U.S. flag

An official website of the United States government

Format
Items per page
Sort by

Send to:

Choose Destination

Links from GEO DataSets

Items: 20

1.

IKZF2 is required for myeloid leukemic stem cells by driving self-renewal and inhibiting the myeloid differentiation program II

(Submitter supplied) We report that IKZF2 is required for maintaining chromatin accessibility in leukemic stem cells in myeloid leukemia. RNA seq and ATAC-seq were performed to investigate the changes in chromatin accessibility of differentially expressed genes in leukemic stem cells when IKZF2 was absent. We found that IKZF2 maintains open accessibility in self-renewal transcription factor motifs such as HOXA9 sites whereas motifs of differentiation transcription factors including C/EBPs are kept closed.
Organism:
Mus musculus
Type:
Other
Platforms:
GPL21103 GPL19057
10 Samples
Download data: TXT
Series
Accession:
GSE120623
ID:
200120623
2.

IKZF2 is required for myeloid leukemic stem cells by driving self-renewal and inhibiting the myeloid differentiation program

(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; Other
Platforms:
GPL21103 GPL19057 GPL13112
18 Samples
Download data: BIGWIG, TXT
Series
Accession:
GSE120630
ID:
200120630
3.

IKZF2 is required for myeloid leukemic stem cells by driving self-renewal and inhibiting the myeloid differentiation program I

(Submitter supplied) We report that IKZF2 is required for maintaining chromatin accessibility in leukemic stem cells in myeloid leukemia. RNA seq and ATAC-seq were performed to investigate the changes in chromatin accessibility of differentially expressed genes in leukemic stem cells when IKZF2 was absent. We found that IKZF2 maintains open accessibility in self-renewal transcription factor motifs such as HOXA9 sites whereas motifs of differentiation transcription factors including C/EBPs are kept closed.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL13112
8 Samples
Download data: BIGWIG, TXT
Series
Accession:
GSE108367
ID:
200108367
4.

Single-cell gene expression analyses reveal distinct self-renewing and proliferating subsets in the leukemia stem cell compartment in murine acute myeloid leukemia

(Submitter supplied) Standard chemotherapy for acute myeloid leukemia (AML) targets proliferative cells and efficiently induces complete remission; however, many patients relapse and die of their disease. Relapse is caused by leukemia stem cells (LSCs), the cells with self-renewal capacity. Self-renewal and proliferation are mutually exclusive in normal hematopoietic stem cells (HSCs) in steady state conditions. If these functions are also mutually exclusive in LSCs, then antiproliferative therapies may fail to target self-renewal, allowing for relapse. more...
Organism:
Homo sapiens; Mus musculus
Type:
Expression profiling by high throughput sequencing
Platforms:
GPL16791 GPL17021
6 Samples
Download data: TXT
Series
Accession:
GSE140896
ID:
200140896
5.

Jmjd1c

(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:
GPL13112
27 Samples
Download data: WIG
Series
Accession:
GSE75581
ID:
200075581
6.

Effect of loss of Jmjd1c on Hoxa9/Meis1 leukemia

(Submitter supplied) Analysis of gene expression profile of Hoxa9/Meis1 leukemia cells 6 days after loss of Jmjd1c. Loss of Jmjd1c induces differentiation and Hoxa9/Meis1 leukemia cells. These results provide insight into the role of Jmjd1c in AML with elelvated expression of Hoxa9.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL13112
6 Samples
Download data: TXT
Series
Accession:
GSE75580
ID:
200075580
7.

Effect of loss of Jmjd1c on normal hematopoiesis

(Submitter supplied) Analysis of gene expression profile of LSK (Lin-Sca-1+ c-Kit+) isolated from Jmjd1c f/f Vav1Cre or Vav1Cre controls. Loss of Jmjd1c minimally affected HSC in homeostatsis while impiars HSC function in response to stree such as transplantation and 5-Fu treatment. These results provide insight into the role of Jmjd1c in normal hematopoiesis.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL13112
7 Samples
Download data: TXT
Series
Accession:
GSE75579
ID:
200075579
8.

Effect of loss of Jmjd1c on H3K9me2 level across the genome

(Submitter supplied) Analysis of H3K9me2 level in MLL-AF9 leukemia cells upon deletion of Jmjd1c. Jmjd1c has been shown to be a H3K9me1/2 demethylase and these results provide insight into its role in MLL-Af9 leukemia
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL13112
6 Samples
Download data: WIG
Series
Accession:
GSE75577
ID:
200075577
9.

