Extreme Vulnerability of IDH1 Mutant Cancers to NAD+ Depletion. - Wikidata - wikimedia - TriplyDB

Extreme Vulnerability of IDH1 Mutant Cancers to NAD+ Depletion.

Extreme Vulnerability of IDH1 Mutant Cancers to NAD+ Depletion.

http://www.wikidata.org/entity/Q36385589

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Emerging therapeutic roles for NAD(+) metabolism in mitochondrial and age-related disorders IDH1 and IDH2 mutations as novel therapeutic targets: current perspectives Integrative Genomic Analysis of Cholangiocarcinoma Identifies Distinct IDH-Mutant Molecular Profiles.Meat Intake and the Dose of Vitamin B3 - Nicotinamide: Cause of the Causes of Disease Transitions, Health Divides, and Health Futures?2-Hydroxyglutarate produced by neomorphic IDH mutations suppresses homologous recombination and induces PARP inhibitor sensitivity.Nicotinamide metabolism regulates glioblastoma stem cell maintenance.Isocitrate Dehydrogenase Mutations Confer Dasatinib Hypersensitivity and SRC Dependence in Intrahepatic Cholangiocarcinoma Molecular Pathways: Isocitrate Dehydrogenase Mutations in Cancer.Myc-Driven Glycolysis Is a Therapeutic Target in Glioblastoma.An NAD+-dependent transcriptional program governs self-renewal and radiation resistance in glioblastoma Chemosensitivity of IDH1-Mutated Gliomas Due to an Impairment in PARP1-Mediated DNA Repair.The emerging role and targetability of the TCA cycle in cancer metabolism.Inhibitor of Nicotinamide Phosphoribosyltransferase Sensitizes Glioblastoma Cells to Temozolomide via Activating ROS/JNK Signaling Pathway.Rapid Conversion of Mutant IDH1 from Driver to Passenger in a Model of Human Gliomagenesis.Correlation of immune phenotype with IDH mutation in diffuse glioma.Targeting the cancer epigenome for therapy.Targeted Therapeutics in Patients With High-Grade Gliomas: Past, Present, and Future.Altered metabolite levels in cancer: implications for tumour biology and cancer therapy.Understanding the Intersections between Metabolism and Cancer Biology.Pharmacotherapy of Glioblastoma: Established Treatments and Emerging Concepts.Perspectives on investigational drugs and immunotherapies for glioblastoma.Isocitrate dehydrogenases in physiology and cancer: biochemical and molecular insight.Mutant IDH1 regulates the tumor-associated immune system in gliomas.The Alkylating Chemotherapeutic Temozolomide Induces Metabolic Stress in IDH1-Mutant Cancers and Potentiates NAD+ Depletion-Mediated Cytotoxicity.PIK3CA mutant tumors depend on oxoglutarate dehydrogenase.Induction of synthetic lethality in IDH1-mutated gliomas through inhibition of Bcl-xL.Clonal expansion and epigenetic reprogramming following deletion or amplification of mutant IDH1.Molecular and Genetic Determinants of Glioma Cell Invasion.Reverse engineering the cancer metabolic network using flux analysis to understand drivers of human disease.Targeting the vulnerability to NAD+ depletion in B-cell acute lymphoblastic leukemia.A Comprehensive Patient-Derived Xenograft Collection Representing the Heterogeneity of Melanoma.Novel NAPRT specific antibody identifies small cell lung cancer and neuronal cancers as promising clinical indications for a NAMPT inhibitor/niacin co-administration strategy.Current trends in mouse models of glioblastoma.Isocitrate dehydrogenase-mutant glioma: Evolving clinical and therapeutic implications.Targeting Metabolism for Cancer Therapy.Wild-type and mutated IDH1/2 enzymes and therapy responses.Glioma CpG Island Methylator Phenotype (G-CIMP): Biological and Clinical Implications.Adaptive Evolution of the GDH2 Allosteric Domain Promotes Gliomagenesis by Resolving IDH1R132H-Induced Metabolic Liabilities.Mutant-IDH1-dependent chromatin state reprogramming, reversibility, and persistence.Metabolism: Totally addicted to NAD(.).

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Extreme Vulnerability of IDH1 Mutant Cancers to NAD+ Depletion.

http://www.wikidata.org/entity/Q36385589

description

2015 nî lūn-bûn

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2015年の論文

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2015年学术文章

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2015年学术文章

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2015年学术文章

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2015年学术文章

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2015年学术文章

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2015年學術文章

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2015年學術文章

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2015年學術文章

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name

Extreme Vulnerability of IDH1 Mutant Cancers to NAD+ Depletion.

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Extreme Vulnerability of IDH1 Mutant Cancers to NAD+ Depletion.

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type

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Extreme Vulnerability of IDH1 Mutant Cancers to NAD+ Depletion.

@ast

Extreme Vulnerability of IDH1 Mutant Cancers to NAD+ Depletion.

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prefLabel

Extreme Vulnerability of IDH1 Mutant Cancers to NAD+ Depletion.

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Extreme Vulnerability of IDH1 Mutant Cancers to NAD+ Depletion.

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J.CCELL.2015.11.006

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Extreme Vulnerability of IDH1 Mutant Cancers to NAD+ Depletion

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A John Iafrate

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Andrew S Chi

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Bailin Zhang

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David E Fisher

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Dmitri Wiederschain

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Fares Nigim

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Franziska Loebel

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Gejing Deng

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Hiroaki Wakimoto

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Jing-Ruey J Yeh

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P2860

Cancer genome landscapes

Cancer-associated IDH1 mutations produce 2-hydroxyglutarate

Mutations in isocitrate dehydrogenase 1 and 2 occur frequently in intrahepatic cholangiocarcinomas and share hypermethylation targets with glioblastomas

Identification of a CpG island methylator phenotype that defines a distinct subgroup of glioma

Oncometabolite 2-hydroxyglutarate is a competitive inhibitor of α-ketoglutarate-dependent dioxygenases

Recurring mutations found by sequencing an acute myeloid leukemia genome

An integrated genomic analysis of human glioblastoma multiforme

IDH1 and IDH2 mutations in gliomas

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

IDH1 mutations are early events in the development of astrocytomas and oligodendrogliomas

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10.1016/J.CCELL.2015.11.006

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6

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Daniel P Cahill

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2015-12-01T00:00:00Z

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