Interleukin-6 gene amplification and shortened survival in glioblastoma patients. - Wikidata - wikimedia - TriplyDB

Interleukin-6 gene amplification and shortened survival in glioblastoma patients.

Interleukin-6 gene amplification and shortened survival in glioblastoma patients.

http://www.wikidata.org/entity/Q42549981

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Molecular and phenotypic characterisation of paediatric glioma cell lines as models for preclinical drug development Clone-specific expression, transcriptional regulation, and action of interleukin-6 in human colon carcinoma cells Targeting interleukin 6 signaling suppresses glioma stem cell survival and tumor growth Interleukin-1β promotes hypoxia-induced apoptosis of glioblastoma cells by inhibiting hypoxia-inducible factor-1 mediated adrenomedullin production Tumor heterogeneity is an active process maintained by a mutant EGFR-induced cytokine circuit in glioblastoma.Hypoxia suppresses cylindromatosis (CYLD) expression to promote inflammation in glioblastoma: possible link to acquired resistance to anti-VEGF therapy.LIF-independent JAK signalling to chromatin in embryonic stem cells uncovered from an adult stem cell disease.The expression of cytoglobin as a prognostic factor in gliomas: a retrospective analysis of 88 patients Adenovirus-mediated delivery of bFGF small interfering RNA reduces STAT3 phosphorylation and induces the depolarization of mitochondria and apoptosis in glioma cells U251.Therapeutic potential of AZD1480 for the treatment of human glioblastoma Studying a complex tumor: potential and pitfalls.Activation of the NF-κB pathway by the STAT3 inhibitor JSI-124 in human glioblastoma cells.Preferential expression of functional IL-17R in glioma stem cells: potential role in self-renewal.Cytokine patterns in brain tumour progression.A highly invasive human glioblastoma pre-clinical model for testing therapeutics.A novel tumor-promoting mechanism of IL6 and the therapeutic efficacy of tocilizumab: Hypoxia-induced IL6 is a potent autophagy initiator in glioblastoma via the p-STAT3-MIR155-3p-CREBRF pathway NF-κB-induced IL-6 ensures STAT3 activation and tumor aggressiveness in glioblastoma NF-kappaB and STAT3 signaling in glioma: targets for future therapies Musashi-1 regulates AKT-derived IL-6 autocrinal/paracrinal malignancy and chemoresistance in glioblastoma Immunotherapy targeting glioma stem cells--insights and perspectives.Promises and challenges of exhausting pediatric neural cancer stem cells.Interleukins in glioblastoma pathophysiology: implications for therapy.Interleukin-6--a key regulator of colorectal cancer development.Using the molecular classification of glioblastoma to inform personalized treatment.Systematic review of protein biomarkers of invasive behavior in glioblastoma.Role of STAT3 in Genesis and Progression of Human Malignant Gliomas.Transcription factor C/EBP-β mediates downregulation of dipeptidyl-peptidase III expression by interleukin-6 in human glioblastoma cells.Interferon regulatory factor 7 regulates glioma stem cells via interleukin-6 and Notch signalling.Effect of 5-FU and MTX on the Expression of Drug-resistance Related Cancer Stem Cell Markers in Non-small Cell Lung Cancer Cells.Interleukin-6 is overexpressed and augments invasiveness of human glioma stem cells in vitro.Glioblastoma-induced inhibition of Langerhans cell differentiation from CD34(+) precursors is mediated by IL-6 but unaffected by JAK2/STAT3 inhibition.Akt signaling pathway: a target for radiosensitizing human malignant glioma.Glioblastoma cellular cross-talk converges on NF-κB to attenuate EGFR inhibitor sensitivity.Identification of expression quantitative trait loci of RPTOR for susceptibility to glioma.Ebselen abrogates TNFalpha induced pro-inflammatory response in glioblastoma.TLR4 interaction with LPS in glioma CD133+ cancer stem cells induces cell proliferation, resistance to chemotherapy and evasion from cytotoxic T lymphocyte-induced cytolysis.Blocking epithelial-to-mesenchymal transition in glioblastoma with a sextet of repurposed drugs: the EIS regimen.Radiotherapy induces an immediate inflammatory reaction in malignant glioma: a clinical microdialysis study.Platelets from glioblastoma patients promote angiogenesis of tumor endothelial cells and exhibit increased VEGF content and release.NFAT1-regulated IL6 signalling contributes to aggressive phenotypes of glioma.

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P2860

Interleukin-6 gene amplification and shortened survival in glioblastoma patients.

http://www.wikidata.org/entity/Q42549981

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name

Interleukin-6 gene amplification and shortened survival in glioblastoma patients.

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Interleukin-6 gene amplification and shortened survival in glioblastoma patients.

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type

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Interleukin-6 gene amplification and shortened survival in glioblastoma patients.

@en

Interleukin-6 gene amplification and shortened survival in glioblastoma patients.

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prefLabel

Interleukin-6 gene amplification and shortened survival in glioblastoma patients.

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Interleukin-6 gene amplification and shortened survival in glioblastoma patients.

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British Journal of Cancer

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A Tchirkov

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B Irthum

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J-L Kémény

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K Mokhtari

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P Verrelle

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T Khalil

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P2860

Targeted anti-interleukin-6 monoclonal antibody therapy for cancer: a review of the rationale and clinical evidence.

The role of IL-6 and STAT3 in inflammation and cancer.

Recent advances in the treatment of malignant astrocytoma.

Clinical implications of quantitative real-time RT-PCR analysis of hTERT gene expression in human gliomas

Interleukin-6-mediated autocrine growth promotion in human glioblastoma multiforme cell line U87MG.

Overexpressed Skp2 within 5p amplification detected by array-based comparative genomic hybridization is associated with poor prognosis of glioblastomas.

Interleukin-6 induces transcriptional activation of vascular endothelial growth factor (VEGF) in astrocytes in vivo and regulates VEGF promoter activity in glioblastoma cells via direct interaction between STAT3 and Sp1.

IL-6 gene amplification and expression in human glioblastomas.

Interleukin-6 inhibits radiation induced apoptosis in pancreatic cancer cells.

Prognostic impact of molecular markers in a series of 220 primary glioblastomas.

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