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Links from GEO DataSets

Items: 20

1.

Loss of TET2 in hematopoietic cells leads to DNA hypermethylation of active enhancers and induction of leukemogenesis [ChIP-seq]

(Submitter supplied) DNA methylation is tightly regulated throughout mammalian development and altered DNA methylation patterns are a general hallmark of cancer. The methylcytosine dioxygenase TET2 is frequently mutated in hematological disorders, including acute myeloid leukemia (AML), and has been suggested to protect CpG islands and promoters from aberrant DNA methylation. In this study, we present a novel Tet2-dependent leukemia mouse model that closely recapitulates gene expression profiles and hallmarks of human AML1-ETO induced AML. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL13112
16 Samples
Download data: BED, BIGWIG
Series
Accession:
GSE68414
ID:
200068414
2.

Loss of TET2 in hematopoietic cells leads to DNA hypermethylation of active enhancers and induction of leukemogenesis [Agilent]

(Submitter supplied) DNA methylation is tightly regulated throughout mammalian development and altered DNA methylation patterns are a general hallmark of cancer. The methylcytosine dioxygenase TET2 is frequently mutated in hematological disorders, including acute myeloid leukemia (AML), and has been suggested to protect CpG islands and promoters from aberrant DNA methylation. In this study, we present a novel Tet2-dependent leukemia mouse model that closely recapitulates gene expression profiles and hallmarks of human AML1-ETO induced AML. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL10787
9 Samples
Download data: TXT
Series
Accession:
GSE68415
ID:
200068415
3.

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

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing; Methylation profiling by high throughput sequencing; Expression profiling by array
Platforms:
GPL16570 GPL13112 GPL10787
53 Samples
Download data: BED, BIGWIG, CEL, TXT
Series
Accession:
GSE59591
ID:
200059591
4.

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

(Submitter supplied) DNA methylation is tightly regulated throughout mammalian development and altered DNA methylation patterns are a general hallmark of cancer. The methylcytosine dioxygenase TET2 is frequently mutated in hematological disorders, including acute myeloid leukemia (AML), and has been suggested to protect CpG islands and promoters from aberrant DNA methylation. In this study, we present a novel Tet2-dependent leukemia mouse model that closely recapitulates gene expression profiles and hallmarks of human AML1-ETO induced AML. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL16570
12 Samples
Download data: CEL
Series
Accession:
GSE59586
ID:
200059586
5.

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

(Submitter supplied) DNA methylation is tightly regulated throughout mammalian development and altered DNA methylation patterns are a general hallmark of cancer. The methylcytosine dioxygenase TET2 is frequently mutated in hematological disorders, including acute myeloid leukemia (AML), and has been suggested to protect CpG islands and promoters from aberrant DNA methylation. In this study, we present a novel Tet2-dependent leukemia mouse model that closely recapitulates gene expression profiles and hallmarks of human AML1-ETO induced AML. more...
Organism:
Mus musculus
Type:
Methylation profiling by high throughput sequencing
Platform:
GPL13112
10 Samples
Download data: TXT
Series
Accession:
GSE59584
ID:
200059584
6.

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

(Submitter supplied) DNA methylation is tightly regulated throughout mammalian development and altered DNA methylation patterns are a general hallmark of cancer. The methylcytosine dioxygenase TET2 is frequently mutated in hematological disorders, including acute myeloid leukemia (AML), and has been suggested to protect CpG islands and promoters from aberrant DNA methylation. In this study, we present a novel Tet2-dependent leukemia mouse model that closely recapitulates gene expression profiles and hallmarks of human AML1-ETO induced AML. more...
Organism:
Mus musculus
Type:
Methylation profiling by high throughput sequencing
Platform:
GPL13112
6 Samples
Download data: BED, BIGWIG
Series
Accession:
GSE59579
ID:
200059579
7.

PU.1-dependent enhancer inhibition separates clonal hematopoiesis from malignant transformation (oxBS-Seq)

(Submitter supplied) Hematopoietic stem cells sustain life-long blood production. While they are the known cellular origin of aging-associated myeloid malignancies, such as acute myeloid leukemia (AML), mechanisms driving their malignant transformation have remained elusive. Epigenetic dysregulation following acquired loss-of-function mutations of DNA methyl-cytosine dioxygenase Ten-Eleven Translocation-2 (TET2) occurs frequently in the elderly leading to cytosine hypermethylation in and around DNA binding sites of master transcription factors, including PU.1. more...
Organism:
Mus musculus
Type:
Methylation profiling by high throughput sequencing
Platform:
GPL21103
16 Samples
Download data: BEDGRAPH
Series
Accession:
GSE194170
ID:
200194170
8.

PU.1-dependent enhancer inhibition separates Tet2 deficient clonal hematopoiesis from malignant transformation

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL21103 GPL17021
41 Samples
Download data: BEDGRAPH
Series
Accession:
GSE191053
ID:
200191053
9.

PU.1-dependent enhancer inhibition separates clonal hematopoiesis from malignant transformation (ATAC-Seq)

(Submitter supplied) Hematopoietic stem cells sustain life-long blood production. While they are the known cellular origin of aging-associated myeloid malignancies, such as acute myeloid leukemia (AML), mechanisms driving their malignant transformation have remained elusive. Epigenetic dysregulation following acquired loss-of-function mutations of DNA methyl-cytosine dioxygenase Ten-Eleven Translocation-2 (TET2) occurs frequently in the elderly leading to cytosine hypermethylation in and around DNA binding sites of master transcription factors, including PU.1. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL21103
8 Samples
Download data: NARROWPEAK
Series
Accession:
GSE191052
ID:
200191052
10.

