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Links from GEO DataSets

Items: 20

1.

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
2.

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
3.

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
4.

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
5.

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
6.

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
7.

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
8.

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
9.

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
10.

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
11.

Identify the key signaling pathway involved in the Tet2 deficiency-induced clonal hematopoiesis

(Submitter supplied) To investigate the signaling pathway required for the Tet2 mutant associated clonal hematopoiesis, we identified the activated signaling pathway in Tet2-deficient hematopoietic stem/progenitor cells compared to WT cells and using transgentic mouse model to validate our findings. In short, the cGAS-STING pathway is activated in Tet2-deficient HSPCs and promotes the development of CH associated with Tet2 deficiency.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24247
55 Samples
Download data: CSV, TXT
Series
Accession:
GSE232384
ID:
200232384
12.

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
13.

Essential role of Jun family transcription factors in PU.1-induced leukemic stem cells

(Submitter supplied) Knockdown of the transcription factor PU.1 (Spi1) leads to acute myeloid leukemia (AML) in mice. We examined the transcriptome of PU.1 knockdown hematopoietic stem cells (HSC) in the preleukemic phase by linear amplification and genome-wide array analysis to identify transcriptional changes preceding malignant transformation. Hierarchical cluster analysis and principal component analysis clearly distinguished PU.1 knockdown from wildtype HSC. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Dataset:
GDS2411
Platform:
GPL1261
6 Samples
Download data
Series
Accession:
GSE5654
ID:
200005654
14.
Full record GDS2411

Transcription factor PU.1 knockdown effect on hematopoietic stem cells

Analysis of preleukemic hematopoietic stem cells from animals knocked down for the transcription factor PU.1. PU.1 knockdown leads to acute myeloid leukemia in the animal. Results provide insight into the molecular changes preceding malignant transformation.
Organism:
Mus musculus
Type:
Expression profiling by array, count, 2 protocol sets
Platform:
GPL1261
Series:
GSE5654
6 Samples
Download data
DataSet
Accession:
GDS2411
ID:
2411
15.

Epigenomic profiling of Acute myeloid leukemia subtypes from primary tumor samples

(Submitter supplied) Here we used Illumina NGS for high-throughput profiling of the DNA methylome(ERRBS) and hydroxymethylome(hMe-Seal) of primary tumor samples with Acute Myeloid Leukemia(AML). The data can be used to compare hydroxymethylation and methylation patterns from different AML subtypes and normal bone marrow samples.
Organism:
Homo sapiens
Type:
Methylation profiling by high throughput sequencing; Other
Platform:
GPL11154
63 Samples
Download data: TXT
Series
Accession:
GSE52945
ID:
200052945
16.

Reduced representation bisulfite-sequencing of human leukemia cells and mouse hematopoietic progenitors

(Submitter supplied) Human leukemia cells treated with vitamin C for 12 and 72hrs and mouse hematopoietic progenitor cells with knockdown and Tet2 restoration
Organism:
Mus musculus; Homo sapiens
Type:
Methylation profiling by high throughput sequencing
Platforms:
GPL17021 GPL16791
34 Samples
Download data: TXT
Series
Accession:
GSE100041
ID:
200100041
17.

hMeDIP sequencing of human leukemia cells

(Submitter supplied) Human leukemia cells treated with vitamin C for 72hrs.
Organism:
Homo sapiens
Type:
Methylation profiling by high throughput sequencing
Platform:
GPL16791
12 Samples
Download data: BED
Series
Accession:
GSE99953
ID:
200099953
18.

Genetic and pharmacological restoration of TET2 function blocks stem cell self-renewal and progression of leukemia

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus; Homo sapiens
Type:
Expression profiling by high throughput sequencing; Methylation profiling by high throughput sequencing
Platforms:
GPL16791 GPL17021
80 Samples
Download data: BED, TXT
Series
Accession:
GSE97442
ID:
200097442
19.

RNA-sequencing of human leukemia cells and mouse hematopoietic progenitors

(Submitter supplied) human leukemia cells treated with vitamin C for 12 and 72hrs and mouse hematopoietic progenitor cells with knockdown and Tet2 restoration
Organism:
Homo sapiens; Mus musculus
Type:
Expression profiling by high throughput sequencing
Platforms:
GPL16791 GPL17021
34 Samples
Download data: CSV
Series
Accession:
GSE97440
ID:
200097440
20.

Gene expression analysis of leukemia-initiating cells of URE-/+::Msh2-/- mice

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6246
9 Samples
Download data: CEL
Series
Accession:
GSE65671
ID:
200065671
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