Activation of HER family members in gastric carcinoma cells mediates resistance to MET inhibition. - Wikidata - awgldk - TriplyDB

Activation of HER family members in gastric carcinoma cells mediates resistance to MET inhibition.

Activation of HER family members in gastric carcinoma cells mediates resistance to MET inhibition.

http://www.wikidata.org/entity/Q33942266

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Clinical significance of MET in gastric cancer MET: a critical player in tumorigenesis and therapeutic target Epidermal growth factor signaling in transformed cells GL-1196 Suppresses the Proliferation and Invasion of Gastric Cancer Cells via Targeting PAK4 and Inhibiting PAK4-Mediated Signaling Pathways A novel SND1-BRAF fusion confers resistance to c-Met inhibitor PF-04217903 in GTL16 cells through [corrected] MAPK activation A novel proteomics-based clinical diagnostics technology identifies heterogeneity in activated signaling pathways in gastric cancers Receptor tyrosine kinases fall into distinct classes based on their inferred signaling networks Exome sequencing deciphers a germline MET mutation in familial epidermal growth factor receptor-mutant lung cancer.LC-0882 targets PAK4 and inhibits PAK4-related signaling pathways to suppress the proliferation and invasion of gastric cancer cells.HGF/MET-directed therapeutics in gastroesophageal cancer: a review of clinical and biomarker development.Outgrowth of drug-resistant carcinomas expressing markers of tumor aggression after long-term TβRI/II kinase inhibition with LY2109761.Synthetic lethal screening reveals FGFR as one of the combinatorial targets to overcome resistance to Met-targeted therapy Truncated RAF kinases drive resistance to MET inhibition in MET-addicted cancer cells.Targeted therapy in the management of advanced gastric cancer: are we making progress in the era of personalized medicine?Overexpression of FGFR2 contributes to inherent resistance to MET inhibitors in MET-amplified patient-derived gastric cancer xenografts.Overexpression of PI3K p110α contributes to acquired resistance to MET inhibitor, in MET-amplified SNU-5 gastric xenografts.Targeted therapy in gastroesophageal cancers: past, present and future.Activation of Pim Kinases Is Sufficient to Promote Resistance to MET Small-Molecule Inhibitors.3-bromopyruvate and sodium citrate target glycolysis, suppress survivin, and induce mitochondrial-mediated apoptosis in gastric cancer cells and inhibit gastric orthotopic transplantation tumor growth.The coexpression and prognostic significance of c-MET, fibroblast growth factor receptor 2, and human epidermal growth factor receptor 2 in resected gastric cancer: a retrospective study.Unraveling trastuzumab and lapatinib inefficiency in gastric cancer: Future steps (Review).Gastric cancer-molecular and clinical dimensions.Targeting MET and EGFR crosstalk signaling in triple-negative breast cancers.c-MET as a potential therapeutic target and biomarker in cancer.Effect of Fluorouracil, Leucovorin, and Oxaliplatin With or Without Onartuzumab in HER2-Negative, MET-Positive Gastroesophageal Adenocarcinoma: The METGastric Randomized Clinical Trial.Promise and challenges on the horizon of MET-targeted cancer therapeutics Emerging kinase inhibitors of the treatment of gastric cancer.Advances of Molecular Targeted Therapy in Gastric Cancer.Dual MET/EGFR therapy leads to complete response and resistance prevention in a MET-amplified gastroesophageal xenopatient cohort.Fangchinoline targets PI3K and suppresses PI3K/AKT signaling pathway in SGC7901 cells Oxymatrine targets EGFR(p-Tyr845) and inhibits EGFR-related signaling pathways to suppress the proliferation and invasion of gastric cancer cells.Comprehensive analyses using next-generation sequencing and immunohistochemistry enable precise treatment in advanced gastric cancer.Increase of MET gene copy number confers resistance to a monovalent MET antibody and establishes drug dependence.A novel bispecific EGFR/Met antibody blocks tumor-promoting phenotypic effects induced by resistance to EGFR inhibition and has potent antitumor activity.MET activation mediates resistance to lapatinib inhibition of HER2-amplified gastric cancer cells.Recombinant immunotoxin anti-c-Met/PE38KDEL inhibits proliferation and promotes apoptosis of gastric cancer cells Rilotumumab plus epirubicin, cisplatin, and capecitabine as first-line therapy in advanced MET-positive gastric or gastro-oesophageal junction cancer (RILOMET-1): a randomised, double-blind, placebo-controlled, phase 3 trial.FOXO1 Suppression is a Determinant of Acquired Lapatinib-Resistance in HER2-Positive Gastric Cancer Cells Through MET Upregulation.The Chemokine Receptor CXCR4 and c-MET Cooperatively Promote Epithelial-Mesenchymal Transition in Gastric Cancer Cells.Expression profiles of HER2, EGFR, MET and FGFR2 in a large cohort of patients with gastric adenocarcinoma.

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Activation of HER family members in gastric carcinoma cells mediates resistance to MET inhibition.

http://www.wikidata.org/entity/Q33942266

description

2010 nî lūn-bûn

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2010 թուականի Մայիսին հրատարակուած գիտական յօդուած

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2010 թվականի մայիսին հրատարակված գիտական հոդված

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2010年の論文

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2010年論文

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2010年論文

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2010年論文

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2010年論文

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2010年論文

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2010年论文

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name

Activation of HER family membe ...... resistance to MET inhibition.

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Activation of HER family membe ...... resistance to MET inhibition.

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type

label

Activation of HER family membe ...... resistance to MET inhibition.

@ast

Activation of HER family membe ...... resistance to MET inhibition.

@en

prefLabel

Activation of HER family membe ...... resistance to MET inhibition.

@ast

Activation of HER family membe ...... resistance to MET inhibition.

@en

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Molecular Cancer

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Activation of HER family membe ...... s resistance to MET inhibition

@en

P2093

Elena Ghiso

http://www.w3.org/2001/XMLSchema#string

J Rafael Sierra

http://www.w3.org/2001/XMLSchema#string

Livio Trusolino

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Virna Cepero

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P2860

The Hallmarks of Cancer

Amplification of MET may identify a subset of cancers with extreme sensitivity to the selective tyrosine kinase inhibitor PHA-665752

ErbB receptors: from oncogenes to targeted cancer therapies

MET amplification leads to gefitinib resistance in lung cancer by activating ERBB3 signaling.

Wild-type BRAF is required for response to panitumumab or cetuximab in metastatic colorectal cancer.

A selective small molecule inhibitor of c-Met kinase inhibits c-Met-dependent phenotypes in vitro and exhibits cytoreductive antitumor activity in vivo

The semaphorin 4D receptor controls invasive growth by coupling with Met

Met, metastasis, motility and more

Targeting the tumor and its microenvironment by a dual-function decoy Met receptor

A multifunctional docking site mediates signaling and transformation by the hepatocyte growth factor/scatter factor receptor family

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10.1186/1476-4598-9-121

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9

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Paolo M. Comoglio

Andrea Bertotti

Silvia Giordano

Cristina Migliore

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2010-05-26T00:00:00Z

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44628839

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1044418682

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20500904

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2892452

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