Effect of loss of Jmjd1c on MLL-AF9 leukemia

(Submitter supplied) Analysis of gene expression profile of MLL-AF9 leukemia cells 6 days after loss of Jmjd1c. Loss of Jmjd1c induces differentiation and apoptosis in MLL-AF9 leukemia cells. These results provide insight into the role of Jmjd1c in MLL leukemia.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL13112
8 Samples
Download data: TXT
Series
Accession:
GSE75576
ID:
200075576
10.

Msi2 sustains the MLL leukemia stem cell regulatory program

(Submitter supplied) Leukemia stem cells (LSCs) are found in most aggressive myeloid diseases and contribute to therapeutic resistance. Genetic and epigenetic alterations cause a dysregulated developmental program in leukemia. The MSI2 RNA binding protein has been previously shown to predict poor survival in leukemia. We demonstrate that the conditional deletion of Msi2 results in delayed leukemogenesis, reduced disease burden and a loss of LSC function. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL13112
4 Samples
Download data: TXT
Series
Accession:
GSE64545
ID:
200064545
11.

Next Generation Sequencing of LSK EpCAM+ and EpCAM- of Zeb1-/-

(Submitter supplied) Zeb1, a zinc finger E-box binding homeobox epithelial-mesenchymal (EMT) transcription factor, confers properties of ‘stemness’, such as self-renewal, in cancer. Yet little is known about the function of Zeb1 in adult stem cells. Here, we used the hematopoietic system, as a well-established paradigm of stem cell biology, to evaluate Zeb1 mediated regulation of adult stem cells. We employed a conditional genetic approach using the Mx1-Cre system to specifically knockout (KO) Zeb1 in adult hematopoietic stem cells (HSCs) and their downstream progeny. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24247
8 Samples
Download data: TXT
Series
Accession:
GSE154615
ID:
200154615
12.

Bortezomib suppresses self-renewal and leukemogenesis of leukemia stem cell by NF-ĸB-dependent inhibition of cyclin dependent kinase 6 in MLL-rearranged myeloid leukemia

(Submitter supplied) Acute myeloid leukemia (AML) with chromosomal rearrangements involving the H3K4 methyltransferase mixed-lineage leukemia (MLL) is an aggressive subtype with low overall survival. MLL rearrangements rapidly transform hematological stem and progenitor cell (HSPC) to leukemia stem cell (LSC). Bortezomib (Velcade) is used widely in hematological malignancies. However, it is still unknown whether bortezomib possesses anti-self-renewal and anti-leukemogenesis of LSC in AML with MLL rearrangements. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11154
2 Samples
Download data: TXT, XLSX
13.

Next Generation Sequencing of Wild Type and Gata2+/- HSCs

(Submitter supplied) Gata2, a zinc finger TF, is essential for the generation and survival of HSCs in the embryo and has been implicated in the pathogenesis of AML, yet the requirement for Gata2 in adult HSCs and LSCs remains unclear. Using a conditional mouse model where Gata2 was deleted specifically in hematopoietic cells, we show that knockout of Gata2 leads to a rapid and complete cell-autonomous loss of adult HSCs. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL21103
8 Samples
Download data: TXT
Series
Accession:
GSE133248
ID:
200133248
14.

Next Generation Sequencing of Wild Type and Gata2-/- LSCs

(Submitter supplied) Gata2, a zinc finger TF, is essential for the generation and survival of HSCs in the embryo and has been implicated in the pathogenesis of AML, yet the requirement for Gata2 in adult HSCs and LSCs remains unclear. Using a conditional mouse model where Gata2 was deleted specifically in hematopoietic cells, we show that knockout of Gata2 leads to a rapid and complete cell-autonomous loss of adult HSCs. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL21103
8 Samples
Download data: TXT
Series
Accession:
GSE133245
ID:
200133245
15.

mRNA expression of murine hematopoietic stem cells and ex vivo murine MLL-AF9 cells deficient for total PRDM16 or f-PRDM16, and AF9 cells overexpressing individual PRDM16 isoforms

(Submitter supplied) Group 1 -- WT or PRDM16-KO ex vivo murine MLL-AF9 cells, and PRDM16-KO AF9 cells overexpressing either f-PRDM16 or s-PRDM16. Group 2 -- WT or total PRDM16-KO murine HSCs isolated from adult BM. Group 3 -- WT or total PRDM16-KO murine HSCs isolated from fetal liver. Group 4 -- WT or f-PRDM16-KO murine HSCs (expressing s-PRDM16 only) isolated from fetal liver.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platforms:
GPL19057 GPL17021
32 Samples
Download data: TXT
Series
Accession:
GSE112860
ID:
200112860
16.

