c-MET Overexpression as a Poor Predictor of MET Amplifications or Exon 14 Mutations in Lung Sarcomatoid Carcinomas
Author:
Publisher
Elsevier BV
Subject
Pulmonary and Respiratory Medicine,Oncology
Reference15 articles.
1. Exon 14 deleted MET receptor as a new biomarker and target in cancers;Cortot;J Natl Cancer Inst,2017
2. Increased MET gene copy number negatively affects survival of surgically resected non–small-cell lung cancer patients;Cappuzzo;J Clin Oncol,2009
3. MET Amplification and exon 14 splice site mutation define unique molecular subgroups of non-small cell lung carcinoma with poor prognosis;Tong;Clin Cancer Res,2016
4. Activation of MET via diverse exon 14 splicing alterations occurs in multiple tumor types and confers clinical sensitivity to MET inhibitors;Frampton;Cancer Discov,2015
5. Activity of crizotinib (PF02341066), a dual mesenchymal-epithelial transition (MET) and anaplastic lymphoma kinase (ALK) inhibitor, in a non–small cell lung cancer patient with de novo MET amplification;Ou;J Thorac Oncol,2011
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3. Unraveling the Significance of MET Focal Amplification in Lung Cancer: Integrative NGS, FISH, and IHC Investigation;Modern Pathology;2024-04
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