Bevacizumab treatment induces metabolic adaptation toward anaerobic metabolism in glioblastomas - Wikidata - wikimedia - TriplyDB

Bevacizumab treatment induces metabolic adaptation toward anaerobic metabolism in glioblastomas

Bevacizumab treatment induces metabolic adaptation toward anaerobic metabolism in glioblastomas

http://www.wikidata.org/entity/Q34807753

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Cancer stem cells: targeting the roots of cancer, seeds of metastasis, and sources of therapy resistance Comprehensive analysis of glycolytic enzymes as therapeutic targets in the treatment of glioblastoma Radiation treatment monitoring using multimodal functional imaging: PET/CT ((18)F-Fluoromisonidazole & (18)F-Fluorocholine) and DCE-US.Biological basis and clinical study of glycogen synthase kinase- 3β-targeted therapy by drug repositioning for glioblastoma.Reactive Oxygen Species-Mediated Mechanisms of Action of Targeted Cancer Therapy Engraftment of Human Glioblastoma Cells in Immunocompetent Rats through Acquired Immunosuppression.Targeted Proteomics to Assess the Response to Anti-Angiogenic Treatment in Human Glioblastoma (GBM).Molecular crosstalk between tumour and brain parenchyma instructs histopathological features in glioblastoma.Bevacizumab and radiotherapy for the treatment of glioblastoma: brothers in arms or unholy alliance?Emerging Approaches for Targeting Metabolic Vulnerabilities in Malignant Glioma.Metabolism of 4-Hydroxy-7-oxo-5-heptenoic Acid (HOHA) Lactone by Retinal Pigmented Epithelial Cells.Limited role for transforming growth factor-β pathway activation-mediated escape from VEGF inhibition in murine glioma models.Glycolysis and the pentose phosphate pathway are differentially associated with the dichotomous regulation of glioblastoma cell migration versus proliferation.In silico gene expression analysis reveals glycolysis and acetate anaplerosis in IDH1 wild-type glioma and lactate and glutamate anaplerosis in IDH1-mutated glioma Treatment of adult and pediatric high-grade gliomas with Withaferin A: antitumor mechanisms and future perspectives.Targeting cancer stem-like cells in glioblastoma and colorectal cancer through metabolic pathways.Trimming the Vascular Tree in Tumors: Metabolic and Immune Adaptations.The interplay between metabolic remodeling and immune regulation in glioblastoma.Nucleus accumbens-associated protein-1 promotes glycolysis and survival of hypoxic tumor cells via the HDAC4-HIF-1α axis.Regulation of hypoxia-induced autophagy in glioblastoma involves ATG9A.Effects of soluble CPE on glioma cell migration are associated with mTOR activation and enhanced glucose flux.Vascular endothelial growth factor blockade elicits a stable metabolic shift in tumor cells: therapeutic implications.Targeting Malignant Brain Tumors with Antibodies.Mammalian target of rapamycin complex 1 activation sensitizes human glioma cells to hypoxia-induced cell death.Induction of reactive oxygen species: an emerging approach for cancer therapy.Metabolic alterations underlying Bevacizumab therapy in glioblastoma cells.Altered metabolic landscape in IDH-mutant gliomas affects phospholipid, energy, and oxidative stress pathways.Hexokinase 2 (HK2), the tumor promoter in glioma, is downregulated by miR-218/Bmi1 pathway.In Vivo Assessment of Ovarian Tumor Response to Tyrosine Kinase Inhibitor Pazopanib by Using Hyperpolarized 13C-Pyruvate MR Spectroscopy and 18F-FDG PET/CT Imaging in a Mouse Model.Suppression of oxidative phosphorylation confers resistance against bevacizumab in experimental glioma.Developmentally regulated signaling pathways in glioma invasion.Multifaceted C-X-C Chemokine Receptor 4 (CXCR4) Inhibition Interferes with Anti-Vascular Endothelial Growth Factor Therapy-Induced Glioma Dissemination.Randomized phase II study of axitinib versus physicians best alternative choice of therapy in patients with recurrent glioblastoma.Temozolomide, sirolimus and chloroquine is a new therapeutic combination that synergizes to disrupt lysosomal function and cholesterol homeostasis in GBM cells.Lack of functional normalisation of tumour vessels following anti-angiogenic therapy in glioblastoma.Large Intergenic Non-coding RNA-RoR Inhibits Aerobic Glycolysis of Glioblastoma Cells via Akt Pathway.Targeting Oxidatively Induced DNA Damage Response in Cancer: Opportunities for Novel Cancer Therapies.

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P2860

Bevacizumab treatment induces metabolic adaptation toward anaerobic metabolism in glioblastomas

http://www.wikidata.org/entity/Q34807753

description

2014 nî lūn-bûn

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2014 թուականի Հոկտեմբերին հրատարակուած գիտական յօդուած

@hyw

2014 թվականի հոտեմբերին հրատարակված գիտական հոդված

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2014年の論文

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2014年論文

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2014年論文

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2014年論文

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2014年論文

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Bevacizumab treatment induces ...... ic metabolism in glioblastomas

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Bevacizumab treatment induces ...... ic metabolism in glioblastomas

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Acta Neuropathologica

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Cecilie B Rygh

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Hrvoje Miletic

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Liang Zheng

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Linda Stuhr

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Nina Obad

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P2860

VEGF inhibits tumor cell invasion and mesenchymal transition through a MET/VEGFR2 complex

β1 integrin targeting potentiates antiangiogenic therapy and inhibits the growth of bevacizumab-resistant glioblastoma

Mechanisms of neovascularization and resistance to anti-angiogenic therapies in glioblastoma multiforme

Mechanisms of evasive resistance to anti-VEGF therapy in glioblastoma

The clonal evolution of tumor cell populations

Why do cancers have high aerobic glycolysis?

Critical appraisal of the side population assay in stem cell and cancer stem cell research

Effects of dual targeting of tumor cells and stroma in human glioblastoma xenografts with a tyrosine kinase inhibitor against c-MET and VEGFR2

Normalization of tumor vasculature: an emerging concept in antiangiogenic therapy

Clonal evolution in cancer

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1

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Patrick N. Harter

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2014-10-17T00:00:00Z

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267044952

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25322816

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metabolic adaptation

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