Hepatocyte growth factor sensitizes brain tumors to c-MET kinase inhibition. - Wikidata - awgldk - TriplyDB

Hepatocyte growth factor sensitizes brain tumors to c-MET kinase inhibition.

Hepatocyte growth factor sensitizes brain tumors to c-MET kinase inhibition.

http://www.wikidata.org/entity/Q30414265

about

microRNA-148a is a prognostic oncomiR that targets MIG6 and BIM to regulate EGFR and apoptosis in glioblastoma.Constitutive and ligand-induced EGFR signalling triggers distinct and mutually exclusive downstream signalling networks.Exogenous HGF Bypasses the Effects of ErbB Inhibition on Tumor Cell Viability in Medulloblastoma Cell Lines The hepatocyte growth factor receptor as a potential therapeutic target for dedifferentiated liposarcoma EGFR wild type antagonizes EGFRvIII-mediated activation of Met in glioblastoma.Impact of MACC1 on human malignant glioma progression and patients' unfavorable prognosis The biologic era of childhood medulloblastoma and clues to novel therapies.Exon 14 Deleted MET Receptor as a New Biomarker and Target in Cancers.Role and Therapeutic Targeting of the HGF/MET Pathway in Glioblastoma.Novel MET/TIE2/VEGFR2 inhibitor altiratinib inhibits tumor growth and invasiveness in bevacizumab-resistant glioblastoma mouse models Cancer stem cells from peritumoral tissue of glioblastoma multiforme: the possible missing link between tumor development and progression.Phase 1 trial, pharmacokinetics, and pharmacodynamics of dasatinib combined with crizotinib in children with recurrent or progressive high-grade and diffuse intrinsic pontine glioma.

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P2860

Hepatocyte growth factor sensitizes brain tumors to c-MET kinase inhibition.

http://www.wikidata.org/entity/Q30414265

description

2013 nî lūn-bûn

@nan

2013 թուականի Փետրուարին հրատարակուած գիտական յօդուած

@hyw

2013 թվականի փետրվարին հրատարակված գիտական հոդված

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2013年の論文

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2013年論文

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2013年論文

@zh-hant

2013年論文

@zh-hk

2013年論文

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2013年論文

@zh-tw

2013年论文

@wuu

name

Hepatocyte growth factor sensitizes brain tumors to c-MET kinase inhibition.

@ast

Hepatocyte growth factor sensitizes brain tumors to c-MET kinase inhibition.

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type

label

Hepatocyte growth factor sensitizes brain tumors to c-MET kinase inhibition.

@ast

Hepatocyte growth factor sensitizes brain tumors to c-MET kinase inhibition.

@en

prefLabel

Hepatocyte growth factor sensitizes brain tumors to c-MET kinase inhibition.

@ast

Hepatocyte growth factor sensitizes brain tumors to c-MET kinase inhibition.

@en

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1078-0432.CCR-12-2832

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Clinical Cancer Research

P1476

Hepatocyte growth factor sensitizes brain tumors to c-MET kinase inhibition.

@en

P2093

Benjamin Purow

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

Charles G Dipierro

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

David Schiff

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

Emanuel Petricoin

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

Fadila Guessous

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

Jae K Lee

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

James Christensen

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

Jianghong Deng

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

Kaitlyn E Farenholtz

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

Roger Abounader

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

P2860

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

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

NK4 (HGF-antagonist/angiogenesis inhibitor) in cancer biology and therapeutics

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

Induction of epithelial tubules by growth factor HGF depends on the STAT pathway

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

Interaction between Gab1 and the c-Met receptor tyrosine kinase is responsible for epithelial morphogenesis

A mammalian cell cycle checkpoint pathway utilizing p53 and GADD45 is defective in ataxia-telangiectasia

Tumor stem cells derived from glioblastomas cultured in bFGF and EGF more closely mirror the phenotype and genotype of primary tumors than do serum-cultured cell lines

Identification of an atypical Grb2 carboxyl-terminal SH3 domain binding site in Gab docking proteins reveals Grb2-dependent and -independent recruitment of Gab1 to receptor tyrosine kinases.

P304

1433-1444

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scholarly article

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10.1158/1078-0432.CCR-12-2832

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6

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19

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2013-02-05T00:00:00Z

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23386689

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3602223

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