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Links from GEO DataSets

Items: 20

1.

HOXA9 Reprograms the Enhancer Landscape During Leukemic 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; Other
Platform:
GPL13112
28 Samples
Download data: BW
Series
Accession:
GSE103508
ID:
200103508
2.

Chromatin state changes in HOXA9/MEIS1 leukemia cells [4C-Seq]

(Submitter supplied) Aberrant expression of homeobox transcription factor HOXA9 is a central component of the leukemogenic program driven by diverse oncogenes. Here we show that HOXA9 overexpression in myeloid progenitor cells and pro-B cells leads to significant rearrangement of the epigenetic landscape with prominent emergence of cancer specific de novo enhancers. HOXA9 acts as a pioneer factor at the de novo enhancers and is required for recruitment of transcription factor CEBP/a and the histone H3K4 methyltransferase MLL3/MLL4 complex. more...
Organism:
Mus musculus
Type:
Other
Platform:
GPL13112
3 Samples
Download data: BW
Series
Accession:
GSE103448
ID:
200103448
3.

RNA expression changes in HOXA9/MEIS1 leukemia cells

(Submitter supplied) Aberrant expression of homeobox transcription factor HOXA9 is a central component of the leukemogenic program driven by diverse oncogenes. Here we show that HOXA9 overexpression in myeloid progenitor cells and pro-B cells leads to significant rearrangement of the epigenetic landscape with prominent emergence of cancer specific de novo enhancers. HOXA9 acts as a pioneer factor at the de novo enhancers and is required for recruitment of transcription factor CEBP/a and the histone H3K4 methyltransferase MLL3/MLL4 complex. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL13112
2 Samples
Download data: TXT
Series
Accession:
GSE103447
ID:
200103447
4.

Chromatin state changes in HOXA9/MEIS1 leukemia cells [ChIP-Seq]

(Submitter supplied) Aberrant expression of homeobox transcription factor HOXA9 is a central component of the leukemogenic program driven by diverse oncogenes. Here we show that HOXA9 overexpression in myeloid progenitor cells and pro-B cells leads to significant rearrangement of the epigenetic landscape with prominent emergence of cancer-specific de novo enhancers. HOXA9 acts as a pioneer factor at the de novo enhancers and is required for recruitment of transcription factor CEBP/ and the histone H3K4 methyltransferase MLL3/MLL4 complex. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL13112
23 Samples
Download data: BW
Series
Accession:
GSE103446
ID:
200103446
5.

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
6.

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:
Homo sapiens; Mus musculus
Type:
Expression profiling by array
Platforms:
GPL5175 GPL6246
48 Samples
Download data: CEL
Series
Accession:
GSE34186
ID:
200034186
7.

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
8.

Affymetrix Human Exon 1.0 ST array assay of 15 human MLL-associated samples and 9 human normal bone marrow [HuEx-1_0-st]

(Submitter supplied) To identify potential target genes of leukemia-related miRNAs such as miR-196b and miR-150 in human MLL-associated leukemia, we performed Affymetrix Human Exon 1.0 ST array assay of 15 human MLL-associated samples and 9 human normal bone marrow (including 3 each of CD34+, CD33+, and MNC) cell samples.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL5175
24 Samples
Download data: CEL
Series
Accession:
GSE34184
ID:
200034184
9.

Trib1 promotes acute myeloid leukemia progression by modulating transcriptional programs of Hoxa9

(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:
GPL11180 GPL16417
15 Samples
Download data: CEL, TDF
Series
Accession:
GSE140315
ID:
200140315
10.

Trib1 promotes acute myeloid leukemia progression by modulating transcriptional programs of Hoxa9 [ChIP-seq]

(Submitter supplied) The pseudokinase Trib1 functions as a myeloid oncogene that recruits E3 ubiquitin ligase COP1 to C/EBP, and interacts with MEK1 to enhance ERK phosphorylation. Close genetic interaction between Trib1 and Hoxa9 has been observed in myeloid leukemogenesis as Trib1 overexpression significantly accelerates Hoxa9-induced leukemia onset. Yet the mechanism how Trib1 functionally modulates Hoxa9 transcription activity is unclear. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL16417
7 Samples
Download data: TDF
Series
Accession:
GSE140313
ID:
200140313
11.

Trib1 promotes acute myeloid leukemia progression by modulating transcriptional programs of Hoxa9 [array]

(Submitter supplied) The pseudokinase Trib1 functions as a myeloid oncogene that recruits E3 ubiquitin ligase COP1 to C/EBPa, and interacts with MEK1 to enhance ERK phosphorylation. Close genetic interaction between Trib1 and Hoxa9 has been observed in myeloid leukemogenesis as Trib1 overexpression significantly accelerates Hoxa9-induced leukemia onset. Yet the mechanism how Trib1 functionally modulates Hoxa9 transcription activity is unclear. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL11180
8 Samples
Download data: CEL
Series
Accession:
GSE139641
ID:
200139641
12.

Regulation of gene expression through genome-wide co-binding of Hoxa9 and C/EBPα in transformed HSCs

(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
9 Samples
Download data: TXT
Series
Accession:
GSE58362
ID:
200058362
13.

