncology · doi:10.1200/jco.2010.33.4235 · Cited by 1,581
Self-citation
Novel D761Y and Common Secondary T790M Mutations in Epidermal Growth Factor Receptor–Mutant Lung Adenocarcinomas with Acquired Resistance to Kinase Inhibitors
Balak, M. N., Gong, Y., Riely, G. J., Somwar, R., Li, A. R., Zakowski, M. F., Chiang, A. C., Yang, G., Ouerfelli, O., Kris, M. G., et al. (2006) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-06-1570 · Cited by 823
First-Line Gefitinib in Patients With Advanced Non–Small-Cell Lung Cancer Harboring Somatic EGFR Mutations
Sequist, L. V., Martins, R. G., Spigel, D., Grunberg, S. M., Spira, A., Jänne, P. A., Joshi, V. A., McCollum, D., Evans, T. L., Muzikansky, A., et al. (2008) · Journal of Clinical Oncology · doi:10.1200/jco.2007.14.8494 · Cited by 820
Self-citation
An Orally Available Small-Molecule Inhibitor of c-Met, PF-2341066, Exhibits Cytoreductive Antitumor Efficacy through Antiproliferative and Antiangiogenic Mechanisms
Zou, H. Y., Li, Q., Lee, J. H., Arango, M. E., McDonnell, S. R. P., Yamazaki, S., Koudriakova, T. B., Alton, G., Cui, J. J., Kung, P., et al. (2007) · Cancer Research · doi:10.1158/0008-5472.can-06-4443 · Cited by 749
Self-citation
PF00299804, an Irreversible Pan-ERBB Inhibitor, Is Effective in Lung Cancer Models with EGFR and ERBB2 Mutations that Are Resistant to Gefitinib
Engelman, J. A., Zejnullahu, K., Gale, C.-M., Lifshits, E., Gonzales, A. J., Shimamura, T., Zhao, F., Vincent, P. W., Naumov, G. N., Bradner, J. E., et al. (2007) · Cancer Research · doi:10.1158/0008-5472.can-07-1885 · Cited by 730
Self-citation
Mechanisms of Acquired Resistance to Epidermal Growth Factor Receptor Tyrosine Kinase Inhibitors in Non–Small Cell Lung Cancer
Engelman, J. A., & Janne, P. A. (2008) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-07-2248 · Cited by 706
Self-citation
Hepatocyte growth factor induces gefitinib resistance of lung adenocarcinoma with epidermal growth factor receptor-activating mutations
Yano, S., Wang, W., Li, Q., Matsumoto, K., Sakurama, H., Nakamura, T., Ogino, H., Kakiuchi, S., Hanibuchi, M., Nishioka, Y., et al. (2008) · Cancer Research · doi:10.1158/0008-5472.can-08-1643 · Cited by 643
Analysis of Epidermal Growth Factor Receptor Gene Mutation in Patients with Non–Small Cell Lung Cancer and Acquired Resistance to Gefitinib
Kosaka, T., Yatabe, Y., Endoh, H., Yoshida, K., Hida, T., Tsuboi, M., Tada, H., Kuwano, H., & Mitsudomi, T. (2006) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-06-0714 · Cited by 598
Acquired resistance to EGFR tyrosine kinase inhibitors in cancer cells is mediated by loss of IGF-binding proteins
Guix, M., Faber, A. C., Wang, S. E., Olivares, M. G., Song, Y., Qu, S., Rinehart, C., Seidel, B., Yee, D., Arteaga, C. L., et al. (2008) · Journal of Clinical Investigation · doi:10.1172/jci34588 · Cited by 525
Self-citation
Several types of mutations of the Abl gene can be found in chronic myeloid leukemia patients resistant to STI571, and they can pre-exist to the onset of treatment
Roche‐Lestienne, C., Soenen, V., Grardel, N., Laï, J., Philippe, N., Facon, T. T. F., Fenaux, P., & Preudhomme, C. (2002) · Blood · doi:10.1182/blood.v100.3.1014 · Cited by 516
Prospective phase II study of gefitinib for chemotherapy-naive patients with advanced non-small-cell lung cancer with epidermal growth factor receptor gene mutations
Inoue, A., Suzuki, T., Fukuhara, T., Maemondo, M., Kimura, Y., Morikawa, N., Watanabe, H., Saijo, Y., & Nukiwa, T. (2006) · Journal of Clinical Oncology · doi:10.1200/jco.2005.05.4692 · Cited by 509
ErbB-3 mediates phosphoinositide 3-kinase activity in gefitinib-sensitive non-small cell lung cancer cell lines
Engelman, J. A., Janne, P. A., Mermel, C. H., Pearlberg, J., Mukohara, T., Fleet, C., Cichowski, K. M., Johnson, B. E., & Cantley, L. C. (2005) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0409773102 · Cited by 500
Self-citation
Allelic dilution obscures detection of a biologically significant resistance mutation in EGFR-amplified lung cancer
Engelman, J. A., Mukohara, T., Zejnullahu, K., Lifshits, E., Borras, A. M., Gale, C.-M., Naumov, G. N., Yeap, B. Y., Jarrell, E., Sun, J., et al. (2006) · Journal of Clinical Investigation · doi:10.1172/jci28656 · Cited by 457
Self-citation
Helical domain and kinase domain mutations in p110α of phosphatidylinositol 3-kinase induce gain of function by different mechanisms
Zhao, L., & Vogt, P. K. (2008) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0712169105 · Cited by 449
A role for common fragile site induction in amplification of human oncogenes
Hellman, A., Zlotorynski, E., Scherer, S. W., Cheung, J., Vincent, J. B., Smith, D. I., Trakhtenbrot, L., & Kerem, B. (2002) · Cancer Cell · doi:10.1016/s1535-6108(02)00017-x · Cited by 300
A phase II trial of gefitinib as first-line therapy for advanced non-small cell lung cancer with epidermal growth factor receptor mutations
Asahina, H., Yamazaki, K., Kinoshita, I., Sukoh, N., Harada, M., Yokouchi, H., Ishida, T., Ogura, S., Kojima, T., Okamoto, Y., et al. (2006) · British Journal of Cancer · doi:10.1038/sj.bjc.6603393 · Cited by 276
A rapid and sensitive enzymatic method for epidermal growth factor receptor mutation screening
Jänne, P. A., Borras, A. M., Kuang, Y., Rogers, A. M., Joshi, V. A., Liyanage, H., Lindeman, N., Lee, J. C., Halmos, B., Maher, E. A., et al. (2006) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-05-2047 · Cited by 214
Self-citation
Multicentre prospective phase II trial of gefitinib for advanced non-small cell lung cancer with epidermal growth factor receptor mutations: results of the West Japan Thoracic Oncology Group trial (WJTOG0403)
Tamura, K., Okamoto, I., Kashii, T., Negoro, S., Hirashima, T., Kudoh, S., Ichinose, Y., Ebi, N., Shibata, K., Nishimura, T., et al. (2008) · British Journal of Cancer · doi:10.1038/sj.bjc.6604249 · Cited by 201
Emergence of Epidermal Growth Factor Receptor T790M Mutation during Chronic Exposure to Gefitinib in a Non–Small Cell Lung Cancer Cell Line
Ogino, A., Kitao, H., Hirano, S., Uchida, A., Ishiai, M., Kozuki, T., Takigawa, N., Takata, M., Kiura, K., & Tanimoto, M. (2007) · Cancer Research · doi:10.1158/0008-5472.can-07-0681 · Cited by 194
Presence of the BCR-ABL mutation Glu255Lys prior to STI571 (imatinib) treatment in patients with Ph+ acute lymphoblastic leukemia
Hofmann, W., Komor, M., Waßmann, B., Jones, L. C., Gschaidmeier, H., Hoelzer, D. F., Koeffler, H. P., & Ottmann, O. G. (2003) · Blood · doi:10.1182/blood-2002-06-1756 · Cited by 124
A Mutation Conferring Resistance to Imatinib at the Time of Diagnosis of Chronic Myelogenous Leukemia
Roche‐Lestienne, C., Laï, J., Darre, S., Facon, T. T. F., & Preudhomme, C. (2003) · New England Journal of Medicine · doi:10.1056/nejmc035089 · Cited by 92
Second-Generation Epidermal Growth Factor Receptor Tyrosine Kinase Inhibitors in Non-small Cell Lung Cancer
Riely, G. J. (2008) · Journal of Thoracic Oncology · doi:10.1097/jto.0b013e318174e96e · Cited by 74
Second-Generation Epidermal Growth Factor Receptor Tyrosine Kinase Inhibitors in Non-Small Cell Lung Cancer
Sequist, L. V. D. (2007) · The Oncologist · doi:10.1634/theoncologist.12-3-325 · Cited by 74
Self-citation
Preliminary activity and safety results from a phase I clinical trial of PF-00299804, an irreversible pan-HER inhibitor, in patients (pts) with NSCLC
Janne, P. A., Schellens, J. H. M., Engelman, J. A., Eckhardt, S. G., Millham, R., Denis, L. J., Britten, C. D., Wong, S. G., Boss, D. S., & Camidge, D. R. (2008) · Journal of Clinical Oncology · doi:10.1200/jco.2008.26.15_suppl.8027 · Cited by 67
Self-citation
First-in-human study of the safety, tolerability, pharmacokinetics (PK), and pharmacodynamics (PD) of PF-00299804, a small molecule irreversible panHER inhibitor in patients with advanced cancer
Schellens, J. H. M., Britten, C. D., Camidge, D. R., Boss, D. S., Wong, S., Diab, S., Guo, F., Maguire, R. P., Letrent, S. P., & Eckhardt, S. (2007) · Journal of Clinical Oncology · doi:10.1200/jco.2007.25.18_suppl.3599 · Cited by 13

