Glucose, not glutamine, is the dominant energy source required for proliferation and survival of head and neck squamous carcinoma cells. - Wikidata - wikimedia - TriplyDB

Glucose, not glutamine, is the dominant energy source required for proliferation and survival of head and neck squamous carcinoma cells.

Glucose, not glutamine, is the dominant energy source required for proliferation and survival of head and neck squamous carcinoma cells.

http://www.wikidata.org/entity/Q35103648

about

Effect of hypoxia on the expression of αB-crystallin in head and neck squamous cell carcinoma Metabolic interplay between glycolysis and mitochondrial oxidation: The reverse Warburg effect and its therapeutic implication Cancer metabolic reprogramming: importance, main features, and potentials for precise targeted anti-cancer therapies Protein N-glycosylation in oral cancer: dysregulated cellular networks among DPAGT1, E-cadherin adhesion and canonical Wnt signaling On metabolic reprogramming and tumor biology: A comprehensive survey of metabolism in breast cancer Metabolic shifts toward glutamine regulate tumor growth, invasion and bioenergetics in ovarian cancer Metabolic interrogation as a tool to optimize chemotherapeutic regimens.Head and Neck Squamous Cell Carcinoma Metabolism Draws on Glutaminolysis, and Stemness Is Specifically Regulated by Glutaminolysis via Aldehyde Dehydrogenase Regulation of the pentose phosphate pathway in cancer Mechanisms by which low glucose enhances the cytotoxicity of metformin to cancer cells both in vitro and in vivo.Delineating metabolic signatures of head and neck squamous cell carcinoma: phospholipase A2, a potential therapeutic target.Restricting carbohydrates to fight head and neck cancer-is this realistic?Individualizing antimetabolic treatment strategies for head and neck squamous cell carcinoma based on TP53 mutational status Magic angle spinning NMR-based metabolic profiling of head and neck squamous cell carcinoma tissues Compartmentalized AMPK signaling illuminated by genetically encoded molecular sensors and actuators Energy metabolism in a matched model of radiation resistance for head and neck squamous cell cancer.Wee-1 Kinase Inhibition Sensitizes High-Risk HPV+ HNSCC to Apoptosis Accompanied by Downregulation of MCl-1 and XIAP Antiapoptotic Proteins.Amino acids in squamous cell carcinomas and adjacent normal tissues from patients with larynx and oral cavity lesions Analysis of glutamine dependency in non-small cell lung cancer: GLS1 splice variant GAC is essential for cancer cell growth.Metformin inhibits gastric cancer cells metastatic traits through suppression of epithelial-mesenchymal transition in a glucose-independent manner.Anti-tumor effects of metformin on head and neck carcinoma cell lines: A systematic review Metformin: Midlife maturity, maiden charm Acute Tumor Lactate Perturbations as a Biomarker of Genotoxic Stress: Development of a Biochemical Model.Cancer metabolism, stemness and tumor recurrence: MCT1 and MCT4 are functional biomarkers of metabolic symbiosis in head and neck cancer.The Influence of Diabetes Mellitus and Metformin on Distant Metastases in Oropharyngeal Cancer: A Multicenter Study Glycolytic inhibition alters anaplastic thyroid carcinoma tumor metabolism and improves response to conventional chemotherapy and radiation.Contextual inhibition of fatty acid synthesis by metformin involves glucose-derived acetyl-CoA and cholesterol in pancreatic tumor cells.Evaluation of hyperpolarized [1-¹³C]-pyruvate by magnetic resonance to detect ionizing radiation effects in real time.2-Deoxy-d-glucose Suppresses the In Vivo Antitumor Efficacy of Erlotinib in Head and Neck Squamous Cell Carcinoma Cells.Regulation of glycolysis in head and neck squamous cell carcinoma.Energy metabolism of cancer: Glycolysis versus oxidative phosphorylation (Review).Proteomics and metabolomics in cancer drug development.Targeting metabolic pathways for head and neck cancers therapeutics.Association of cancer metabolism-related proteins with oral carcinogenesis - indications for chemoprevention and metabolic sensitizing of oral squamous cell carcinoma?Energy metabolism characterization of a novel cancer stem cell-like line 3AB-OS.Real-Time Genomic Characterization Utilizing Circulating Cell-Free DNA in Patients with Anaplastic Thyroid Carcinoma.HPV-associated differential regulation of tumor metabolism in oropharyngeal head and neck cancer Partial Substitution of Glucose with Xylitol Suppressed the Glycolysis and Selectively Inhibited the Proliferation of Oral Cancer Cells.Prognostic relevance of insulin resistance on disease-free survival in head and neck squamous cell carcinomas: Preliminary results.2-Deoxy-d-glucose enhances tonic inhibition through the neurosteroid-mediated activation of extrasynaptic GABAA receptors.

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P2860

Glucose, not glutamine, is the dominant energy source required for proliferation and survival of head and neck squamous carcinoma cells.

http://www.wikidata.org/entity/Q35103648

description

2011 nî lūn-bûn

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2011 թուականի Յունուարին հրատարակուած գիտական յօդուած

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2011 թվականի հունվարին հրատարակված գիտական հոդված

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2011年の論文

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2011年論文

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2011年論文

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2011年論文

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2011年論文

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2011年論文

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2011年论文

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name

Glucose, not glutamine, is the ...... neck squamous carcinoma cells.

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Glucose, not glutamine, is the ...... neck squamous carcinoma cells.

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type

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Glucose, not glutamine, is the ...... neck squamous carcinoma cells.

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Glucose, not glutamine, is the ...... neck squamous carcinoma cells.

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Glucose, not glutamine, is the ...... neck squamous carcinoma cells.

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P2093

Curtis R Pickering

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Ge Zhou

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

Izabela Fokt

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Jeffrey N Myers

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Melinda Davis-Malesevich

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Mitchell J Frederick

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Thomas J Ow

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Waldemar Priebe

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P2860

Glucose catabolism in cancer cells. The type II hexokinase promoter contains functionally active response elements for the tumor suppressor p53

Pyruvate dehydrogenase complex activity controls metabolic and malignant phenotype in cancer cells

Understanding the Warburg effect: the metabolic requirements of cell proliferation

KEGG for representation and analysis of molecular networks involving diseases and drugs

Metabolomic profiles delineate potential role for sarcosine in prostate cancer progression

Glycolysis inhibition for anticancer treatment

Myc regulates a transcriptional program that stimulates mitochondrial glutaminolysis and leads to glutamine addiction

Beyond aerobic glycolysis: transformed cells can engage in glutamine metabolism that exceeds the requirement for protein and nucleotide synthesis

Elevated tumor lactate concentrations predict for an increased risk of metastases in head-and-neck cancer.

DNA fluorometric assay in 96-well tissue culture plates using Hoechst 33258 after cell lysis by freezing in distilled water.

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2926-2938

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10.1002/CNCR.25868

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13

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117

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Vlad C. Sandulache

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2011-01-10T00:00:00Z

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51237300

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21692052

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