Dysfunctional oxidative phosphorylation makes malignant melanoma cells addicted to glycolysis driven by the (V600E)BRAF oncogene. - Wikidata - awgldk - TriplyDB

Dysfunctional oxidative phosphorylation makes malignant melanoma cells addicted to glycolysis driven by the (V600E)BRAF oncogene.

Dysfunctional oxidative phosphorylation makes malignant melanoma cells addicted to glycolysis driven by the (V600E)BRAF oncogene.

http://www.wikidata.org/entity/Q37038401

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Intrinsic and Tumor Microenvironment-Induced Metabolism Adaptations of T Cells and Impact on Their Differentiation and Function Energy metabolic dysfunction as a carcinogenic factor in cancer cells Targeting hypoxic response for cancer therapy Somatic mutations in solid tumors: a spectrum at the service of diagnostic armamentarium or an indecipherable puzzle? The morphological eyes looking for BRAF and somatic molecular detections on cyto-histological samples Capturing the biological impact of CDKN2A and MC1R genes as an early predisposing event in melanoma and non melanoma skin cancer The Synthetic β-Nitrostyrene Derivative CYT-Rx20 Inhibits Esophageal Tumor Growth and Metastasis via PI3K/AKT and STAT3 Pathways A DNA repair pathway score predicts survival in human multiple myeloma: the potential for therapeutic strategy Immune-based antitumor effects of BRAF inhibitors rely on signaling by CD40L and IFNγ.ERK-mediated phosphorylation of TFAM downregulates mitochondrial transcription: implications for Parkinson's disease Potential clinical implications of BRAF mutations in histiocytic proliferations.The stress phenotype makes cancer cells addicted to CDT2, a substrate receptor of the CRL4 ubiquitin ligase.Metabolic determinants of cancer cell sensitivity to glucose limitation and biguanides.Autophagy: In the cROSshairs of cancer.Mitochondria as new therapeutic targets for eradicating cancer stem cells: Quantitative proteomics and functional validation via MCT1/2 inhibition.High Id1 expression, a generally negative prognostic factor, paradoxically predicts a favorable prognosis for adjuvant paclitaxel plus cisplatin therapy in surgically treated lung cancer patients.Targeting ornithine decarboxylase reverses the LIN28/Let-7 axis and inhibits glycolytic metabolism in neuroblastoma.Resistance to BRAF inhibitors induces glutamine dependency in melanoma cells Targeting metabolic flexibility by simultaneously inhibiting respiratory complex I and lactate generation retards melanoma progression.Application of mitochondrial pyruvate carrier blocker UK5099 creates metabolic reprogram and greater stem-like properties in LnCap prostate cancer cells in vitro.The metabolic microenvironment of melanomas: Prognostic value of MCT1 and MCT4 Mitochondrial oxidative stress is the Achille's heel of melanoma cells resistant to Braf-mutant inhibitor.Mitochondrial oxidative phosphorylation controls cancer cell's life and death decisions upon exposure to MAPK inhibitors.The "melanoma-enriched" microRNA miR-4731-5p acts as a tumour suppressor.Cancer as a metabolic disease: implications for novel therapeutics.Dependence On Glycolysis Sensitizes BRAF-mutated Melanomas For Increased Response To Targeted BRAF Inhibition.Pyruvate dehydrogenase expression is negatively associated with cell stemness and worse clinical outcome in prostate cancers.Papillary thyroid microcarcinoma: how to diagnose and manage this epidemic?Mitochondrial dysfunction: a neglected component of skin diseases.Targeting T cell metabolism for therapy.Overexpression of pyruvate dehydrogenase kinase supports dichloroacetate as a candidate for cutaneous melanoma therapy.MAGeCK enables robust identification of essential genes from genome-scale CRISPR/Cas9 knockout screens.Myc and Ras oncogenes engage different energy metabolism programs and evoke distinct patterns of oxidative and DNA replication stress.Poly(3-hydroxybutyrate-co-R-3-hydroxyhexanoate) nanoparticles with polyethylenimine coat as simple, safe, and versatile vehicles for cell targeting: population characteristics, cell uptake, and intracellular trafficking.Polyplex Evolution: Understanding Biology, Optimizing Performance.Metabolic Hallmarks of Tumor and Immune Cells in the Tumor Microenvironment Engineering Chimeric Antigen Receptor T-Cells for Racing in Solid Tumors: Don't Forget the Fuel Dasatinib modulates sensitivity to pemetrexed in malignant pleural mesothelioma cell lines.The PWWP domain of the human oncogene WHSC1L1/NSD3 induces a metabolic shift toward fermentation.Impact of the Tumor Microenvironment on Tumor-Infiltrating Lymphocytes: Focus on Breast Cancer.Resistance to Dasatinib in primary chronic lymphocytic leukemia lymphocytes involves AMPK-mediated energetic re-programming.

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Dysfunctional oxidative phosphorylation makes malignant melanoma cells addicted to glycolysis driven by the (V600E)BRAF oncogene.

http://www.wikidata.org/entity/Q37038401

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article científic

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bilimsel makale

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scientific article published on April 2013

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vedecký článok

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vetenskaplig artikel

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videnskabelig artikel

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vědecký článek

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name

Dysfunctional oxidative phosph ...... n by the (V600E)BRAF oncogene.

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Dysfunctional oxidative phosph ...... ed to glycolysis driven by the

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Dysfunctional oxidative phosph ...... n by the (V600E)BRAF oncogene.

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Dysfunctional oxidative phosph ...... ed to glycolysis driven by the

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Dysfunctional oxidative phosph ...... n by the (V600E)BRAF oncogene.

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Dysfunctional oxidative phosph ...... ed to glycolysis driven by the

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Dysfunctional oxidative phosph ...... en by the (V600E)BRAF oncogene

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Arnaldur Hall

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Christina Dahl

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Claus Christensen

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Jiri Bartek

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Kathrine Damm Meyle

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Katrine Thorup

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Marina Krarup Lange

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Martin Klima

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May Sanderhoff

http://www.w3.org/2001/XMLSchema#string

Per Bo Jensen

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P2860

Understanding the Warburg effect: the metabolic requirements of cell proliferation

Improved survival with vemurafenib in melanoma with BRAF V600E mutation

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

Discovery of a selective inhibitor of oncogenic B-Raf kinase with potent antimelanoma activity

Mutations of the BRAF gene in human cancer

On the Origin of Cancer Cells

Targeting RAS signalling pathways in cancer therapy

Mammalian MAP kinase signalling cascades

Mechanism of activation of the RAF-ERK signaling pathway by oncogenic mutations of B-RAF

Regulation of cancer cell metabolism

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584-599

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scholarly article

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10.18632/ONCOTARGET.965

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4

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4

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Seyed Moein Moghimi

Cecilie Abildgaard

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2013-04-01T00:00:00Z

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236252489

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23603840

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phosphorylation

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3720606

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