Compensatory glutamine metabolism promotes glioblastoma resistance to mTOR inhibitor treatment. - Wikidata - wikimedia - TriplyDB

Compensatory glutamine metabolism promotes glioblastoma resistance to mTOR inhibitor treatment.

Compensatory glutamine metabolism promotes glioblastoma resistance to mTOR inhibitor treatment.

http://www.wikidata.org/entity/Q35408838

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Novel drugs that target the metabolic reprogramming in renal cell cancer Retinoblastoma tumor suppressor functions shared by stem cell and cancer cell strategies MYC, Metabolism, and Cancer Non-invasive metabolic imaging of brain tumours in the era of precision medicine.Phosphorylation by mTORC1 stablizes Skp2 and regulates its oncogenic function in gastric cancer Rapamycin (mTORC1 inhibitor) reduces the production of lactate and 2-hydroxyglutarate oncometabolites in IDH1 mutant fibrosarcoma cells From Krebs to clinic: glutamine metabolism to cancer therapy.Compensatory metabolic networks in pancreatic cancers upon perturbation of glutamine metabolism Supramolecular Probes for Assessing Glutamine Uptake Enable Semi-Quantitative Metabolic Models in Single Cells.In search of druggable targets for GBM amino acid metabolism.Alterations in cellular metabolome after pharmacological inhibition of Notch in glioblastoma cells.2-Aminobutyric acid modulates glutathione homeostasis in the myocardium Selenite inhibits glutamine metabolism and induces apoptosis by regulating GLS1 protein degradation via APC/C-CDH1 pathway in colorectal cancer cells.Glutaminase 1 plays a key role in the cell growth of fibroblast-like synoviocytes in rheumatoid arthritis.Targeting Glutamine Induces Apoptosis: A Cancer Therapy Approach.How does metabolism affect cell death in cancer?Glutaminolysis as a target for cancer therapy.Dying glioma cells establish a proangiogenic microenvironment through a caspase 3 dependent mechanism.Blockage of glutaminolysis enhances the sensitivity of ovarian cancer cells to PI3K/mTOR inhibition involvement of STAT3 signaling.Blocking autophagy enhanced leukemia cell death induced by recombinant human arginase.Glutamate and α-ketoglutarate: key players in glioma metabolism.Glutamine Addiction In Gliomas.Hopefully devoted to Q: targeting glutamine addiction in cancer.Metabolic Reprogramming in Glioma.Glutaminase sustains cell survival via the regulation of glycolysis and glutaminolysis in colorectal cancer Glutaminase and poly(ADP-ribose) polymerase inhibitors suppress pyrimidine synthesis and VHL-deficient renal cancers.Targeting hexokinase 2 enhances response to radio-chemotherapy in glioblastoma.Nuclear Compartmentalization of Serine Racemase Regulates D-Serine Production: IMPLICATIONS FOR N-METHYL-D-ASPARTATE (NMDA) RECEPTOR ACTIVATION.Targeted Inhibition of EGFR and Glutaminase Induces Metabolic Crisis in EGFR Mutant Lung Cancer.Glutaminase is essential for the growth of triple-negative breast cancer cells with a deregulated glutamine metabolism pathway and its suppression synergizes with mTOR inhibition.Diagnostic value of glutamate with 2-hydroxyglutarate in magnetic resonance spectroscopy for IDH1 mutant glioma.Targeting glutaminase and mTOR.Drug repurposing for the treatment of glioblastoma multiforme.Myo-inositol concentration in MR spectroscopy for differentiating high grade glioma from primary central nervous system lymphoma.p53 Nongenotoxic Activation and mTORC1 Inhibition Lead to Effective Combination for Neuroblastoma Therapy.Targeting Glutamine Metabolism for Cancer Treatment.Glutaminolysis is a metabolic dependency in FLT3ITD acute myeloid leukemia unmasked by FLT3 tyrosine kinase inhibition.Exploiting Metabolic Vulnerabilities of Cancer with Precision and Accuracy.Autophagy mediates glucose starvation-induced glioblastoma cell quiescence and chemoresistance through coordinating cell metabolism, cell cycle, and survival.Glutaminolysis Promotes Collagen Translation and Stability via α-ketoglutarate Mediated mTOR Activation and Proline Hydroxylation.

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P2860

Compensatory glutamine metabolism promotes glioblastoma resistance to mTOR inhibitor treatment.

http://www.wikidata.org/entity/Q35408838

description

2015 nî lūn-bûn

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2015 թվականի մարտին հրատարակված գիտական հոդված

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2015年の論文

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2015年論文

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Compensatory glutamine metabol ...... e to mTOR inhibitor treatment.

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Compensatory glutamine metabol ...... e to mTOR inhibitor treatment.

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Compensatory glutamine metabol ...... e to mTOR inhibitor treatment.

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Beatrice Gini

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Eiji Kohmura

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Hiroaki Nagashima

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Huijun Yang

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Katsusuke Kyotani

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Kazuhiro Tanaka

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Kenta Masui

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Kohkichi Hosoda

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Kumi Takata

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Naoko Satoh

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P2860

Tyrosine phosphorylation of mitochondrial pyruvate dehydrogenase kinase 1 is important for cancer metabolism

Understanding the Warburg effect: the metabolic requirements of cell proliferation

Glucose deprivation contributes to the development of KRAS pathway mutations in tumor cells

Comprehensive genomic characterization defines human glioblastoma genes and core pathways

mTOR kinase structure, mechanism and regulation

Molecular determinants of the response of glioblastomas to EGFR kinase inhibitors.

Defining the role of mTOR in cancer

Prolonged rapamycin treatment inhibits mTORC2 assembly and Akt/PKB

Antitumor activity of rapamycin in a Phase I trial for patients with recurrent PTEN-deficient glioblastoma

Glucose-independent glutamine metabolism via TCA cycling for proliferation and survival in B cells

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1591-1602

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10.1172/JCI78239

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4

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125

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Taichiro Imahori

Takashi Sasayama

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2015-03-23T00:00:00Z

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25798620

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4396477

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