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Links from GEO DataSets

Items: 20

1.

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
2.

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
3.

Transcriptomic and epigenomic profiling of SETDB1 mediated repression in Acute Myeloid Leukemia

(Submitter supplied) Epigenetic regulators play a critical role in normal and malignant hematopoiesis. We recently showed that the Histone 3 Lysine 9 (H3K9) methyltransferase SETDB1 negatively regulates the expression of the pro-leukemic genes HoxA9 and its cofactor Meis1 through deposition of promoter H3K9 trimethylation (H3K9me3) in MLL-AF9 AML cells. Here, we investigated the microbiological impact of altered SETDB1 expression in AML cells. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL19057 GPL17021
26 Samples
Download data: BW, TXT
Series
Accession:
GSE136850
ID:
200136850
4.

ZNF521 enhances MLL-AF9-dependent hematopoietic stem cell transformation in acute myeloid leukemias by altering the gene expression landscape

(Submitter supplied) Leukemias derived from the MLL-AF9 rearrangement rely on deranged transcriptional networks. ZNF521, a transcription co-factor implicated in the control of hematopoiesis, has been proposed to sustain leukemic transformation in collaboration with other oncogenes. We demonstrate here that ZNF521 mRNA levels correlate with specific genetic aberrations: in particular, the highest expression is observed in AMLs bearing MLL rearrangements, while the lowest is detected in AMLs with FLT3-ITD, NPM1 or CEBPα double mutations. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL23126
10 Samples
Download data: CEL
Series
Accession:
GSE181006
ID:
200181006
5.

Epigenetic profiling of hematopoietic stem cells and leukemia stem cells

(Submitter supplied) The histone 3 lysine 79 (H3K79) methyltransferase Dot1l has been implicated in the development of leukemias bearing translocations that involve the Mixed Lineage Leukemia (MLL) gene. We identified the MLL-fusion targets in a murine MLL-AF9 leukemia model, and conducted epigenetic profiling for H3K79me2, H3K4me3, H3K27me3 and H3K36me3. Histone methylation patterns are highly abnormal on MLL-AF9 fusion target loci, defining a distinct epigenetic lesion involving H3K79. more...
Organism:
Mus musculus; Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL11002 GPL10999 GPL13112
15 Samples
Download data: WIG
Series
Accession:
GSE29130
ID:
200029130
6.

Expression changes after loss of Dot1l in murine MLL-AF9 leukemia cells

(Submitter supplied) MLL-fusions may induce leukemogenic gene expression programs by recruiting the histone H3K79 methyltransferase to MLL-target promoters. We evaluated gene expression changes after cre-mediated loss of Dot1l in leukemia cells obtained from mice injected with MLL-9 transformed lineage negative bone marrow cells.
Organism:
Mus musculus
Type:
Expression profiling by array
Dataset:
GDS4295
Platform:
GPL1261
26 Samples
Download data: CEL
Series
Accession:
GSE25911
ID:
200025911
7.
Full record GDS4295

Histone methyltransferase H3K79 Dot1l deletion effect on MLL-AF9 leukemia cells: time course

Analysis of Mixed Lineage Leukemia (MLL)-AF9 leukemia cells after loss of Dot1l for up to 7 days. Loss of Dot1l leads to decreased growth, differentiation, and apoptosis of MLL-AF9 cells. Results provide insight into role of Dot1l in MLL-rearranged leukemia.
Organism:
Mus musculus
Type:
Expression profiling by array, count, 2 genotype/variation, 3 time sets
Platform:
GPL1261
Series:
GSE25911
26 Samples
Download data: CEL
8.

PBX3 cooperates with MEISI in causing rapid acute myeloid leukemia and recapitulates the core transcriptome of MLL-rearranged leukemia

(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
Series
Accession:
GSE68643
ID:
200068643
9.

Gene expression profiling of the MLL-AF9 induced AML cells (wild type and Dnmt3b-KO)

(Submitter supplied) Acute myeloid leukemia (AML) is a heterogeneous hematopoietic disorder with a poor prognosis. Abnormal DNA methylation is involved in the initiation and development of AML. The de novo methyltransferases Dnmt3a and Dnmt3b are responsible for the generation of genomic methylation patterns. While DNMT3A is frequently mutated in hematologic malignancies, DNMT3B is rarely mutated. To investigate the role of Dnmt3b in AML, we genetically inactivated Dnmt3b in an MLL-AF9 induced AML mouse model. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL20775
6 Samples
Download data: CEL
Series
Accession:
GSE75401
ID:
200075401
10.

MLL-AF9 Expression in Hematopoietic Stem Cells Drives a Highly Invasive AML Expressing EMT-Related Genes Linked to Poor Outcome

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing; Expression profiling by array
Platforms:
GPL13112 GPL6246
41 Samples
Download data: CEL
Series
Accession:
GSE65384
ID:
200065384
11.

