Type and frequency of IDH1 and IDH2 mutations are related to astrocytic and oligodendroglial differentiation and age: a study of 1,010 diffuse gliomas

By C. Hartmann, Jochen Meyer, Jörg Balss, D. Capper, W. Mueller, Arne Christians, J. Felsberg, M. Wolter, C. Mawrin, Wolfgang Wick and 7 more. Acta Neuropathologica, 2009

1,146 citations recorded by the source corpus.

Subfields: Epidemiology, Genetics, Neurology

View Paper: https://www.semanticscholar.org/paper/3499545e35fd47b5d84058d7550ece82d3432120

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Citations in the corpus

Identification of a CpG island methylator phenotype that defines a distinct subgroup of glioma. (2010, background): “Mutations in the related IDH2 gene are of lower frequency and generally nonoverlapping with tumors containing IDH1 mutations (Hartmann et al., 2009; Yan et al., 2009).”
Glioblastoma: pathology, molecular mechanisms and markers (2015, background): “In addition to providing insights about the origin of gliomas, the mutational status of IDH1/2 serves as a prognostic marker in patients with WHO grade II and III gliomas [58, 123, 141, 181] and GBMs [172].”
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].”
Leukemic IDH1 and IDH2 mutations result in a hypermethylation phenotype, disrupt TET2 function, and impair hematopoietic differentiation (2010, background): “Although mutations in IDH1 and IDH2 are thought to be mutually exclusive based on mutational studies in malignant gliomas (Hartmann et al., 2009; Yan et al., 2009), occasional rare AML patients have been reported with concurrent mutations in both IDH1 and IDH2 (Paschka et al., 2010).”
The common feature of leukemia-associated IDH1 and IDH2 mutations is a neomorphic enzymatic activity that converts α-ketoglutarate to 2-hydroxyglutarate (2010, result): “This is in contrast to the data reported for gliomas in which less than 5% of IDH mutations were in IDH2 (Hartmann et al., 2009; Yan et al., 2009).”
Cancer-associated metabolite 2-hydroxyglutarate accumulates in acute myelogenous leukemia with isocitrate dehydrogenase 1 and 2 mutations (2010, background): “…has revealed that this mutation is present in a high proportion of gliomas and secondary glioblastomas, but not in other human malignancies (Balss et al., 2008; Bleeker et al., 2009; Hartmann et al., 2009; Kang et al., 2009; Sanson et al., 2009; Watanabe et al., 2009; Yan et al., 2009).”