Oligodendrogliomas: Molecular Biology and Treatment

Bromberg, J.E.C.; Bent, Martin J. van den

doi:10.1634/theoncologist.2008-0248

Cited by 73 publications

(47 citation statements)

References 61 publications

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“…Oligodendrogliomas have long been known to contain characteristic losses of chromosome arms 1p and 19q, and these losses reflect inactivation of the CIC gene on chromosome 19q and in some cases, inactivation of the FUBP1 gene on chromosome 1p (34)(35)(36). Accordingly, 78% of 45 oligodendrogliomas contained chromosome arm 1p or 19q losses of heterozygosity (Fig.…”

Section: Resultsmentioning

confidence: 99%

TERT promoter mutations occur frequently in gliomas and a subset of tumors derived from cells with low rates of self-renewal

Killela

Reitman

Jiao

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

1,245

1,230

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Malignant cells, like all actively growing cells, must maintain their telomeres, but genetic mechanisms responsible for telomere maintenance in tumors have only recently been discovered. In particular, mutations of the telomere binding proteins alpha thalassemia/ mental retardation syndrome X-linked (ATRX) or death-domain associated protein (DAXX) have been shown to underlie a telomere maintenance mechanism not involving telomerase (alternative lengthening of telomeres), and point mutations in the promoter of the telomerase reverse transcriptase (TERT) gene increase telomerase expression and have been shown to occur in melanomas and a small number of other tumors. To further define the tumor types in which this latter mechanism plays a role, we surveyed 1,230 tumors of 60 different types. We found that tumors could be divided into types with low (<15%) and high (≥15%) frequencies of TERT promoter mutations. The nine TERT-high tumor types almost always originated in tissues with relatively low rates of self renewal, including melanomas, liposarcomas, hepatocellular carcinomas, urothelial carcinomas, squamous cell carcinomas of the tongue, medulloblastomas, and subtypes of gliomas (including 83% of primary glioblastoma, the most common brain tumor type). TERT and ATRX mutations were mutually exclusive, suggesting that these two genetic mechanisms confer equivalent selective growth advantages. In addition to their implications for understanding the relationship between telomeres and tumorigenesis, TERT mutations provide a biomarker that may be useful for the early detection of urinary tract and liver tumors and aid in the classification and prognostication of brain tumors.

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Section: Resultsmentioning

confidence: 99%

TERT promoter mutations occur frequently in gliomas and a subset of tumors derived from cells with low rates of self-renewal

Killela

Reitman

Jiao

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

1,245

1,230

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“…We first screened for combined LOH on 1p and 19q; chromosomal losses that are frequently observed in oligodendrogliomas and relatively rare in astrocytic tumors (Ohgaki and Kleihues 2009;Bromberg and van den Bent 2009)). These losses are caused by an unbalanced translocation between chromosomes 1 and 19 [t(1;19)(q10,p10)] (Griffin et al, 2006;Jenkins et al, 2006).…”

Section: Non-pr132h Mutations In Idh1 Segregate In Distinct Glioma Smentioning

confidence: 99%

Segregation of non-p.R132H mutations inIDH1in distinct molecular subtypes of glioma

et al. 2010

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Mutations in the gene encoding the isocitrate dehydrogenase 1 gene (IDH1) occur at a high frequency (up to 80%) in many different subtypes of glioma. In this study, we have screened for IDH1 mutations in a cohort of 496 gliomas. IDH1 mutations were most frequently observed in low grade gliomas with c.395G>A (p.R132H) representing >90% of all IDH1 mutations. Interestingly, non-p.R132H mutations segregate in distinct histological and molecular subtypes of glioma. Histologically, they occur sporadically in classic oligodendrogliomas and at significantly higher frequency in other grade II and III gliomas. Genetically, non-p.R132H mutations occur in tumors with TP53 mutation, are virtually absent in tumors with loss of heterozygosity on 1p and 19q and accumulate in distinct (gene-expression profiling based) intrinsic molecular subtypes. The IDH1 mutation type does not affect patient survival. Our results were validated on an independent sample cohort, indicating that the IDH1 mutation spectrum may aid glioma subtype classification. Functional differences between p.R132H and non-p.R132H mutated IDH1 may explain the segregation in distinct glioma subtypes.

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“…3 The characteristic feature of oligodendrogliomas at the molecular level is loss of the shorter arm of chromosome 1 (1p) or codeletion of 1p and the longer arm of chromosome 19 mutation that harbors tumor suppressor genes. Whereas isolated 19q LOH occurs in astrocytomas, 1p LOH or combined 1p/19q LOH is uncommon in gliomas other than oligodendrogliomas and oligoastrocytomas.…”

mentioning

confidence: 99%

Differentiation between Oligodendroglioma Genotypes Using Dynamic Susceptibility Contrast Perfusion-Weighted Imaging and Proton MR Spectroscopy

Chawla¹,

Krejza²,

Vossough³

et al. 2013

AJNR Am J Neuroradiol

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Oligodendrogliomas: Molecular Biology and Treatment

Cited by 73 publications

References 61 publications

TERT promoter mutations occur frequently in gliomas and a subset of tumors derived from cells with low rates of self-renewal

TERT promoter mutations occur frequently in gliomas and a subset of tumors derived from cells with low rates of self-renewal

Segregation of non-p.R132H mutations inIDH1in distinct molecular subtypes of glioma

Differentiation between Oligodendroglioma Genotypes Using Dynamic Susceptibility Contrast Perfusion-Weighted Imaging and Proton MR Spectroscopy

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