GEO DataSets

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

(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

(Submitter supplied) Aberrant activation of β-catenin is a common event in Acute Myeloid Leukemia (AML), and is recognized as an independent predictor of poor prognosis. Although increased β-catenin signaling in AML has been associated with AML1-ETO and PML-RARα translocation products, and activating mutations in the FLT3 receptor, it remains unclear which mechanisms activate β-catenin in AML more broadly. Here, we describe a novel link between interleukin-3 (IL-3) signaling and the regulation of β-catenin in myeloid transformation and AML. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Dataset:

GDS4868

Platform:

GPL6244

16 Samples

Download data: CEL

Analysis of mononuclear cells from acute myeloid leukemia patients (AML 1-4) cultured in the presence of interleukin-3 (IL-3) for up to 16hrs. The overexpression of IL-3Rα in AML has been associated with reduced overall survival. Results provide insight into the role of IL-3 signaling in AML.

Organism:

Homo sapiens

Type:

Expression profiling by array, transformed count, 2 agent, 3 genotype/variation, 4 individual, 2 time sets

Platform:

GPL6244

Series:

GSE51402

16 Samples

Download data: CEL

(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

(Submitter supplied) Analysis of gene expression change after galectin-9 stimulation in primary CD34+TIM-3+ AML cells

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL10558

6 Samples

Download data: IDAT

(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:

GPL17021 GPL16791

6 Samples

Download data: TXT

(Submitter supplied) To investigate whether co-expression of PBX3/MEIS1 can mimic that of MLL-AF9, HOXA9/MEIS1 or HOXA9/PBX3 in inducing leukemogenesis, we conducted in vivo mouse bone marrow transplantation (BMT) assays. Briefly, normal mouse bone marrow (BM) progenitor (i.e., lineage negative; Lin-) cells collected from B6.SJL (CD45.1) donor mice (CD45.1) were retrovirally co-transduced with MSCVneo-MLL-AF9+MSCV-PIG (MLL-AF9), MSCVneo-HOXA9+MSCV-PIG (HOXA9), MSCVneo-HOXA9+MSCV-PIG-MEIS1 (HOXA9+MEIS1), MSCVneo-HOXA9+MSCV-PIG-PBX3 (HOXA9+PBX3), MSCV-PIG-PBX3+MSCVneo-MEIS1 (PBX3+MEIS1), MSCVneo+MSCV-PIG-PBX3 (PBX3) , MSCVneo+MSCV-PIG-MEIS1 (MEIS1), or MSCVneo+MSCV-PIG (normal control; NC). more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL16570

20 Samples

Download data: CEL

(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

(Submitter supplied) MLL-AF9 expression in normal human umbilical cord blood CD34+ cells leads to long-term proliferation of a myeloid progenitor cell with leukemogenic potential. Expression of a Core Binding Factor leukemia fusion (AML1-ETO or CBFbeta-SMMHC) in human CD34+ cells results in self-renewal of primitive progenitor cells with multilineage potential and stem cell ability, but these cells do not induce leukemia in immunodeficient mice. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL570

18 Samples

Download data: CEL

(Submitter supplied) Purpose: To clarify the function of TIM-3 signaling in AML cells. Analysis of lentiviral shRNA-mediated knockdown of TIM-3 in TIM-3+ acute myeloid leukemia (AML) cell line, KASUMI-3. Consistent with our previous study (Kikushige et al., Cell Stem Cell 2015) revealing the presence of TIM-3/galectin-9 autocrine loop and its constitutive signaling in AML, KD of receptor,TIM-3, alone significantly impaired the proliferation of KASUMI-3 in vitro and in vivo.

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL17077

6 Samples

Download data: TXT

(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 GPL13112 GPL19057

18 Samples

Download data: BIGWIG, TXT

(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

(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

(Submitter supplied) Ecotropic virus integration site 1 (EVI1), whose overexpression characterizes a particularly aggressive subtype of acute myeloid leukemia (AML), enhanced anti-leukemic activities of all-trans retinoic acid (atRA) in cell lines and patient samples. However, the drivers of leukemia formation, therapy resistance, and relapse are leukemic stem cells (LSCs), whose properties were hardly reflected in these experimental setups. more...

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL21493

10 Samples

Download data: TXT

(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

(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

(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

(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

(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