Sorted by citations

Cancer Genome Landscapes
Vogelstein, B., Papadopoulos, N., Velculescu, V. E., Zhou, S., Diaz, L. A., & Kinzler, K. W. (2013) · Science · doi:10.1126/science.1235122 · Cited by 7,863
The biology and management of non-small cell lung cancer
Herbst, R. S., Morgensztern, D., & Boshoff, C. (2018) · Nature · doi:10.1038/nature25183 · Cited by 4,891
Tumour heterogeneity and resistance to cancer therapies
Dagogo-Jack, I., & Shaw, A. T. (2018) · Nature Reviews Clinical Oncology · doi:10.1038/nrclinonc.2017.166 · Cited by 3,846
Genotypic and Histological Evolution of Lung Cancers Acquiring Resistance to EGFR Inhibitors
Sequist, L. V., Waltman, B. A., Dias-Santagata, D., Digumarthy, S., Turke, A. B., Fidias, P., Bergethon, K., Shaw, A. T., Gettinger, S., Cosper, A. K., et al. (2011) · Science Translational Medicine · doi:10.1126/scitranslmed.3002003 · Cited by 3,499
Self-citation
Clonal evolution in cancer
Greaves, M., & Maley, C. C. (2012) · Nature · doi:10.1038/nature10762 · Cited by 3,162

See all 1,059

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

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review

Preexistence and Clonal Selection of MET Amplification in EGFR Mutant NSCLC

Abstract

Overview

Integrity signals

Verification

Claims the paper makes

Claims other papers make about this one

Self-check

Citations

Cites

Cited by

Related

Metadata

Record

About these checks