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Links from GEO DataSets

Items: 11

1.

Both gain and loss of function of miR-126 promote t(8;21) leukemia progression with different consequences and through different mechanisms

(Submitter supplied) To investigate the pathological effect of miR-126 on the progression of acute myeloid leukemia (AML) induced by AML1-ETO9a (AE9a), we conducted a series of mouse bone marrow transplantation (BMT) assays with the following groups: AE9a (primary donor cells were wild-type mouse bone marrow progenitor (i.e., lineage negative; Lin-) cells retrovirally transduced with MSCV-PIG-AE9a), AE9a+miR-126 (primary donor cells were wild-type mouse bone marrow progenitor (i.e., Lin-) cells retrovirally transduced with MSCV-PIG-AE9a-miR-126), and miR-126KO+AE9a (primary donor cells were miR-126 knockout mouse bone marrow progenitor (i.e., Lin-) cells retrovirally transduced with MSCV-PIG-AE9a), along with a control group (primary donor cells were wild-type mouse bone marrow progenitor (i.e., Lin-) cells retrovirally transduced with MSCV-PIG empty vector). more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL16570
39 Samples
Download data: CEL
Series
Accession:
GSE65939
ID:
200065939
2.

Epigenetic regulation of the apoptosis program in t(8;21) AMLs by an AML1-ETO, ERG and RUNX1 triad

(Submitter supplied) The t(8;21) acute myeloid leukemia associated oncoprotein AML1-ETO is a transcription factor that aberrantly regulates the pathways that lead to myeloid differentiation. Here, we set out to investigate the effects of AML1-ETO on gene expression and the epigenome in patient blast cells. We identify two modules, one in which AML1-ETO binds promoter regions of active genes and one represented by non-promoter binding to accessible, yet inactive chromatin regions. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing
Platforms:
GPL11154 GPL10999
16 Samples
Download data: WIG
Series
Accession:
GSE76464
ID:
200076464
3.

Genome-wide studies identify a novel interplay between AML1 and AML1/ETO in t(8;21) acute myeloid leukemia

(Submitter supplied) The AML1/ETO fusion protein is essential to the development of acute myeloid leukemia (AML), and is well recognized for its dominant-negative effect on the co-existing wild-type protein AML1. However, the involvement of wild-type AML1 in AML1/ETO-driven leukemogenesis remains elusive. Through chromatin immunoprecipitation sequencing, computational analysis plus a series of experimental validations, we report here that AML1 is able to orchestrate the expression of AML1/ETO targets regardless of being activated or repressed, via forming a complex with AML1/ETO and via recruiting the cofactor.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL9115
6 Samples
Download data: BED, BIGWIG
Series
Accession:
GSE65427
ID:
200065427
4.

Expression profiling of primary leukemia initiating cell-enriched population induced by AML1-ETO9a

(Submitter supplied) Combined gene expression and DNA occupancy profiling identifies JAK/STAT signaling as a valid therapeutic target of t(8;21) AML t(8;21) is commonly associated with acute myeloid leukemia (AML). The resulting AML1-ETO fusion proteins are involved in the pathogenesis of AML. To identify novel molecular and therapeutic targets, we performed combined gene expression and promoter occupancy profiling using a primary leukemia initiating cell-enriched population induced by AML1-ETO9a (AE9a). more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL1261
6 Samples
Download data: CEL, EXP
Series
Accession:
GSE15195
ID:
200015195
5.

Targeting miR-126 in inv(16) acute myeloid leukemia inhibits leukemia development and leukemia stem cell maintenance

(Submitter supplied) Acute myeloid leukemia (AML) harboring inv(16)(p13q22) expresses high levels of miR-126. Here we show that the CBFB-MYH11 (CM) fusion gene upregulates miR-126 expression through aberrant miR-126 transcription and perturbed miR-126 biogenesis via the HDAC8/RAN-XPO5-RCC1 axis. Aberrant miR-126 upregulation promotes survival of leukemia-initiating progenitors and is critical for initiating and maintaining CM-driven AML. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
10 Samples
Download data: TXT
Series
Accession:
GSE184015
ID:
200184015
6.

