MET amplification occurs with or without T790M mutations in EGFR mutant lung tumors with acquired resistance to gefitinib or erlotinib
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Summary
Analysis of tumor samples from multiple independent patient cohorts and array-based comparative genomic hybridization suggest that MET amplification occurs independently of EGFRT790M mutations and that MET may be a clinically relevant therapeutic target for some patients with acquired resistance to gefitinib or erlotinib.
- Type
- article
- Published
- 2007-11-01
- Cited by
- 1,699
- References
- 37
- OpenAlex
- https://openalex.org/W2093613683
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:1393504
Keywords
T790M, Gefitinib, Erlotinib, Cancer research, Lung cancer
References
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- Germline and somatic mutations in the tyrosine kinase domain of the MET proto-oncogene in papillary renal carcinomas
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- Acquired Resistance of Lung Adenocarcinomas to Gefitinib or Erlotinib Is Associated with a Second Mutation in the EGFR Kinase Domain
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- Therapeutic targeting of receptor tyrosine kinases in lung cancer
- Tyrosine kinase receptor indistinguishable from the c-met protein
- An alternative inhibitor overcomes resistance caused by a mutation of the epidermal growth factor receptor.
- Anticancer drugs: To the rescue?
- Lung cancer cell lines harboring MET gene amplification are dependent on Met for growth and survival.
- Novel D761Y and Common Secondary T790M Mutations in Epidermal Growth Factor Receptor–Mutant Lung Adenocarcinomas with Acquired Resistance to Kinase Inhibitors
Cited by
- Analyzing the Impact of EGFR-induced c-Met Phosphorylation in Non-Small Cell Lung Cancer
- Metastasis: from dissemination to organ-specific colonization
- Lessons learnt from gefitinib and erlotinib: Key insights into small-molecule EGFR-targeted kinase inhibitors in non-small cell lung cancer.
- Antagonism between Gefitinib and Cisplatin in Non-small Cell Lung Cancer Cells: Why Randomized Trials Failed?
- Genetic determinants of anticancer drug activity: towards a global approach to personalized cancer medicine
- Gefitinib resistance of cancer cells correlated with TM4SF5-mediated epithelial-mesenchymal transition.
- Overcoming acquired resistance to kinase inhibition: the cases of EGFR, ALK and BRAF.
- Analysis of Tumor Specimens at the Time of Acquired Resistance to EGFR TKI therapy in 155 patients with EGFR mutant Lung Cancers
- Personalizing Therapy in Advanced Non–Small Cell Lung Cancer
- EGFR: The Paradigm of an Oncogene-Driven Lung Cancer
- TARGETED THERAPY IN CANCER
- Intermittent high-dose treatment with erlotinib enhances therapeutic efficacy in EGFR-mutant lung cancer
- ROR1 sustains caveolae and survival signalling as a scaffold of cavin-1 and caveolin-1
- Intrinsic resistance to EGFR tyrosine kinase inhibitors in advanced non-small-cell lung cancer with activating EGFR mutations
- Expanded molecular interrogation for potential actionable targets in non-squamous non-small cell lung cancer.
- EGFR-TKI resistance in NSCLC patients: mechanisms and strategies.
- Clonal MET Amplification as a Determinant of Tyrosine Kinase Inhibitor Resistance in Epidermal Growth Factor Receptor-Mutant Non-Small-Cell Lung Cancer.
- Targeted therapies for advanced non-small cell lung cancer
- Exploiting MET dysregulation in EGFR-addicted non-small-cell lung carcinoma: a further step toward personalized medicine.
- A personalized treatment for lung cancer: molecular pathways, targeted therapies, and genomic characterization.
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