Ras inhibition in glioblastoma down-regulates hypoxia-inducible factor-1alpha, causing glycolysis shutdown and cell death.
about
Pyruvate dehydrogenase complex activity controls metabolic and malignant phenotype in cancer cellsGlucose deprivation contributes to the development of KRAS pathway mutations in tumor cellsOvarian clear cell carcinoma meets metabolism; HNF-1β confers survival benefits through the Warburg effect and ROS reductionOncogenes strike a balance between cellular growth and homeostasisGlucose transport: meeting the metabolic demands of cancer, and applications in glioblastoma treatmentRAS oncogenes: weaving a tumorigenic webThe transcription factor HIF-1alpha plays a critical role in the growth factor-dependent regulation of both aerobic and anaerobic glycolysisNatural product-based inhibitors of hypoxia-inducible factor-1 (HIF-1).Inhibition of hypoxia-inducible factor-1alpha (HIF-1alpha) protein synthesis by DNA damage inducing agentsThe inflammatory cytokine TNFα cooperates with Ras in elevating metastasis and turns WT-Ras to a tumor-promoting entity in MCF-7 cells.Positron emission tomography imaging of DMBA/TPA mouse skin multi-step tumorigenesis.Perturbational profiling of a cell-line model of tumorigenesis by using metabolic measurements.Oncogene activation induces metabolic transformation resulting in insulin-independence in human breast cancer cells.Integrating diverse genomic data using gene setsMiR-124 governs glioma growth and angiogenesis and enhances chemosensitivity by targeting R-Ras and N-RasHIF-1α overexpression in ductal carcinoma in situ of the breast in BRCA1 and BRCA2 mutation carriersThe Bmi-1/NF-κB/VEGF story: another hint for proteasome involvement in glioma angiogenesis?Modulation of A1 and A2B adenosine receptor activity: a new strategy to sensitise glioblastoma stem cells to chemotherapy.Interplay Between HGF/SF-Met-Ras Signaling, Tumor Metabolism and Blood Flow as a Potential Target for Breast Cancer TherapyInhibitors of Glioma Growth that Reveal the Tumour to the Immune System.Inhibition of Ras for cancer treatment: the search continues.Analysis of gene expression array in TSC2-deficient AML cells reveals IRF7 as a pivotal factor in the Rheb/mTOR pathway.Oxidative Dimerization of PHD2 is Responsible for its Inactivation and Contributes to Metabolic Reprogramming via HIF-1α ActivationHighly porous drug-eluting structures: from wound dressings to stents and scaffolds for tissue regenerationSynthesis and evaluation of quinazolin-4-ones as hypoxia-inducible factor-1α inhibitors.Design and in vitro activities of N-alkyl-N-[(8-R-2,2-dimethyl-2H-chromen-6-yl)methyl]heteroarylsulfonamides, novel, small-molecule hypoxia inducible factor-1 pathway inhibitors and anticancer agents.Tumour hypoxia induces a metabolic shift causing acidosis: a common feature in cancer.Is cancer a disease of abnormal cellular metabolism? New angles on an old ideaGroup IIa secretory phospholipase expression correlates with group IIa secretory phospholipase inhibition-mediated cell death in K-ras mutant lung cancer cells.Metabolism addiction in pancreatic cancer.Metabolic assessment of the action of targeted cancer therapeutics using magnetic resonance spectroscopyTargeting Ras-RAF-ERK and its interactive pathways as a novel therapy for malignant gliomas.Exploiting metabolic differences in glioma therapy.KRAS: feeding pancreatic cancer proliferation.Secreted Glioblastoma Nanovesicles Contain Intracellular Signaling Proteins and Active Ras Incorporated in a Farnesylation-dependent Manner.MTH1 expression is required for effective transformation by oncogenic HRAS.Involvement of mitophagy in oncogenic K-Ras-induced transformation: overcoming a cellular energy deficit from glucose deficiencyTargeting Tumor Adaption to Chronic Hypoxia: Implications for Drug Resistance, and How It Can Be Overcome.HIF-1alpha partners with FoxA2, a neuroendocrine-specific transcription factor, to promote tumorigenesis.The role of glucose metabolism and glucose-associated signalling in cancer.
P2860
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P2860
Ras inhibition in glioblastoma down-regulates hypoxia-inducible factor-1alpha, causing glycolysis shutdown and cell death.
description
2005 nî lūn-bûn
@nan
2005 թուականի Փետրուարին հրատարակուած գիտական յօդուած
@hyw
2005 թվականի փետրվարին հրատարակված գիտական հոդված
@hy
2005年の論文
@ja
2005年論文
@yue
2005年論文
@zh-hant
2005年論文
@zh-hk
2005年論文
@zh-mo
2005年論文
@zh-tw
2005年论文
@wuu
name
Ras inhibition in glioblastoma ...... lysis shutdown and cell death.
@ast
Ras inhibition in glioblastoma ...... lysis shutdown and cell death.
@en
Ras inhibition in glioblastoma ...... lysis shutdown and cell death.
@nl
type
label
Ras inhibition in glioblastoma ...... lysis shutdown and cell death.
@ast
Ras inhibition in glioblastoma ...... lysis shutdown and cell death.
@en
Ras inhibition in glioblastoma ...... lysis shutdown and cell death.
@nl
prefLabel
Ras inhibition in glioblastoma ...... lysis shutdown and cell death.
@ast
Ras inhibition in glioblastoma ...... lysis shutdown and cell death.
@en
Ras inhibition in glioblastoma ...... lysis shutdown and cell death.
@nl
P2093
P1433
P1476
Ras inhibition in glioblastoma ...... lysis shutdown and cell death.
@en
P2093
Gideon Rechavi
Jasmine Jacob-Hirsch
Ninette Amariglio
Yoel Kloog
P304
P407
P577
2005-02-01T00:00:00Z