Results 21 to 30 of about 58,205 (308)

Metabolic Profiling of IDH Mutation and Malignant Progression in Infiltrating Glioma. [PDF]

open access: yes, 2017
Infiltrating low grade gliomas (LGGs) are heterogeneous in their behavior and the strategies used for clinical management are highly variable. A key factor in clinical decision-making is that patients with mutations in the isocitrate dehydrogenase 1 and ...
Berger, Mitchel S   +12 more
core   +1 more source

Mutation of Isocitrate Dehydrogenase 1 in Cholangiocarcinoma Impairs Tumor Progression by Inhibiting Isocitrate Metabolism

open access: yesFrontiers in Endocrinology, 2020
Aim: Isocitrate dehydrogenase 1 (IDH1) is key enzyme involved in cellular metabolism and DNA repair. Mutations in IDH1 occur in up to 25% of cholangiocarcinomas.
Li Su   +5 more
doaj   +1 more source

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   +1 more source

Factors associated with increased survival after surgical resection of glioblastoma in octogenarians. [PDF]

open access: yes, 2015
Elderly patients with glioblastoma represent a clinical challenge for neurosurgeons and oncologists. The data available on outcomes of patients greater than 80 undergoing resection is limited.
Abdullah, Kalil G   +6 more
core   +6 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   +1 more source

Allosteric Mutant IDH1 Inhibitors Reveal Mechanisms for IDH1 Mutant and Isoform Selectivity [PDF]

open access: yesStructure, 2017
Oncogenic IDH1 and IDH2 mutations contribute to cancer via production of R-2-hydroxyglutarate (2-HG). Here, we characterize two structurally distinct mutant- and isoform-selective IDH1 inhibitors that inhibit 2-HG production. Both bind to an allosteric pocket on IDH1, yet shape it differently, highlighting the plasticity of this site.
Xiaoling, Xie   +22 more
openaire   +2 more sources

Metabolism, Gliomas, andIDH1 [PDF]

open access: yesNew England Journal of Medicine, 2010
A mutation in IDH1, which encodes an isocitrate dehydrogenase, is associated with susceptibility to glioma. This mutation results in an acquired enzyme activity that points to a potential biomarker of the mutant tumor.
Smeitink, J.A.M., Smeitink, J.A.M.
openaire   +3 more sources

Immunohistochemical Expression of IDH1, ATRX, Ki67, GFAP, and Prognosis in Indonesian Glioma Patients

open access: yesInternational Journal of General Medicine, 2023
Dody Priambada,1 Muhamad Thohar Arifin,1 Abdi Saputro,1 Azka Muzakka,1 Vega Karlowee,2 Udadi Sadhana,2 Yuriz Bakhtiar,1 Krisna Tsaniadi Prihastomo,1 Ajid Risdianto,1 Happy Kurnia Brotoarianto,1 Erie Andar,1 Zainal Muttaqin1 1Department of Neurosurgery ...
Priambada D   +11 more
doaj  

In vivo investigation of hyperpolarized [1,3-13C2]acetoacetate as a metabolic probe in normal brain and in glioma. [PDF]

open access: yes, 2019
Dysregulation in NAD+/NADH levels is associated with increased cell division and elevated levels of reactive oxygen species in rapidly proliferating cancer cells.
Batsios, Georgios   +7 more
core   +3 more sources

IDH1 R132H Mutation Enhances Cell Migration by Activating AKT-mTOR Signaling Pathway, but Sensitizes Cells to 5-FU Treatment as NADPH and GSH Are Reduced. [PDF]

open access: yesPLoS ONE, 2017
Mutations of isocitrate dehydrogenase 1 and 2 (IDH1 and IDH2) gene were recently discovered in vast majority of World Health Organization (WHO) grade II/III gliomas.
Huixia Zhu   +6 more
doaj   +1 more source

Home - About - Disclaimer - Privacy