Codeletion of 1p and 19q determines distinct gene methylation and expression profiles in IDH-mutated oligodendroglial tumors View Full Text


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Article Info

DATE

2013-05-21

AUTHORS

Pilar Mur, Manuela Mollejo, Yolanda Ruano, Ángel Rodríguez de Lope, Concepción Fiaño, Juan Fernando García, Javier S. Castresana, Aurelio Hernández-Laín, Juan A. Rey, Bárbara Meléndez

ABSTRACT

Oligodendroglial tumors (OTs) are primary brain tumors that show variable clinical and biological behavior. The 1p/19q codeletion is frequent in these tumors, indicating a better prognosis and/or treatment response. Recently, the prognostically favorable CpG island methylator phenotype (CIMP) in gliomas (G-CIMP+) was associated with mutations in the isocitrate dehydrogenase 1 and isocitrate dehydrogenase 2 (IDH) genes, as opposed to G-CIMP− tumors, highlighting the relevance of epigenetic mechanisms. We performed a whole-genome methylation study in 46 OTs, and a gene expression study of 25 tumors, correlating the methylation and transcriptomic profiles with molecular and clinical variables. Here, we identified two different epigenetic patterns within the previously described main G-CIMP+ profile. Both IDH mutation-associated methylation profiles featured one group of OTs with 1p/19q loss (CD-CIMP+), most of which were pure oligodendrogliomas, and a second group with intact 1p/19q and frequent TP53 mutation (CIMP+), most of which exhibited a mixed histopathology. A third group of OTs lacking the CIMP profile (CIMP−), and with a wild-type IDH and an intact 1p/19q, similar to the G-CIMP− subgroup, was also observed. The three CIMP groups presented a significantly better (CD-CIMP+), intermediate (CIMP+) or worse (CIMP−) prognosis. Furthermore, transcriptomic analyses revealed CIMP-specific gene expression signatures, indicating the impact of genetic status (IDH mutation, 1p/19q codeletion, TP53 mutation) on gene expression, and pointing to candidate biomarkers. Therefore, the CIMP profiles contributed to the identification of subgroups of OTs characterized by different prognoses, histopathologies, molecular features and gene expression signatures, which may help in the classification of OTs. More... »

PAGES

277-289

References to SciGraph publications

  • 2012-05-17. CIC and FUBP1 mutations in oligodendrogliomas, oligoastrocytomas and astrocytomas in ACTA NEUROPATHOLOGICA
  • 2008-11-05. Analysis of the IDH1 codon 132 mutation in brain tumors in ACTA NEUROPATHOLOGICA
  • 2008-12-18. Systematic and integrative analysis of large gene lists using DAVID bioinformatics resources in NATURE PROTOCOLS
  • 2012-02-15. IDH1 mutation is sufficient to establish the glioma hypermethylator phenotype in NATURE
  • 2012-10-14. Epigenomic analysis detects widespread gene-body DNA hypomethylation in chronic lymphocytic leukemia in NATURE GENETICS
  • 2009-06-25. Type and frequency of IDH1 and IDH2 mutations are related to astrocytic and oligodendroglial differentiation and age: a study of 1,010 diffuse gliomas in ACTA NEUROPATHOLOGICA
  • <error retrieving object. in <ERROR RETRIEVING OBJECT
  • 2011-12-12. Downregulation of PRDX1 by promoter hypermethylation is frequent in 1p/19q-deleted oligodendroglial tumours and increases radio- and chemosensitivity of Hs683 glioma cells in vitro in ONCOGENE
  • 2012-07-19. MGMT methylation analysis of glioblastoma on the Infinium methylation BeadChip identifies two distinct CpG regions associated with gene silencing and outcome, yielding a prediction model for comparisons across datasets, tumor grades, and CIMP-status in ACTA NEUROPATHOLOGICA
  • 2012-01-29. Somatic Histone H3 Alterations in Paediatric Diffuse Intrinsic Pontine Gliomas and Non-Brainstem Glioblastomas in NATURE GENETICS
  • 2007-07-06. The 2007 WHO Classification of Tumours of the Central Nervous System in ACTA NEUROPATHOLOGICA
  • 2012-01-29. Driver mutations in histone H3.3 and chromatin remodelling genes in paediatric glioblastoma in NATURE
  • Identifiers

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    http://scigraph.springernature.com/pub.10.1007/s00401-013-1130-9

    DOI

    http://dx.doi.org/10.1007/s00401-013-1130-9

    DIMENSIONS

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    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/23689617


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