State-Transition Analysis of Time-Sequential microRNA Expression Predicts Development of Acute Myeloid Leukemia

(Submitter supplied) We show that the microRNA transcriptome undergoes a global state transition during the initiation and progression of acute myeloid leukemia, and accurately predicts time to disease development.
Organism:
Mus musculus
Type:
Non-coding RNA profiling by high throughput sequencing
Platform:
GPL17021
231 Samples
Download data: TSV
Series
Accession:
GSE173785
ID:
200173785
7.

State-Transition Analysis of Time-Sequential Gene Expression Identifies Critical Points That Predict Leukemia Development

(Submitter supplied) Temporal dynamics of gene expression are informative of changes associated with disease development and evolution. Given the complexity of high-dimensionaltemporal datasets, an analytical framework guided by a robust theory is needed to interpret time-sequential changes and to predict system dynamics. Herein, we use acute myeloid leukemia as a proof-of-principle to model gene expression dynamics in a transcriptome state-space constructed based on time-sequential RNA-sequencing data. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
248 Samples
Download data: TSV, TXT
Series
Accession:
GSE133642
ID:
200133642
8.

Genome-wide co-occupancy of AML1-ETO and N-CoR defines the t(8;21) AML signature in leukemic cells

(Submitter supplied) This study characterizes the genome-side occupancy of AML1, AML1-ETO and the cofactors N-CoR and p300 in leukemics cells (Kasumi-1) to discover novel regulatory mechanisms involving genes bound by the t(8:21) fusion protein AML1-ETO. A significant discovery of our study is the co-localization of AML1-ETO with the N-CoR co-repressor on genomic regions that are primarily distal to the transcriptional start sites (TSSs). more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL9115
7 Samples
Download data: BED, BW
Series
Accession:
GSE62847
ID:
200062847
9.

Epigenetic silencing of UBXN8 contributes to leukemogenesis of t(8;21) acute myeloid leukemia

(Submitter supplied) The formation of the AML1-ETO fusion protein, resulting from the t(8;21) translocation, is considered to be among the t(8;21) acute myeloid leukemia (AML) initiating events. However, the mechanisms of the oncogenic activity of AML1-ETO remains unclear. In this study, we found that AML1-ETO triggers the heterochromatic silencing of UBXN8 by recognizing the AML1 binding sites and recruiting chromatin remodeling enzymes to the UBXN8 promoter region. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL16791
2 Samples
Download data: TXT
Series
Accession:
GSE155466
ID:
200155466
10.

microRNA profiling in pediatric AML

(Submitter supplied) MicroRNAs (miRNAs) play a pivotal role in the regulation of hematopoiesis and development of leukemia. Great interest emerged in modulating miRNA expression for therapeutic purposes. In order to identify miRNAs, which specifically suppress leukemic growth of AML with t(8;21), inv(16) or MLL-rearrangement by inducing differentiation, we conducted a miRNA expression profiling in a cohort of 90 cytogenetically characterized, de novo pediatric AML cases. more...
Organism:
Homo sapiens
Type:
Expression profiling by RT-PCR
Platform:
GPL16566
90 Samples
Download data: TXT
Series
Accession:
GSE52541
ID:
200052541
11.

Expression data for hematopoietic stem cells (lin- sca1+ ckit+) isolated from the bone marrow of Ercc1-deficient and proficient littermates

(Submitter supplied) To identify cellular and genetic abnormalities involved in interstrand cross link repair-deficient bone marrow failure and its transformation to leukemia, we used an Ercc1 hypomorphic mouse model (Ercc1 -/d). Gene expression profiling was done to determine which genes are differentially expressed
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL1261
6 Samples
Download data: CEL
Series
Accession:
GSE47700
ID:
200047700
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