Four individually druggable MET hotspots mediate HGF-driven tumor progression
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Title
Four individually druggable MET hotspots mediate HGF-driven tumor progression
Authors
Keywords
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Journal
JOURNAL OF CLINICAL INVESTIGATION
Volume 124, Issue 7, Pages 3172-3186
Publisher
American Society for Clinical Investigation
Online
2014-05-27
DOI
10.1172/jci72316
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- The MET Oncogene Is a Functional Marker of a Glioblastoma Stem Cell Subtype
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- Induction of MET by Ionizing Radiation and Its Role in Radioresistance and Invasive Growth of Cancer
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- Breast Cancer Cells Induce Cancer-Associated Fibroblasts to Secrete Hepatocyte Growth Factor to Enhance Breast Tumorigenesis
- (2011) Shiaw-Wei Tyan et al. PLoS One
- Hepatocyte growth factor (HGF) autocrine activation predicts sensitivity to MET inhibition in glioblastoma
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- Preexistence and Clonal Selection of MET Amplification in EGFR Mutant NSCLC
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- Monovalency Unleashes the Full Therapeutic Potential of the DN-30 Anti-Met Antibody
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- MetMAb, the One-Armed 5D5 Anti-c-Met Antibody, Inhibits Orthotopic Pancreatic Tumor Growth and Improves Survival
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- Mechanisms of Acquired Resistance to Epidermal Growth Factor Receptor Tyrosine Kinase Inhibitors in Non-Small Cell Lung Cancer
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- Drug development of MET inhibitors: targeting oncogene addiction and expedience
- (2008) Paolo M. Comoglio et al. NATURE REVIEWS DRUG DISCOVERY
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