PU.1-dependent enhancer inhibition separates clonal hematopoiesis from malignant transformation (RNA-Seq)

(Submitter supplied) Hematopoietic stem cells sustain life-long blood production. While they are the known cellular origin of aging-associated myeloid malignancies, such as acute myeloid leukemia (AML), mechanisms driving their malignant transformation have remained elusive. Epigenetic dysregulation following acquired loss-of-function mutations of DNA methyl-cytosine dioxygenase Ten-Eleven Translocation-2 (TET2) occurs frequently in the elderly leading to cytosine hypermethylation in and around DNA binding sites of master transcription factors, including PU.1. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
17 Samples
Download data: TXT
Series
Accession:
GSE186146
ID:
200186146
11.

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

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Expression profiling by array; Methylation profiling by genome tiling array
Platforms:
GPL13534 GPL6244
40 Samples
Download data: CEL
Series
Accession:
GSE37365
ID:
200037365
12.

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

(Submitter supplied) 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:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL6244
9 Samples
Download data: CEL
Series
Accession:
GSE37363
ID:
200037363
13.

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

(Submitter supplied) 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.
Organism:
Homo sapiens
Type:
Methylation profiling by genome tiling array
Platform:
GPL13534
31 Samples
Download data: TXT
Series
Accession:
GSE37362
ID:
200037362
14.

Rational targeting of cooperating layers of the epigenome yields enhanced therapeutic efficacy against AML

(Submitter supplied) Disruption of epigenetic regulation is a hallmark of Acute Myeloid Leukemia (AML), but therapeutic interventions are difficult by the interplay of epigenetic mechanisms controlling genomic elements. We hypothesized that concurrent targeting of aberrant promoter and enhancer epigenetic silencing improves efficacy against AML. To test this, we developed an ex vivo culturing system and treated 52 patient-derived AML with low-dose 5-Azacytidine and specific LSD1 inhibitors. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing; Methylation profiling by high throughput sequencing
Platform:
GPL16791
28 Samples
Download data: TXT
15.

TET2 coactivates gene expression through demethylation of enhancers

(Submitter supplied) The tet methylcytosine dioxygenase 2 (TET2) enzyme catalyzes the conversion of the modified DNA base 5-methylcytosine to 5-hydroxymethylcytosine. TET2 is frequently mutated or dysregulated in multiple human cancers, and loss of TET2 is associated with changes in DNA methylation patterns. Here, using newly developed TET2-specific antibodies and the estrogen response as a model system for studying the regulation of gene expression, we demonstrate that endogenous TET2 occupies active enhancers and facilitates the proper recruitment of ERalpha. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing; Methylation profiling by high throughput sequencing
Platform:
GPL18573
79 Samples
Download data: BW, TXT
16.

TET2 binding to enhancers facilitates transcription factor recruitment in hematopoietic cells

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL21626
66 Samples
Download data: BIGWIG, NARROWPEAK
Series
Accession:
GSE115972
ID:
200115972
17.

TET2 binding to enhancers facilitates transcription factor recruitment in hematopoietic cells [RNA-Seq]

(Submitter supplied) The epigenetic regulator TET2 is frequently mutated in hematological diseases. Mutations have been shown to arise in hematopoietic stem cells early in disease development, lead to altered DNA methylation landscapes and to an increased risk of hematopoietic malignancy. Here, we show by genome-wide mapping of TET2 binding sites in different cell types that TET2 localizes to regions of open chromatin and cell-type specific enhancers. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL21626
16 Samples
Download data: TXT
Series
Accession:
GSE115967
ID:
200115967
18.

TET2 binding to enhancers facilitates transcription factor recruitment in hematopoietic cells [TET2 ChIP-seq hematopoietic cells]

(Submitter supplied) The epigenetic regulator TET2 is frequently mutated in hematological diseases. Mutations have been shown to arise in hematopoietic stem cells early in disease development, lead to altered DNA methylation landscapes and to an increased risk of hematopoietic malignancy. Here, we show by genome-wide mapping of TET2 binding sites in different cell types that TET2 localizes to regions of open chromatin and cell-type specific enhancers. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL21626
12 Samples
Download data: TXT
Series
Accession:
GSE115965
ID:
200115965
19.

TET2 binding to enhancers facilitates transcription factor recruitment in hematopoietic cells [TET2 ChIP-seq ES cells]

(Submitter supplied) The epigenetic regulator TET2 is frequently mutated in hematological diseases. Mutations have been shown to arise in hematopoietic stem cells early in disease development, lead to altered DNA methylation landscapes and to an increased risk of hematopoietic malignancy. Here, we show by genome-wide mapping of TET2 binding sites in different cell types that TET2 localizes to regions of open chromatin and cell-type specific enhancers. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL21626
10 Samples
Download data: BIGWIG, NARROWPEAK
Series
Accession:
GSE115964
ID:
200115964
20.

TET2 binding to enhancers facilitates transcription factor recruitment in hematopoietic cells [ATAC-Seq]

(Submitter supplied) The epigenetic regulator TET2 is frequently mutated in hematological diseases. Mutations have been shown to arise in hematopoietic stem cells early in disease development, lead to altered DNA methylation landscapes and to an increased risk of hematopoietic malignancy. Here, we show by genome-wide mapping of TET2 binding sites in different cell types that TET2 localizes to regions of open chromatin and cell-type specific enhancers. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL21626
28 Samples
Download data: BIGWIG
Series
Accession:
GSE115962
ID:
200115962
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