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

By Takuya Watanabe, S. Nobusawa, P. Kleihues, H. Ohgaki. American Journal of Pathology, 2009

1,019 citations recorded by the source corpus.

Subfields: Cancer Research, Genetics, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/dc65640bc46542e3c383d1f88da15cdbdfcd0d89

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Citations in the corpus

The Definition of Primary and Secondary Glioblastoma (2012, background): “Furthermore, the analysis of multiple biopsies from the same patient revealed that there were no cases in which an IDH1 mutation occurred after the acquisition of a TP53 mutation or loss of 1p/19q (11, 33).”
Patients with IDH1 wild type anaplastic astrocytomas exhibit worse prognosis than IDH1-mutated glioblastomas, and IDH1 mutation status accounts for the unfavorable prognostic effect of higher age: implications for classification of gliomas (2010, background): “Cytosolic isocitrate dehydrogenase 1 (IDH1) mutations were initially detected in a fraction of glioblastomas [14] followed by the observation that they are present in the majority of diffuse astrocytomas, oligodendrogliomas and mixed oligoastrocytomas of WHO grades II and III [1, 7, 9, 22, 26].”
Targeting Metabolism for Cancer Therapy (2017, background): “IDH1 mutations are early events in the development of glial cancer (Watanabe et al., 2009), raising the possibility that IDH mutations are important for tumor initiation, but accumulation of additional oncogenic mutations renders GBM tumors less dependent on constitutive expression of mutant IDH for”
Oncometabolite 2-Hydroxyglutarate Is a Competitive Inhibitor of α-Ketoglutarate-Dependent Dioxygenases (2011, positive): “Given that both mutations of IDH1 and TET2 have been reported to occur at a very early stage during glioma and leukemia development (Delhommeau et al., 2009; Langemeijer et al., 2009; Watanabe et al., 2009), alteration of histone and DNA methylations resulting from IDH1 and IDH2 mutations may contri”
Type and frequency of IDH1 and IDH2 mutations are related to astrocytic and oligodendroglial differentiation and age: a study of 1,010 diffuse gliomas (2009, background): “5% for O III comparing to 67% [1], 86% [21], 75% [17] and 60% [8].”
Genetics of adult glioma. (2012, background): “The high prevalence of TP53 and IDH1mutations in low-grade astrocyomas (as well as in secondary glioblastomas) provides evidence that these alterations are among the earliest genetic abnormalities in the development of lowgrade astrocytomas (41,43) (Figure 1).”
Hexokinase 2 is a key mediator of aerobic glycolysis and promotes tumor growth in human glioblastoma multiforme (2011, background): “Highthroughput genomic screening of GBMs identified a point mutation (predominantly R132H) in the IDH1 gene in 12% of all GBMs (Parsons et al., 2008) and 80% of lowgrade astrocytomas (LGA) or secondary GBMs that developed from their malignant progression (Watanabe et al., 2009; Yan et al., 2009).”
Mutational Analysis Reveals the Origin and Therapy-driven Evolution of Recurrent Glioma (2013, neutral): “This further implicates IDH1 mutations as an initiating event in low-grade gliomagenesis (12).”
Cancer-associated IDH1 mutations produce 2-hydroxyglutarate (2009, neutral): “The reaction product from R132H co-eluted with the R(2)-2HG peak, demonstrating that the R(2) stereoisomer is the product produced from a-ketoglutarate by R132H mutant IDH1.”