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TET2 loss-of-function mutations associate with a DNA hypermethylation signature in diffuse large B-cell lymphoma (mRNA)

ABSTRACT: Global gene expression in TET2 mutant and Wild type patients. We performed an integrated analysis of global DNA methylation and gene expression data to investigate the effects of DNA hypermethylation on gene expression.

ORGANISM(S): Homo sapiens

PROVIDER: GSE37363 | GEO | 2013/10/10

SECONDARY ACCESSION(S): PRJNA159821

REPOSITORIES: GEO

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TET2 loss-of-function mutations associate with a DNA hypermethylation signature in diffuse large B-cell lymphoma (DNA methylation)

Project description:Genome wide DNA methylation profiling of patient samples with TET2 mutations and Wild type TET2 status . The Illumina Infinium HumanMethylation 450_15017482_v.1.1 was used to obtain DNA methylation profiles across approximately 482,421 CpGs in fresh frozen lymphoma samples. Samples include 19 TET2 wild type and 12 TET2 mutant samples. Bisulphite converted DNA from the 31 samples were hybridised to the Illumina Infinium HM450K Human Methylation Beadchip v1.2

2013-10-10 | E-GEOD-37362 | biostudies-arrayexpress

TET2 loss-of-function mutations associate with a DNA hypermethylation signature in diffuse large B-cell lymphoma (DNA methylation)

2013-10-10 | GSE37362 | GEO

Transcription profiling by array of TET2 wild type and TET2 mutant patients with diffuse large B-cell derived lymphoma

Project description:Global gene expression in TET2 mutant and Wild type patients. We performed an integrated analysis of global DNA methylation and gene expression data to investigate the effects of DNA hypermethylation on gene expression. Total RNA was isolated from 4 TET2mut and 5 TET2wt were isolated using standard RNAeasy kit protocol (Qiagen). Their gene expression profiles were obtained using the[HuGene-1_0-st] Affymetrix.

2013-10-10 | E-GEOD-37363 | biostudies-arrayexpress

Leukemic IDH1 and IDH2 mutations result in a hypermethylation phenotype, disrupt TET2 function, and impair hematopoietic differentiation

Project description:Cancer-associated IDH mutations are characterized by neomorphic enzyme activity and resultant 2 hydroxyglutarate (2HG) production. Mutational and epigenetic profiling of a large AML patient cohort revealed that IDH1/2-mutant AMLs display global DNA hypermethylation and a specific hypermethylation signature. Furthermore, expression of 2HG-producing IDH alleles in cells rapidly induced global DNA hypermethylation. In the AML cohort, IDH1/2 mutations were mutually exclusive with mutations in the α-ketoglutarate-dependent enzyme TET2, and TET2 loss-of function mutations associated with similar epigenetic defects as IDH1/2 mutants. Consistent with these genetic and epigenetic data, expression of IDH mutants impaired TET2 catalytic function in cells. Finally, either expression of mutant IDH1/2 or Tet2 depletion impaired hematopoietic differentiation and increased stem cell marker expression, suggesting a shared pro-leukemogenic effect. DNA methylation and gene expression profiling in IDH1/2 mutant vs. IDH1/2 wild-type AML

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TET2 loss-of-function mutations associate with a DNA hypermethylation signature in diffuse large B-cell lymphoma

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2013-10-10 | E-GEOD-37365 | biostudies-arrayexpress

Loss of TET2 in hematopoietic cells leads to DNA hypermethylation of active enhancers and induction of leukemogenesis (Affymetrix)

Project description:DNA methylation is tightly regulated throughout mammalian development and altered methylation patterns are a hallmark of cancer. The methylcytosine dioxygenase TET2 is frequently mutated in acute myeloid leukemia (AML) and has been suggested to protect CpG islands and promoters from aberrant methylation. By generating a novel mouse model of Tet2-deficient AML we show that loss of Tet2 in hematopoietic cells leads to progressive hypermethylation of active enhancer elements and altered expression of genes implicated in tumorigenesis. In contrast, CpG island and promoter methylation does not change in a Tet2-dependent manner. Furthermore, we confirm this specific enhancer hypermethylation phenotype in human AML patients. Thus, we propose that TET2 prevents leukemic transformation of hematopoietic cells by protecting enhancers from aberrant DNA methylation. Gene expression profiles from Tet2-/-;AML1-ETO and Tet2fl/fl;AML1-ETO in vitro-grown hematopoietic cells were compared using GeneChip Mouse Gene ST 2.0 Arrays (Affymetrix). Expression changes were investigated at early (passage 2) and late (passage 10) timepoints after Tet2 disruption.

2015-04-22 | E-GEOD-59586 | biostudies-arrayexpress

Loss of TET2 in hematopoietic cells leads to DNA hypermethylation of active enhancers and induction of leukemogenesis (eRRBS)

Project description:DNA methylation is tightly regulated throughout mammalian development and altered methylation patterns are a hallmark of cancer. The methylcytosine dioxygenase TET2 is frequently mutated in acute myeloid leukemia (AML) and has been suggested to protect CpG islands and promoters from aberrant methylation. By generating a novel mouse model of Tet2-deficient AML we show that loss of Tet2 in hematopoietic cells leads to progressive hypermethylation of active enhancer elements and altered expression of genes implicated in tumorigenesis. In contrast, CpG island and promoter methylation does not change in a Tet2-dependent manner. Furthermore, we confirm this specific enhancer hypermethylation phenotype in human AML patients. Thus, we propose that TET2 prevents leukemic transformation of hematopoietic cells by protecting enhancers from aberrant DNA methylation. Enhanced Reduced Representation Bisulfite Sequencing (eRRBS) analysis of in vitro-grown hematopoietic cells transduced with AML1-ETO or MLL-AF9

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TET2 loss-of-function mutations associate with a DNA hypermethylation signature in diffuse large B-cell lymphoma

Project description:This SuperSeries is composed of the SubSeries listed below.

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Loss of TET2 in hematopoietic cells leads to DNA hypermethylation of active enhancers and induction of leukemogenesis (MeDIP-seq)

Project description:DNA methylation is tightly regulated throughout mammalian development and altered methylation patterns are a hallmark of cancer. The methylcytosine dioxygenase TET2 is frequently mutated in acute myeloid leukemia (AML) and has been suggested to protect CpG islands and promoters from aberrant methylation. By generating a novel mouse model of Tet2-deficient AML we show that loss of Tet2 in hematopoietic cells leads to progressive hypermethylation of active enhancer elements and altered expression of genes implicated in tumorigenesis. In contrast, CpG island and promoter methylation does not change in a Tet2-dependent manner. Furthermore, we confirm this specific enhancer hypermethylation phenotype in human AML patients. Thus, we propose that TET2 prevents leukemic transformation of hematopoietic cells by protecting enhancers from aberrant DNA methylation. 5hmC-DIP-seq analysis for distribution of 5hmC in in vitro-grown hematopoietic cells transduced with AML1-ETO

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