Modulation of angiogenic and inflammatory response in glioblastoma by hypoxia - Wikidata - awgldk - TriplyDB

Modulation of angiogenic and inflammatory response in glioblastoma by hypoxia

Modulation of angiogenic and inflammatory response in glioblastoma by hypoxia

http://www.wikidata.org/entity/Q33470265

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Zinc finger proteins in cancer progression Potential prognostic, diagnostic and therapeutic markers for human gastric cancer Kisspeptin Activates Ankrd 26 Gene Expression in Migrating Embryonic GnRH Neurons.Genomic estimates of aneuploid content in glioblastoma multiforme and improved classification The tumor microenvironment underlies acquired resistance to CSF-1R inhibition in gliomas Global gene expression profiling in three tumor cell lines subjected to experimental cycling and chronic hypoxia.Identification of hypoxia-induced genes in human SGBS adipocytes by microarray analysis.Hypoxic signature of microRNAs in glioblastoma: insights from small RNA deep sequencing.Increased microglia/macrophage gene expression in a subset of adult and pediatric astrocytomas Immunotherapy coming of age: what will it take to make it standard of care for glioblastoma?Choline metabolism, proliferation, and angiogenesis in nonenhancing grades 2 and 3 astrocytoma.Molecular biomarkers of vascular dysfunction in obstructive sleep apnea.Induction of the unfolded protein response drives enhanced metabolism and chemoresistance in glioma cells The hypoxia-inducible transcription factor ZNF395 is controlled by IĸB kinase-signaling and activates genes involved in the innate immune response and cancer.Glioma IL13Rα2 is associated with mesenchymal signature gene expression and poor patient prognosis Glioma-associated microglia/macrophages display an expression profile different from M1 and M2 polarization and highly express Gpnmb and Spp1.The Wnt inhibitory factor 1 (WIF1) is targeted in glioblastoma and has a tumor suppressing function potentially by induction of senescence Hypoxia induces macrophage polarization and re-education toward an M2 phenotype in U87 and U251 glioblastoma models Diversity and divergence of the glioma-infiltrating T-cell receptor repertoire.A20 deficiency leads to angiogenesis of pulmonary artery endothelial cells through stronger NF-κB activation under hypoxia Mesenchymal differentiation mediated by NF-κB promotes radiation resistance in glioblastoma.Assessment of tumour hypoxia for prediction of response to therapy and cancer prognosis.Elevated Pentraxin 3 in bone metastatic breast cancer is correlated with osteolytic function.Analysis of the inhibitors of apoptosis identifies BIRC3 as a facilitator of malignant progression in glioma.Presence of an oligodendroglioma-like component in newly diagnosed glioblastoma identifies a pathogenetically heterogeneous subgroup and lacks prognostic value: central pathology review of the EORTC_26981/NCIC_CE.3 trial.Myeloid-derived suppressor cells (MDSCs) in gliomas and glioma-development.Brain and retinal microglia in health and disease: an unrecognized target of the renin-angiotensin system.Myeloid-derived suppressor cells in glioma.Emerging roles for triggering receptor expressed on myeloid cells receptor family signaling in inflammatory diseases.ZNF395 Is an Activator of a Subset of IFN-Stimulated Genes.The Transcription Factor ZNF395 Is Required for the Maximal Hypoxic Induction of Proinflammatory Cytokines in U87-MG Cells.A biology-driven approach identifies the hypoxia gene signature as a predictor of the outcome of neuroblastoma patients.Ectopic overexpression of Nanog induces tumorigenesis in non-tumorous fibroblasts.Modulating glioma-mediated myeloid-derived suppressor cell development with sulforaphane.Regulation of Human Macrophage M1-M2 Polarization Balance by Hypoxia and the Triggering Receptor Expressed on Myeloid Cells-1.Reductive Metabolism Influences the Toxicity and Pharmacokinetics of the Hypoxia-Targeted Benzotriazine Di-Oxide Anticancer Agent SN30000 in Mice.BIRC3 is a biomarker of mesenchymal habitat of glioblastoma, and a mediator of survival adaptation in hypoxia-driven glioblastoma habitats.High sensitivity to carcinogens in the brain of a mouse model of Alzheimer's disease.Interactive phenotyping of large-scale histology imaging data with HistomicsML.The angiogenic switch leads to a metabolic shift in human glioblastoma.

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Modulation of angiogenic and inflammatory response in glioblastoma by hypoxia

http://www.wikidata.org/entity/Q33470265

description

2009 nî lūn-bûn

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2009 թուականի Յունիսին հրատարակուած գիտական յօդուած

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2009 թվականի հունիսին հրատարակված գիտական հոդված

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2009年の論文

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2009年学术文章

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2009年学术文章

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2009年学术文章

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2009年學術文章

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name

Modulation of angiogenic and inflammatory response in glioblastoma by hypoxia

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Modulation of angiogenic and inflammatory response in glioblastoma by hypoxia

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type

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Modulation of angiogenic and inflammatory response in glioblastoma by hypoxia

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Modulation of angiogenic and inflammatory response in glioblastoma by hypoxia

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Modulation of angiogenic and inflammatory response in glioblastoma by hypoxia

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Modulation of angiogenic and inflammatory response in glioblastoma by hypoxia

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Modulation of angiogenic and inflammatory response in glioblastoma by hypoxia

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Amy B Heimberger

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Anastasia Murat

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Curzio Rüegg

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Eugenia Migliavacca

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Isabelle Desbaillets

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Marie-France Hamou

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Mauro Delorenzi

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Roger Stupp

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S Farzana Hussain

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P2860

Cutting edge: inflammatory responses can be triggered by TREM-1, a novel receptor expressed on neutrophils and monocytes

Novel nuclear shuttle proteins, HDBP1 and HDBP2, bind to neuronal cell-specific cis-regulatory element in the promoter for the human Huntington's disease gene

Antiangiogenic therapy elicits malignant progression of tumors to increased local invasion and distant metastasis

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MGMT gene silencing and benefit from temozolomide in glioblastoma.

Radiotherapy plus concomitant and adjuvant temozolomide for glioblastoma

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TREM-1 amplifies inflammation and is a crucial mediator of septic shock

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