Glioblastoma resistance to anti-VEGF therapy is associated with myeloid cell infiltration, stem cell accumulation, and a mesenchymal phenotype. - Wikidata - wikimedia - TriplyDB

Glioblastoma resistance to anti-VEGF therapy is associated with myeloid cell infiltration, stem cell accumulation, and a mesenchymal phenotype.

Glioblastoma resistance to anti-VEGF therapy is associated with myeloid cell infiltration, stem cell accumulation, and a mesenchymal phenotype.

http://www.wikidata.org/entity/Q39281709

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Myeloid cell signatures in tumor microenvironment predicts therapeutic response in cancer Autophagy in stem cells.Dynamic quantitative intravital imaging of glioblastoma progression reveals a lack of correlation between tumor growth and blood vessel density Contribution of the Microenvironmental Niche to Glioblastoma Heterogeneity.Macrophage migration inhibitory factor downregulation: a novel mechanism of resistance to anti-angiogenic therapy.Integrin inhibitor suppresses bevacizumab-induced glioma invasion.Hypoxia suppresses cylindromatosis (CYLD) expression to promote inflammation in glioblastoma: possible link to acquired resistance to anti-VEGF therapy.An orthotopic glioblastoma mouse model maintaining brain parenchymal physical constraints and suitable for intravital two-photon microscopy.The impact of bevacizumab treatment on survival and quality of life in newly diagnosed glioblastoma patients.RAGE expression in tumor-associated macrophages promotes angiogenesis in glioma.Glial progenitors as targets for transformation in glioma.Bevacizumab treatment induces metabolic adaptation toward anaerobic metabolism in glioblastomas Survival outcome of early versus delayed bevacizumab treatment in patients with recurrent glioblastoma Upregulation of hypoxia-inducible factors and autophagy in von Hippel-Lindau-associated retinal hemangioblastoma.Neutrophils promote the malignant glioma phenotype through S100A4.Characterization of Arginase Expression in Glioma-Associated Microglia and Macrophages Expression and prognostic impact of matrix metalloproteinase-2 (MMP-2) in astrocytomas.Bone marrow derived myeloid cells orchestrate antiangiogenic resistance in glioblastoma through coordinated molecular networks.Tumor angiogenesis and anti-angiogenic therapy in malignant gliomas revisited.Differential expression of vascular endothelial growth factor A, its receptors VEGFR-1, -2, and -3 and co-receptors neuropilin-1 and -2 does not predict bevacizumab response in human astrocytomas.Arsenic trioxide disrupts glioma stem cells via promoting PML degradation to inhibit tumor growth Induction of WNT11 by hypoxia and hypoxia-inducible factor-1α regulates cell proliferation, migration and invasion.Glioblastoma: Defining Tumor Niches.The role of microglia and macrophages in glioma maintenance and progression Cytokine patterns in brain tumour progression.Periostin (POSTN) Regulates Tumor Resistance to Antiangiogenic Therapy in Glioma Models.Six-color intravital two-photon imaging of brain tumors and their dynamic microenvironment.Tissue factor expression provokes escape from tumor dormancy and leads to genomic alterations.Assessment of bevacizumab resistance increased by expression of BCAT1 in IDH1 wild-type glioblastoma: application of DSC perfusion MR imaging.Tumor-associated macrophages induce vasculogenic mimicry of glioblastoma multiforme through cyclooxygenase-2 activation Current status of antiangiogenic therapies for glioblastomas.Resistance to antiangiogenic therapy.Bevacizumab for the treatment of high-grade glioma: an update after phase III trials.Reciprocal Supportive Interplay between Glioblastoma and Tumor-Associated Macrophages.CNS macrophages and peripheral myeloid cells in brain tumours.Current evidence of temozolomide and bevacizumab in treatment of gliomas.Resistance to antiangiogenic therapies.Interferon-regulatory factor-1 (IRF1) regulates bevacizumab induced autophagy.Antiangiogenic therapies for glioblastoma.Bevacizumab in high-grade gliomas: past, present, and future.

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Glioblastoma resistance to anti-VEGF therapy is associated with myeloid cell infiltration, stem cell accumulation, and a mesenchymal phenotype.

http://www.wikidata.org/entity/Q39281709

description

2012 nî lūn-bûn

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2012年论文

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name

Glioblastoma resistance to ant ...... , and a mesenchymal phenotype.

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Glioblastoma resistance to ant ...... , and a mesenchymal phenotype.

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Glioblastoma resistance to ant ...... , and a mesenchymal phenotype.

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Glioblastoma resistance to ant ...... , and a mesenchymal phenotype.

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Glioblastoma resistance to ant ...... , and a mesenchymal phenotype.

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Glioblastoma resistance to ant ...... , and a mesenchymal phenotype.

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Glioblastoma resistance to ant ...... , and a mesenchymal phenotype.

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Amado J Zurita

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Ji Liang

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John F de Groot

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Lindsay Holmes

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Verlene Henry

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Yuji Piao

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P2860

Modes of resistance to anti-angiogenic therapy

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

Benefits of targeting both pericytes and endothelial cells in the tumor vasculature with kinase inhibitors

Hypoxia attenuates the expression of E-cadherin via up-regulation of SNAIL in ovarian carcinoma cells

Normalization of tumor vasculature: an emerging concept in antiangiogenic therapy

The role of myeloid cells in the promotion of tumour angiogenesis

Accelerated metastasis after short-term treatment with a potent inhibitor of tumor angiogenesis

Bevacizumab alone and in combination with irinotecan in recurrent glioblastoma

Phase III randomized trial comparing the efficacy of cediranib as monotherapy, and in combination with lomustine, versus lomustine alone in patients with recurrent glioblastoma

Bevacizumab and irinotecan in the treatment of recurrent malignant gliomas.

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