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 fully automated artificial intelligence method for non-invasive, imaging-based identification of genetic alterations in glioblastomas. 
  • 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. 
  • Association of Maximal Extent of Resection of Contrast-Enhanced and Non-Contrast-Enhanced Tumor With Survival Within Molecular Subgroups of Patients With Newly Diagnosed Glioblastoma. 
  • 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. 
  • CRISPR Editing of Mutant IDH1 R132H Induces a CpG Methylation-Low State in Patient-Derived Glioma Models of G-CIMP. 
  • 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. 
  • Decoupling genetics, lineages, and microenvironment in IDH-mutant gliomas by single-cell RNA-seq. 
  • Disruption of wild-type IDH1 suppresses D-2-hydroxyglutarate production in IDH1-mutated gliomas. 
  • Distinct Roles of Glutamine Metabolism in Benign and Malignant Cartilage Tumors With IDH Mutations. 
  • 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. 
  • Genetic Determinants of Outcome in Intrahepatic Cholangiocarcinoma. 
  • Genetic dissection of leukemia-associated IDH1 and IDH2 mutants and D-2-hydroxyglutarate in Drosophila. 
  • Glioma Groups Based on 1p/19q, IDH, and TERT Promoter Mutations in Tumors. 
  • Glioma progression is shaped by genetic evolution and microenvironment interactions. 
  • Heterogeneity of tumor-induced gene expression changes in the human metabolic network. 
  • Hitting Gliomas When They Are Down: Exploiting IDH-Mutant Metabolic Vulnerabilities. 
  • 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. 
  • IDH3α regulates one-carbon metabolism in glioblastoma. 
  • Imaging correlates for the 2016 update on WHO classification of grade II/III gliomas: implications for IDH, 1p/19q and ATRX status. 
  • Immune Microenvironment Landscape in CNS Tumors and Role in Responses to Immunotherapy. 
  • 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. 
  • Intracellular cholesterol biosynthesis in enchondroma and chondrosarcoma. 
  • 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 is important for nitrosative stress resistance in Cryptococcus neoformans, but oxidative stress resistance is not dependent on glucose-6-phosphate dehydrogenase. 
  • 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. 
  • Ivosidenib induces deep durable remissions in patients with newly diagnosed IDH1-mutant acute myeloid leukemia. 
  • Longitudinal molecular trajectories of diffuse glioma in adults. 
  • Management of glioblastoma: State of the art and future directions. 
  • Mitochondrial acetylome analysis in a mouse model of alcohol-induced liver injury utilizing SIRT3 knockout mice. 
  • Molecular Profiling Reveals Biologically Discrete Subsets and Pathways of Progression in Diffuse Glioma. 
  • Molecular biomarker-defined brain tumors: Epidemiology, validity, and completeness in the United States. 
  • Molecular profiling of different glioma specimens from an Ollier disease patient suggests a multifocal disease process in the setting of IDH mosaicism. 
  • Multiscale, multimodal analysis of tumor heterogeneity in IDH1 mutant vs wild-type diffuse gliomas. 
  • 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. 
  • National-level overall survival patterns for molecularly-defined diffuse glioma types in the United States. 
  • Outcomes of patients with IDH1-mutant relapsed or refractory acute myeloid leukemia receiving ivosidenib who proceeded to hematopoietic stem cell transplant. 
  • Overcoming Resistance to Targeted Therapies in Gastrointestinal Cancers: Progress to Date and Progress to Come. 
  • Pattern of failure in anaplastic glioma patients with an IDH1/2 mutation. 
  • Profiling the effects of isocitrate dehydrogenase 1 and 2 mutations on the cellular metabolome. 
  • Radiation and chemotherapy for high-risk lower grade gliomas: Choosing between temozolomide and PCV. 
  • 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. 
  • Reductive TCA cycle metabolism fuels glutamine- and glucose-stimulated insulin secretion. 
  • Reflecting on survivorship outcomes to aid initial decision making in patients treated for IDH-mutated anaplastic glioma. 
  • Releasing the block: setting differentiation free with mutant IDH inhibitors. 
  • Role of Ethnicity and Geographic Location on Glioblastoma IDH1/IDH2 Mutations. 
  • Sensitive and rapid detection of TERT promoter and IDH mutations in diffuse gliomas. 
  • Single-cell RNA-seq supports a developmental hierarchy in human oligodendroglioma. 
  • Synthesis and evaluation of radiolabeled AGI-5198 analogues as candidate radiotracers for imaging mutant IDH1 expression in tumors. 
  • Targeting Isocitrate Dehydrogenase Mutations in Cancer: Emerging Evidence and Diverging Strategies. 
  • The Cancer Genome Atlas expression profiles of low-grade gliomas. 
  • The genomic landscape of TERT promoter wildtype-IDH wildtype glioblastoma. 
  • The implications of IDH mutations for cancer development and therapy. 
  • The preparation of stereospecific tritium-labeled reduced nicotinamide adenine dinucleotide phosphate. 
  • Transformation by the (R)-enantiomer of 2-hydroxyglutarate linked to EGLN activation. 
  • Understanding the Genetic Risk of IDH-Mutant Glioma. 
  • Vitamin A and biochemical development. II. Effect of postnatal excess vitamin-A administration on the activity of pyridine nucleotide-linked dehydrogenases. 
  • Volumetric analysis of IDH-mutant lower-grade glioma: a natural history study of tumor growth rates before and after treatment. 
  • Vorasidenib, a Dual Inhibitor of Mutant IDH1/2, in Recurrent or Progressive Glioma; Results of a First-in-Human Phase I Trial. 
  • Vulnerabilities in mIDH2 AML confer sensitivity to APL-like targeted combination therapy. 
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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, Biomedical Engineering