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Meta-analysis of IDH-mutant cancers identifies EBF1 as an interaction partner for TET2

ABSTRACT: Illumina Infinium 450k Human DNA Methylation BeadChip was used to obtain DNA methylation profiles across approximately 450,000 CpGs in 51 central chondrosarcoma.

ORGANISM(S): Homo sapiens

PROVIDER: GSE40853 | GEO | 2013/07/15

SECONDARY ACCESSION(S): PRJNA175115

REPOSITORIES: GEO

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Meta-analysis of IDH mutant-mediated hypermethylation identifies tissue-specific effectors within a shared pathway in multiple cancers.

Project description:Illumina Infinium 450k Human DNA Methylation BeadChip was used to obtain DNA methylation profiles across approximately 450,000 CpGs in 51 central chondrosarcoma. Bisulphite converted DNA from each sample was hybridised to the Illumina Infinium 450k Human Methylation BeadChip.

2013-07-15 | E-GEOD-40853 | biostudies-arrayexpress

Meta-analysis of IDH-mutant cancers identifies EBF1 as an interaction partner for TET2.

Project description:Isocitrate dehydrogenase (IDH) genes 1 and 2 are frequently mutated in acute myeloid leukaemia (AML), low-grade glioma, cholangiocarcinoma (CC) and chondrosarcoma (CS). For AML, low-grade glioma and CC, mutant IDH status is associated with a DNA hypermethylation phenotype, implicating altered epigenome dynamics in the aetiology of these cancers. Here we show that the IDH variants in CS are also associated with a hypermethylation phenotype and display increased production of the oncometabolite 2-hydroxyglutarate, supporting the role of mutant IDH-produced 2-hydroxyglutarate as an inhibitor of TET-mediated DNA demethylation. Meta-analysis of the acute myeloid leukaemia, low-grade glioma, cholangiocarcinoma and CS methylation data identifies cancer-specific effectors within the retinoic acid receptor activation pathway among the hypermethylated targets. By analysing sequence motifs surrounding hypermethylated sites across the four cancer types, and using chromatin immunoprecipitation and western blotting, we identify the transcription factor EBF1 (early B-cell factor 1) as an interaction partner for TET2, suggesting a sequence-specific mechanism for regulating DNA methylation.

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