Activation or maintenance of a leukemia stem cell self-renewal pathway in downstream myeloid cells

(Submitter supplied) Activation or maintenance of a leukemia stem cell self-renewal pathway in downstream myeloid cells is an important component of AML development We generated either MLL-AF9 mediated murine leukemias that originate from committed progenitor (GMP) cells or Hoxa9/Meis1a mediated murine leukemias that originate from hematopoietic stem cells (HSC). The leukemia stem cell fraction in these two type of leukemias shared a common self-renewal pathway with normal hematopoietic stem cells. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Dataset:
GDS3839
Platform:
GPL8321
15 Samples
Download data: CEL
Series
Accession:
GSE20377
ID:
200020377
17.
Full record GDS3839

Acute myelogenous leukemia stem cells

Analysis of acute myelogenous leukemia (AML) leukemia stem cells (LSC) induced either by Hoxa9/Meis1a oncogenes or MLL-AF9 oncoprotein. LSC self-renewal pathway in myeloid cells is central to AML development. Results provide insight into the molecular mechanisms underlying development of LSC in AML.
Organism:
Mus musculus
Type:
Expression profiling by array, count, 4 cell line, 5 cell type, 2 disease state sets
Platform:
GPL8321
Series:
GSE20377
15 Samples
Download data: CEL
18.

Expression data from Ezh2-null leukemic cells

(Submitter supplied) The polycomb group (PcG) proteins function in gene silencing through histone modifications. They form chromatin-associated multiprotein complexes, termed polycomb repressive complex (PRC) 1 and PRC2. These two complexes work in a coordinated manner in the maintenance of cellular memories through transcriptional repression of target genes. EZH2 is a catalytic component of PRC2 and trimethylates histone H3 at lysine 27 to transcriptionally repress the target genes. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL1261
4 Samples
Download data: CEL, CHP
Series
Accession:
GSE33808
ID:
200033808
19.

H3K9me3 ChIP-seq in MLL-rearranged leukemic stem cells and hematopoietic stem cells

(Submitter supplied) Acute myeloid leukemia (AML) with rearrangement of the mixed-lineage leukemia (MLL) gene are the most aggressive hematopoietic malignancies. Previous studies demonstrated the distribution of several epigenetic modifications including H3K9me3, H3K79me2, H3K36me3, H3K4me3 and H3K27me3, in MLL-AF9 transformed murine cells. Here, we examined the H3K9me3 distribution in c-Kit+ cells (enriched with stem/progenitor cells) from both MLL-AF9 transformed murine cells in parallel with control wild-type cells, and found an overall lower distribution of H3K9me3 in leukemia stem cells than normal hematopoietic stem/progenitor cells.
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL17021
8 Samples
Download data: WIG
Series
Accession:
GSE132175
ID:
200132175
20.

RNA profiling of Suv39h1 overexpressed MLL-AF9 induced acute myeloid leukemia (AML) cells

(Submitter supplied) Acute myeloid leukemias (AMLs) with rearrangement of the mixed-lineage leukemia (MLL) gene are the most aggressive hematopoietic malignancies. By analyzing the clinical data, we found the expression of SUV39H1 was significantly decreased in AML patients and MLL-AF9 (MA9) induced AML mice, in comparison with controls. Remarkably, when overexpress Suv39h1 in MA9 AML mice, the survival of AML mice was significantly prolonged.To examined the mechanism mediated by Suv39h1 overexpression (SUV-OE), we performed the RNAseq profiling of SUV-OE MA9 AML cells and control cells.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL13112
4 Samples
Download data: TXT
Series
Accession:
GSE115549
ID:
200115549
Format
Items per page
Sort by

Send to:

Choose Destination

Supplemental Content

db=gds|term=|query=1|qty=3|blobid=MCID_67596684c087e367329ecb31|ismultiple=true|min_list=5|max_list=20|def_tree=20|def_list=|def_view=|url=/Taxonomy/backend/subset.cgi?|trace_url=/stat?
   Taxonomic Groups  [List]
Tree placeholder
    Top Organisms  [Tree]

Find related data

Recent activity

Your browsing activity is empty.

Activity recording is turned off.

Turn recording back on

See more...
Support Center