DLL4-Notch signaling mediates tumor resistance to anti-VEGF therapy in vivo. - Wikidata - awgldk - TriplyDB

DLL4-Notch signaling mediates tumor resistance to anti-VEGF therapy in vivo.

DLL4-Notch signaling mediates tumor resistance to anti-VEGF therapy in vivo.

http://www.wikidata.org/entity/Q39497811

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Mechanisms of neovascularization and resistance to anti-angiogenic therapies in glioblastoma multiforme Tumor cell vasculogenic mimicry: from controversy to therapeutic promise Compensatory angiogenesis and tumor refractoriness Angiogenesis in metastatic colorectal cancer and the benefits of targeted therapy Eph receptors as therapeutic targets in glioblastoma Brain tumor stem cells: Molecular characteristics and their impact on therapy In vitro and in vivo models for analysis of resistance to anticancer molecular therapies Resistance and escape from antiangiogenesis therapy: clinical implications and future strategies Targeted therapies in development for non-small cell lung cancer Metabolic and hypoxic adaptation to anti-angiogenic therapy: a target for induced essentiality The Notch pathway: a crossroad between the life and death of the endothelium Gene expression profiling identifies EPHB4 as a potential predictive biomarker in colorectal cancer patients treated with bevacizumab.ROS, Notch, and Wnt signaling pathways: crosstalk between three major regulators of cardiovascular biology Epidermal growth factor receptor inhibition reduces angiogenesis via hypoxia-inducible factor-1α and Notch1 in head neck squamous cell carcinoma γ-Secretase inhibitor enhances antitumour effect of radiation in Notch-expressing lung cancer Anti-angiogenic therapy for cancer: current progress, unresolved questions and future directions.Macrophage migration inhibitory factor downregulation: a novel mechanism of resistance to anti-angiogenic therapy.Vascular Mimicry: A Novel Neovascularization Mechanism Driving Anti-Angiogenic Therapy (AAT) Resistance in Glioblastoma Inhibition of Notch signaling alters the phenotype of orthotopic tumors formed from glioblastoma multiforme neurosphere cells but does not hamper intracranial tumor growth regardless of endogene Notch pathway signature Endothelial Delta-like 4 (DLL4) promotes renal cell carcinoma hematogenous metastasis.Essential roles of EphB receptors and EphrinB ligands in endothelial cell function and angiogenesis.Fatty acid-binding protein 4, a point of convergence for angiogenic and metabolic signaling pathways in endothelial cells.The antiangiogenic 16K prolactin impairs functional tumor neovascularization by inhibiting vessel maturation.Gene Expression Analysis Reveals Distinct Pathways of Resistance to Bevacizumab in Xenograft Models of Human ER-Positive Breast Cancer Molecular pathways: vasculogenic mimicry in tumor cells: diagnostic and therapeutic implications.Novel paracrine modulation of Notch-DLL4 signaling by fibulin-3 promotes angiogenesis in high-grade gliomas.Role of anti-angiogenesis therapy in the management of hepatocellular carcinoma: The jury is still out.Bevacizumab treatment induces metabolic adaptation toward anaerobic metabolism in glioblastomas Genetic modification of neurons to express bevacizumab for local anti-angiogenesis treatment of glioblastoma.Lenvatinib in combination with golvatinib overcomes hepatocyte growth factor pathway-induced resistance to vascular endothelial growth factor receptor inhibitor.Dll4 blockade potentiates the anti-tumor effects of VEGF inhibition in renal cell carcinoma patient-derived xenografts Angiogenesis-related protein expression in bevacizumab-treated metastatic colorectal cancer: NOTCH1 detrimental to overall survival Combined vaccine+axitinib therapy yields superior antitumor efficacy in a murine melanoma model.High delta-like ligand 4 (DLL4) is correlated with peritumoral brain edema and predicts poor prognosis in primary glioblastoma.Requirement of novel amino acid fragments of orphan nuclear receptor TR3/Nur77 for its functions in angiogenesis PAT4 levels control amino-acid sensitivity of rapamycin-resistant mTORC1 from the Golgi and affect clinical outcome in colorectal cancer Targeting the tumour microenvironment in ovarian cancer Combination therapy of RY10-4 with the γ-secretase inhibitor DAPT shows promise in treating HER2-amplified breast cancer.Differential function and regulation of orphan nuclear receptor TR3 isoforms in endothelial cells.Development and characterization of a high-throughput in vitro cord formation model insensitive to VEGF inhibition.

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P2860

DLL4-Notch signaling mediates tumor resistance to anti-VEGF therapy in vivo.

http://www.wikidata.org/entity/Q39497811

description

2011 nî lūn-bûn

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2011年の論文

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2011年学术文章

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2011年学术文章

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2011年学术文章

@zh-hans

2011年学术文章

@zh-my

2011年学术文章

@zh-sg

2011年學術文章

@yue

2011年學術文章

@zh

2011年學術文章

@zh-hant

name

DLL4-Notch signaling mediates tumor resistance to anti-VEGF therapy in vivo.

@en

DLL4-Notch signaling mediates tumor resistance to anti-VEGF therapy in vivo.

@nl

type

label

DLL4-Notch signaling mediates tumor resistance to anti-VEGF therapy in vivo.

@en

DLL4-Notch signaling mediates tumor resistance to anti-VEGF therapy in vivo.

@nl

prefLabel

DLL4-Notch signaling mediates tumor resistance to anti-VEGF therapy in vivo.

@en

DLL4-Notch signaling mediates tumor resistance to anti-VEGF therapy in vivo.

@nl

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0008-5472.CAN-11-1704

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Cancer Research

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DLL4-Notch signaling mediates tumor resistance to anti-VEGF therapy in vivo.

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Craig P Montgomery

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Emma T Bowden

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Esther Bridges

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Helen Sheldon

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Helen Turley

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Herren Wu

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Ji-Liang Li

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Partha S Chowdhury

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Richard C A Sainson

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Richard Poulsom

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6073-6083

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scholarly article

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10.1158/0008-5472.CAN-11-1704

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18

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Adrian L Harris

Angela J Russell

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2011-07-29T00:00:00Z

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21803743

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