EGFR mutation-induced alternative splicing of Max contributes to growth of glycolytic tumors in brain cancer. - Wikidata - wikimedia - TriplyDB

EGFR mutation-induced alternative splicing of Max contributes to growth of glycolytic tumors in brain cancer.

EGFR mutation-induced alternative splicing of Max contributes to growth of glycolytic tumors in brain cancer.

http://www.wikidata.org/entity/Q36920081

about

Autophagy in hepatocellular carcinomas: from pathophysiology to therapeutic response Ligand-Independent EGFR Signaling MYC and metabolism on the path to cancer Defective control of pre-messenger RNA splicing in human disease Non-invasive metabolic imaging of brain tumours in the era of precision medicine.Inositol phosphate recycling regulates glycolytic and lipid metabolism that drives cancer aggressiveness.mTORC2 in the center of cancer metabolic reprogramming Cancer metabolism as a central driving force of glioma pathogenesis Epidermal growth factor receptor (EGFR) signaling regulates global metabolic pathways in EGFR-mutated lung adenocarcinoma.A Comprehensive Analysis of CXCL12 Isoforms in Breast Cancer(1,2.)Emerging function of mTORC2 as a core regulator in glioblastoma: metabolic reprogramming and drug resistance.Compensatory glutamine metabolism promotes glioblastoma resistance to mTOR inhibitor treatment.Arsenic trioxide sensitizes glioblastoma to a myc inhibitor.EGFR Mutation Promotes Glioblastoma through Epigenome and Transcription Factor Network Remodeling.Inhibition of Acetyl-CoA Carboxylase 1 (ACC1) and 2 (ACC2) Reduces Proliferation and De Novo Lipogenesis of EGFRvIII Human Glioblastoma Cells.Differential expression of alternatively spliced transcripts related to energy metabolism in colorectal cancer.mTORC2 and Metabolic Reprogramming in GBM: at the Interface of Genetics and Environment.Glucose-Mediated N-glycosylation of SCAP Is Essential for SREBP-1 Activation and Tumor Growth.Biophysical characterization of the b-HLH-LZ of ΔMax, an alternatively spliced isoform of Max found in tumor cells: Towards the validation of a tumor suppressor role for the Max homodimers.Sex Difference of Egfr Expression and Molecular Pathway in the Liver: Impact on Drug Design and Cancer Treatments?Mechanistic Target of Rapamycin (mTOR) Inhibition Synergizes with Reduced Internal Ribosome Entry Site (IRES)-mediated Translation of Cyclin D1 and c-MYC mRNAs to Treat Glioblastoma.mTOR complex 2 controls glycolytic metabolism in glioblastoma through FoxO acetylation and upregulation of c-Myc.RNA splicing factors as oncoproteins and tumour suppressors.An overview of MYC and its interactome.Tumor metabolism of malignant gliomas.EGFR signaling and autophagy dependence for growth, survival, and therapy resistance.Alternative splicing in cancer: implications for biology and therapy.Mitochondrial p32 is upregulated in Myc expressing brain cancers and mediates glutamine addiction.Glutamate and α-ketoglutarate: key players in glioma metabolism.The role of RNA alternative splicing in regulating cancer metabolism.RNA processing as an alternative route to attack glioblastoma.MicroRNA Regulation of Glycolytic Metabolism in Glioblastoma.Hypoxia reduces MAX expression in endothelial cells by unproductive splicing.mTORC2 dictates Warburg effect and drug resistance.Cytoplasmic p53 couples oncogene-driven glucose metabolism to apoptosis and is a therapeutic target in glioblastoma.Emerging functions of the EGFR in cancer.MAX Mutations in Endometrial Cancer: Clinicopathologic Associations and Recurrent MAX p.His28Arg Functional Characterization.Differential Response of Glioma Stem Cells to Arsenic Trioxide Therapy Is Regulated by MNK1 and mRNA Translation.Value of (18)F-FDG PET/CT for predicting EGFR mutations and positive ALK expression in patients with non-small cell lung cancer: a retrospective analysis of 849 Chinese patients.Emerging roles of hnRNPA1 in modulating malignant transformation.

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P2860

EGFR mutation-induced alternative splicing of Max contributes to growth of glycolytic tumors in brain cancer.

http://www.wikidata.org/entity/Q36920081

description

2013 nî lūn-bûn

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name

EGFR mutation-induced alternat ...... olytic tumors in brain cancer.

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EGFR mutation-induced alternat ...... olytic tumors in brain cancer.

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EGFR mutation-induced alternat ...... olytic tumors in brain cancer.

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J.CMET.2013.04.013

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Cell Metabolism

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EGFR mutation-induced alternat ...... olytic tumors in brain cancer.

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Ascia Eskin

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Beatrice Gini

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Bing Li

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Carolina Espindola Camacho

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David Akhavan

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Deliang Guo

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Douglas L Black

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Erik S Anderson

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Genaro R Villa

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P2860

Max: a helix-loop-helix zipper protein that forms a sequence-specific DNA-binding complex with Myc

Gene set enrichment analysis: a knowledge-based approach for interpreting genome-wide expression profiles.

Mammalian target of rapamycin up-regulation of pyruvate kinase isoenzyme type M2 is critical for aerobic glycolysis and tumor growth

Understanding the Warburg effect: the metabolic requirements of cell proliferation

An integrated genomic analysis of human glioblastoma multiforme

Integrated genomic analysis identifies clinically relevant subtypes of glioblastoma characterized by abnormalities in PDGFRA, IDH1, EGFR, and NF1

Comprehensive genomic characterization defines human glioblastoma genes and core pathways

Pyruvate kinase M2 is a phosphotyrosine-binding protein

Alternative mRNA forms and open reading frames of the max gene

Alternative forms of Max as enhancers or suppressors of Myc-ras cotransformation

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1000-1008

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6

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17

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Heather R Christofk

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2013-05-23T00:00:00Z

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236938220

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