Genome-wide co-occupancy of Hoxa9 and C/EBPα in Hoxa9/Meis1 transformed HSCs [ChIP-seq]

(Submitter supplied) Identification of the genome-wide binding sites of Hoxa9 and C/EBPα in a murine myeloblastic cell line transformed by Hoxa9/Meis1. Over 50% of Hoxa9 binding sites are co-bound by C/EBPα, providing mechanistic insight into the requirement of C/EBPα for Hoxa9-mediated leukemogenesis. Additionally, genome-wide occupancy of H3K4 monomethylation and H3K27 trimethylation provide additional information on the functionality of Hoxa9/C/EBPα cobound loci.
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL13112
5 Samples
Download data: TXT
Series
Accession:
GSE58361
ID:
200058361
14.

Gene expression changes after loss of C/EBPα in transformed HSCs [CEBPA RNA-seq]

(Submitter supplied) RNAseq characterization of gene expression changes 72 hours after genomic excision of Cebpa in murine hematopoietic progenitors from Cebpaf/f;CreER mice transformed by Hoxa9/Meis1. In the presence of tamoxifen (4OHT), Cre-ER localizes to the nucleus of cells allowing for excision of Cebpa and loss of C/EBPα protein levels. Loss of C/EBPα leads to a decrease in cellular proliferation.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL13112
2 Samples
Download data: TXT
Series
Accession:
GSE58360
ID:
200058360
15.

Gene expression changes after loss of Hoxa9 in transformed HSCs [HOXA9 RNA-seq]

(Submitter supplied) Characterization of gene expression changes 72 hours after withdrawal of tamoxifen in murine hematopoietic progenitors transformed by Hoxa9-ER/Meis1 using RNAseq. In the presence of tamoxifen (4OHT), Hoxa9-ER localizes to the nucleus of cells allowing for transformation, while withdrawal of 4OHT (culture in EtOH) leads to loss of nuclear Hoxa9-ER. Loss of Hoxa9-ER leads to a decrease in cellular proliferation and differentiation along the myeloid lineage.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL13112
2 Samples
Download data: TXT
Series
Accession:
GSE58359
ID:
200058359
16.

The role of Hoxa9 and Meis1 in development of acute myeloid leukemia (mRNA)

(Submitter supplied) OBJECTIVE: MEIS1, a HOX cofactor, collaborates with multiple HOX proteins, such as HOXA9, to accelerate the onset of acute myeloid leukemia (AML) through largely unknown molecular mechanisms. To further resolve these mechanisms, we conducted a structure-function analysis of Meis1 and gene expression profiling, in the context of Hoxa9 leukemogenesis. RESULTS: We show, in a murine bone marrow transplantation model, that the homeodomain of Meis1 is required for leukemogenic collaboration with Hoxa9. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6193
12 Samples
Download data: CEL, CHP
Series
Accession:
GSE75272
ID:
200075272
17.

Function of MLL4 in mouse embryonic stem cells and somatic cell reprogramming

(Submitter supplied) Enhancers control cell type-specific gene expression and direct cell fate transition. Enhancers are marked by H3K4me1/2. MLL4 (KMT2D) is a major enhancer H3K4me1/2 methyltransferase. Here we show in embryonic stem cells (ESCs), MLL4 associates with, but is dispensable for the maintenance of, active enhancers of ESC identity genes. As a result, MLL4 is dispensable for cell identity gene expression and self-renewal in ESCs. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL17021 GPL13112
36 Samples
Download data: TXT, WIG
Series
Accession:
GSE50534
ID:
200050534
18.

MLL is essential for NUP98-HOXA9-induced leukemia

(Submitter supplied) Rearrangements involving the NUP98 gene resulting in fusions to several partner genes occur in acute myeloid leukemia and myelodysplastic syndromes. This study demonstrates that the second FG repeat domain of the NUP98 moiety of the NUP98-HOXA9 fusion protein is important for its cell immortalization and leukemogenesis activities. We demonstrate that NUP98-HOXA9 interacts with MLL via this FG repeat domain and that, in the absence of MLL, NUP98-HOXA9-induced cell immortalization and leukemogenesis are severely inhibited. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6246
8 Samples
Download data: CEL
Series
Accession:
GSE93923
ID:
200093923
19.

MicroRNA-155 is a direct target of Meis1, but not a driver in acute myeloid leukemia

(Submitter supplied) OBJECTIVE: The microRNA miR-155 is upregulated by Hoxa9 and Meis1, and accelerate the onset of acute myeloid leukemia (AML) together with Hoxa9 but through largely unknown molecular mechanisms. To further resolve these mechanisms, we performed a gene expression profiling, in the context of Hoxa9 leukemogenesis with our without overexpression of miR-155. RESULTS: Gene expression profiling of a Hoxa9 preleukemic cell line transduced with miR-155 leads to differential expression of multiple genes, including a set not previously implicated as miR-155 targets.
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6096
12 Samples
Download data: CEL, CHP
Series
Accession:
GSE76113
ID:
200076113
20.

Effect of RBM5 knockout or overexpression on transcription in MOLM13 AML cells

(Submitter supplied) Background: The oncogenic protein HOXA9 plays a critical role in leukemia transformation and maintenance, and its aberrant expression is a hallmark of most aggressive acute leukemia. Although inhibiting the upstream regulators of HOXA9 has been proven as a significant therapeutic intervention, the comprehensive regulation network controlling HOXA9 expression in leukemia has not been systematically investigated. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24676
9 Samples
Download data: TSV
Series
Accession:
GSE225633
ID:
200225633
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