MLL-AF9 Expression in Hematopoietic Stem Cells Drives a Highly Invasive AML Expressing EMT-Related Genes Linked to Poor Outcome [RNA-Seq]

(Submitter supplied) To address the impact of cellular origin on AML, we generated an inducible transgenic mouse model for MLL-AF9 driven leukemia. MLL-AF9 expression in long-term hematopoietic stem cells (LT-HSCs) in vitro resulted in unprecedented clonogenic growth and expression of genes involved in migration and invasion. In vivo, some LT-HSC-derived AMLs were particularly aggressive with extensive tissue infiltration, chemo-resistance and expression of genes related to epithelial-mesenchymal transition (EMT) in solid cancers. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL13112
15 Samples
Download data: TXT
Series
Accession:
GSE65383
ID:
200065383
12.

MLL-AF9 Expression in Hematopoietic Stem Cells Drives a Highly Invasive AML Expressing EMT-Related Genes Linked to Poor Outcome [Microarray]

(Submitter supplied) To address the impact of cellular origin on AML, we generated an inducible transgenic mouse model for MLL-AF9 driven leukemia. MLL-AF9 expression in long-term hematopoietic stem cells (LT-HSCs) in vitro resulted in unprecedented clonogenic growth and expression of genes involved in migration and invasion. In vivo, some LT-HSC-derived AMLs were particularly aggressive with extensive tissue infiltration, chemo-resistance and expression of genes related to epithelial-mesenchymal transition (EMT) in solid cancers. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6246
26 Samples
Download data: CEL
Series
Accession:
GSE65382
ID:
200065382
13.

Zinc finger protein 521 overexpression is a feature of MLL-rearranged acute myeloid leukemia and contributes to the maintenance of myeloid differentiation block

(Submitter supplied) ZNF521 is a multiple zinc finger transcription factor previously identified because abundantly and selectively expressed in normal CD34+ hematopoietic stem and progenitor cells. From microarray datasets, aberrant expression of ZNF521 has been reported in both pediatric and adult acute myeloid leukemia (AML) patients with MLL gene rearrangements. However, a proper validation of microarray data is lacking, likewise ZNF521 contribution in MLL-rearranged AML is still uncertain. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
6 Samples
Download data: CEL
Series
Accession:
GSE79110
ID:
200079110
14.

miR-196b targets both oncogenic and tumor suppressor genes in MLL-associated leukemia

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus; Homo sapiens
Type:
Expression profiling by array
Platforms:
GPL6246 GPL5175
48 Samples
Download data: CEL
Series
Accession:
GSE34186
ID:
200034186
15.

Affymetrix gene arrays of leukemic BM samples from 24 mice including 9 primary

(Submitter supplied) To identify such targets of leukemia-related miRNAs such as miR-196b, we conducted Affymetrix gene arrays of leukemic BM samples from 24 mice including 9 primary (including 3 each of negative control, MLL-AF9, and miR-196b+MLL-AF9) and 15 secondary (including 3 negative control, 6 MLL-AF9, and 6 miR-196b+MLL-AF9) recipient mice
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6246
24 Samples
Download data: CEL
Series
Accession:
GSE34185
ID:
200034185
16.

Identification of miR-181 target genes and a common prognostic gene signature in AML

(Submitter supplied) Increased expression levels of miR-181 family members have been shown to be associated with favorable outcome in patients with cytogenetically normal acute myeloid leukemia. Here we show that increased expression of miR-181a and miR-181b is also significantly (P < .05; Cox regression) associated with favorable overall survival in cytogenetically abnormal AML (CA-AML) patients. We further show that up-regulation of a gene signature composed of 4 potential miR-181 targets (including HOXA7, HOXA9, HOXA11, and PBX3), associated with down-regulation of miR-181 family members, is an independent predictor of adverse overall survival on multivariable testing in analysis of 183 CA-AML patients. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL13781
65 Samples
Download data: TXT
Series
Accession:
GSE30258
ID:
200030258
17.

Transcriptome analysis of Cdc73 deletion in AML cells

(Submitter supplied) The Polymerase Associated Factor (PAFc) complex is an epigenetic regulating complex that has been shown to to be important for Acute Myeloid Leukemias harboring an MLL chromosomal translocations, such as MLL-AF9 leukemias. This study describes the transcriptomic profiling of AML cells following genetic deletion of the PAFc subunit Cdc73.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL13112
8 Samples
Download data: TXT
Series
Accession:
GSE90136
ID:
200090136
18.

The Polycomb Repressive Complex 2 Is Required For MLL-AF9 Leukemia

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Expression profiling by array; Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL13112 GPL1261
23 Samples
Download data: CEL, WIG
Series
Accession:
GSE34963
ID:
200034963
19.

Epigenetic profiling of WT and Ezh2-null MLL-AF9 murine leukemic cells

(Submitter supplied) Chromatin immunoprecipitation (ChIP) for H3K27me3 followed by Solexa sequencing in WT and Ezh2-null leukemic cells from primary and secondary recipients.
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL13112
4 Samples
Download data: WIG
Series
Accession:
GSE34962
ID:
200034962
20.

Expression profiling of secondary wild type (WT) and Ezh2-null murine MLL-AF9 AML

(Submitter supplied) We evaluated gene expression changes in secondary recipient murine leukemia caused by retroviral overexpression of MLL-AF9. We compared wild-type (WT) leukemia cells with mutant leukemia cells after cre-mediated inactivation of a homozygous conditional allele for Ezh2, a component of the Polycomb Repressive Complex2.
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL1261
9 Samples
Download data: CEL, TXT
Series
Accession:
GSE34961
ID:
200034961
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