Isocitrate Dehydrogenase

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  Subject Areas on Research

  • 2-hydroxyglutarate production, but not dominant negative function, is conferred by glioma-derived NADP-dependent isocitrate dehydrogenase mutations. 
  • A heterozygous IDH1R132H/WT mutation induces genome-wide alterations in DNA methylation. 
  • A low-frequency variant at 8q24.21 is strongly associated with risk of oligodendroglial tumors and astrocytomas with IDH1 or IDH2 mutation. 
  • A monoclonal antibody IMab-1 specifically recognizes IDH1R132H, the most common glioma-derived mutation. 
  • A pyruvate cycling pathway involving cytosolic NADP-dependent isocitrate dehydrogenase regulates glucose-stimulated insulin secretion. 
  • Adaptive Evolution of the GDH2 Allosteric Domain Promotes Gliomagenesis by Resolving IDH1R132H-Induced Metabolic Liabilities. 
  • Adult infiltrating gliomas with WHO 2016 integrated diagnosis: additional prognostic roles of ATRX and TERT. 
  • An SOD mimic protects NADP+-dependent isocitrate dehydrogenase against oxidative inactivation. 
  • An integrated genomic analysis of human glioblastoma multiforme. 
  • Biological Role and Therapeutic Potential of IDH Mutations in Cancer. 
  • Breaking Cryo-EM Resolution Barriers to Facilitate Drug Discovery. 
  • CDKN2A loss is associated with shortened overall survival in lower-grade (World Health Organization Grades II-III) astrocytomas. 
  • Cancer-associated isocitrate dehydrogenase 1 (IDH1) R132H mutation and d-2-hydroxyglutarate stimulate glutamine metabolism under hypoxia. 
  • Cancer-associated isocitrate dehydrogenase mutations induce mitochondrial DNA instability. 
  • Centronuclear myopathy: histochemistry and electron microscopy. Report of two cases. 
  • Control of voltage-gated potassium channel Kv2.2 expression by pyruvate-isocitrate cycling regulates glucose-stimulated insulin secretion. 
  • Culture kinetics of glycolytic enzyme induction, glucose utilization, and thymidine incorporation of extended-exposure phytohemagglutinin-stimulated human lymphocytes. 
  • Disruption of wild-type IDH1 suppresses D-2-hydroxyglutarate production in IDH1-mutated gliomas. 
  • Durable Remissions with Ivosidenib in IDH1-Mutated Relapsed or Refractory AML. 
  • Enzyme redesign guided by cancer-derived IDH1 mutations. 
  • Exome sequencing identifies distinct mutational patterns in liver fluke-related and non-infection-related bile duct cancers. 
  • Frequent ATRX, CIC, FUBP1 and IDH1 mutations refine the classification of malignant gliomas. 
  • Functional requirement of a wild-type allele for mutant IDH1 to suppress anchorage-independent growth through redox homeostasis. 
  • Genetic dissection of leukemia-associated IDH1 and IDH2 mutants and D-2-hydroxyglutarate in Drosophila. 
  • Glioblastoma with PNET-like components has a higher frequency of isocitrate dehydrogenase 1 (IDH1) mutation and likely a better prognosis than primary glioblastoma. 
  • Glioma Groups Based on 1p/19q, IDH, and TERT Promoter Mutations in Tumors. 
  • Heterogeneity of tumor-induced gene expression changes in the human metabolic network. 
  • IDH1 and IDH2 hotspot mutations are not found in canine glioma. 
  • IDH1 and IDH2 mutations in gliomas. 
  • IDH1(R132) mutation identified in one human melanoma metastasis, but not correlated with metastases to the brain. 
  • Improved grading of IDH-mutated astrocytic gliomas. 
  • Inherited variant on chromosome 11q23 increases susceptibility to IDH-mutated but not IDH-normal gliomas regardless of grade or histology. 
  • Isocitrate dehydrogenase 1 and 2 mutations in cancer: alterations at a crossroads of cellular metabolism. 
  • Isocitrate dehydrogenase 1: what it means to the neurosurgeon: a review. 
  • Isocitrate dehydrogenase mutations in gliomas. 
  • Isocitrate dehydrogenase mutations in gliomas: mechanisms, biomarkers and therapeutic target. 
  • Isocitrate-to-SENP1 signaling amplifies insulin secretion and rescues dysfunctional β cells. 
  • Mitochondrial acetylome analysis in a mouse model of alcohol-induced liver injury utilizing SIRT3 knockout mice. 
  • Molecular profiling of different glioma specimens from an Ollier disease patient suggests a multifocal disease process in the setting of IDH mosaicism. 
  • Mutant IDH is sufficient to initiate enchondromatosis in mice. 
  • Mutant IDH1 Disrupts the Mouse Subventricular Zone and Alters Brain Tumor Progression. 
  • Mutant IDH1 Expression Drives TERT Promoter Reactivation as Part of the Cellular Transformation Process. 
  • Mutant IDH1 is required for IDH1 mutated tumor cell growth. 
  • Mutant metabolic enzymes are at the origin of gliomas. 
  • Mutations in IDH1, IDH2, and in the TERT promoter define clinically distinct subgroups of adult malignant gliomas. 
  • Mutations in isocitrate dehydrogenase 1 and 2 occur frequently in intrahepatic cholangiocarcinomas and share hypermethylation targets with glioblastomas. 
  • Profiling the effects of isocitrate dehydrogenase 1 and 2 mutations on the cellular metabolome. 
  • Radiogenomics of lower-grade glioma: algorithmically-assessed tumor shape is associated with tumor genomic subtypes and patient outcomes in a multi-institutional study with The Cancer Genome Atlas data. 
  • Radiolabeled inhibitors as probes for imaging mutant IDH1 expression in gliomas: Synthesis and preliminary evaluation of labeled butyl-phenyl sulfonamide analogs. 
  • Radioprotection of lipogenesis from glucose (U-14C) and activities of pyridine nucleotide dehydrogenases in liver of gamma-irradiated female rats by cystamine. 
  • Releasing the block: setting differentiation free with mutant IDH inhibitors. 
  • Synthesis and evaluation of radiolabeled AGI-5198 analogues as candidate radiotracers for imaging mutant IDH1 expression in tumors. 
  • TERT promoter mutations contribute to IDH mutations in predicting differential responses to adjuvant therapies in WHO grade II and III diffuse gliomas. 
  • The genomic landscape of TERT promoter wildtype-IDH wildtype glioblastoma. 
  • Transformation by the (R)-enantiomer of 2-hydroxyglutarate linked to EGLN activation. 
  • Vitamin A and biochemical development. II. Effect of postnatal excess vitamin-A administration on the activity of pyridine nucleotide-linked dehydrogenases. 
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  Keywords of People

  • McLendon, Roger Edwin, Professor of Pathology, Pathology
  • Sampson, John Howard, Robert H., M.D. and Gloria Wilkins Professor of Neurosurgery, in the School of Medicine, Immunology
  • Yan, Hai, Henry S. Friedman Professor of Neuro-Oncology in the School of Medicine, Pathology