Results 1 to 10 of about 34,660 (223)

Mutant IDH1 is required for IDH1 mutated tumor cell growth [PDF]

open access: greenOncotarget, 2012
Frequent somatic hotspot mutations in isocitrate dehydrogenase 1 (IDH1) have been identified in gliomas, acute myeloid leukemias, chondrosarcomas, and other cancers, providing a likely avenue for targeted cancer therapy. However, whether mutant IDH1 protein is required for maintaining IDH1 mutated tumor cell growth remains unknown.
Genglin Jin   +9 more
openalex   +5 more sources

Recent advances of IDH1 mutant inhibitor in cancer therapy

open access: yesFrontiers in Pharmacology, 2022
Isocitrate dehydrogenase (IDH) is the key metabolic enzyme that catalyzes the conversion of isocitrate to α-ketoglutarate (α-KG). Two main types of IDH1 and IDH2 are present in humans.
Wangqi Tian   +7 more
doaj   +2 more sources

IDH1 and IDH2 mutations in gliomas. [PDF]

open access: yesNew England Journal of Medicine, 2009
BACKGROUND A recent genomewide mutational analysis of glioblastomas (World Health Organization [WHO] grade IV glioma) revealed somatic mutations of the isocitrate dehydrogenase 1 gene (IDH1) in a fraction of such tumors, most frequently in tumors that ...
Hai Yan   +17 more
semanticscholar   +7 more sources

Secondary IDH1 resistance mutations and oncogenic IDH2 mutations cause acquired resistance to ivosidenib in cholangiocarcinoma

open access: yesnpj Precision Oncology, 2022
The mutant IDH1 inhibitor ivosidenib improves outcomes for patients with IDH1-mutated cholangiocarcinoma, but resistance inevitably develops. Mechanisms of resistance and strategies to overcome resistance are poorly understood.
James M. Cleary   +11 more
doaj   +2 more sources

IDH1 and IDH2 Mutations in Gliomas [PDF]

open access: greenCurrent Neurology and Neuroscience Reports, 2013
Mutations in isocitrate dehydrogenase (IDH) 1 and 2, originally discovered in 2008, occur in the vast majority of low-grade gliomas and secondary high-grade gliomas. These mutations, which occur early in gliomagenesis, change the function of the enzymes, causing them to produce 2-hydroxyglutarate, a possible oncometabolite, and to not produce NADPH ...
Adam L. Cohen   +2 more
openalex   +5 more sources

HDAC1 and HDAC6 are essential for driving growth in IDH1 mutant glioma

open access: yesScientific Reports, 2023
Low-grade and secondary high-grade gliomas frequently contain mutations in the IDH1 or IDH2 metabolic enzymes that are hypothesized to drive tumorigenesis by inhibiting many of the chromatin-regulating enzymes that regulate DNA structure.
Matthew C. Garrett   +18 more
doaj   +2 more sources

Expanding the spectrum of IDH1 mutations in gliomas [PDF]

open access: bronzeModern Pathology, 2013
Mutations in isocitrate dehydrogenase -1 or -2 (IDH1 or IDH2) are found in the majority of WHO grade II and III diffuse gliomas and secondary glioblastomas. IDH mutation screening is rapidly becoming part of the routine pathological work up of human brain tumors, providing both diagnostic and prognostic information.
Ruta Gupta   +7 more
openalex   +4 more sources

IDH1 mutation impairs antiviral response and potentiates oncolytic virotherapy in glioma

open access: yesNature Communications, 2023
IDH1 mutations frequently occur early in human glioma. While IDH1 mutation has been shown to promote gliomagenesis via DNA and histone methylation, little is known regarding its regulation in antiviral immunity.
Xueqin Chen   +24 more
doaj   +2 more sources

The roles of IDH1 in tumor metabolism and immunity.

open access: yesFuture Oncology, 2023
IDH1 is a key metabolic enzyme for cellular respiration in the tricarboxylic acid (TCA) cycle that can convert isocitrate into α-ketoglutarate (α-KG) and generate NADPH.
Yingqian Ni   +5 more
semanticscholar   +3 more sources

The expression and significance of IDH1 and p53 in osteosarcoma [PDF]

open access: yesJournal of Experimental & Clinical Cancer Research, 2010
Background To detect the expression of isocitrate dehydrogenase 1 (IDH1) and transformation-related protein 53 (p53) in osteosarcoma and analyze the correlation between them and the clinico-pathological features.
Zhou Min   +7 more
doaj   +4 more sources

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