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Links from GEO DataSets

Items: 18

1.

Trancriptome profiling of human THP-1 knockdown for HOXA9 vs treated with DB1055

(Submitter supplied) Effect of HOXA9 shRNA versus DB1055 treatment of human THP-1 AML cell line
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL16699
20 Samples
Download data: TXT
Series
Accession:
GSE106831
ID:
200106831
2.

Trancriptome profiling of murine Hoxa9-transformed MigA9 cell line treated or not with DB818

(Submitter supplied) Effect of DB818 treatment on murine Hoxa9-transformed MigA9 cell line Effect of DB818 treatment on murine Hoxa9-transformed MigA9 cell line
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL2872
3 Samples
Download data: TXT
Series
Accession:
GSE111109
ID:
200111109
3.

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
4.

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
5.

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
6.

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
7.

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
8.

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
9.

HOXA9 cooperates with activated JAK/STAT signaling to drive leukemia development

(Submitter supplied) Leukemia is caused by the accumulation of multiple genomic lesions in hematopoietic precursor cells. However, how these events cooperate during oncogenic transformation remains poorly understood. We studied the cooperation between activated JAK3/STAT5 signaling and HOXA9 overexpression, two events identified as significantly co-occuring in T-cell acute lymphoblastic leukemia. Expression of mutant JAK3 and HOXA9 led to a rapid development of leukemia originating from multipotent or lymphoid-committed progenitors, with a significant decrease in disease latency compared to JAK3 or HOXA9 alone. more...
Organism:
Homo sapiens; Mus musculus
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL16791 GPL17021
32 Samples
Download data: BEDGRAPH, NARROWPEAK, TXT
Series
Accession:
GSE109653
ID:
200109653
10.

RNA sequencing analysis of adult mixed phenotype acute leukemia (MPAL)

(Submitter supplied) RNA sequencing analysis was performed from bone marrow samples of 24 adult mixed phenotype acute leukemia (MPAL) patients
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11154
24 Samples
Download data: TXT
11.

Cytosine methylation analysis of adult mixed phenotype acute leukemia (MPAL)

(Submitter supplied) Cytosine methylation analysis of genomic DNA from 31 MPAL patients bone marrow samples was performed using Illumina’s Infinium MethylationEPIC Kit (EPIC) that covers approximately 850,000 CpG probes (Illumina, San Diego, CA).
Organism:
Homo sapiens
Type:
Methylation profiling by genome tiling array
Platform:
GPL21145
31 Samples
Download data: IDAT
Series
Accession:
GSE113545
ID:
200113545
12.

Cohesin in AML

(Submitter supplied) Depletion of Rad21 in murine bone marrow leads to enhanced self-renewal in vitro
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL8321
6 Samples
Download data: CEL
Series
Accession:
GSE76320
ID:
200076320
13.

The Histone Methyltransferases MLL1 and DOT1L Cooperate with Meningioma-1 to Induce AML

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens; Mus musculus
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL13112 GPL11154
27 Samples
Download data: BW, TXT
Series
Accession:
GSE76750
ID:
200076750
14.

The Histone Methyltransferases MLL1 and DOT1L Cooperate with Meningioma-1 to Induce AML [Mouse Mll1 ko RNA-seq]

(Submitter supplied) Purpose: To characterize transcriptional changes associated with homozygous inactivation of Dot1l or Mll1 in MN1 driven AML Methods: We sequenced mRNA from murine LSK-cells transformed using forced expression of MN1 (MSCV-MN1-IRES-GFP), and transduced with Cre-vector to inactivate either Dot1l or Mll1. Cells were sorted for Cre-expression (pTomato fluorescent marker) or expression of an inert control vector. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL13112
5 Samples
Download data: TXT
Series
Accession:
GSE76749
ID:
200076749
15.

The Histone Methyltransferases MLL1 and DOT1L Cooperate with Meningioma-1 to Induce AML [Mouse Dot1l ko RNA-seq]

(Submitter supplied) Purpose: To characterize transcriptional changes associated with homozygous inactivation of Dot1l or Mll1 in MN1 driven AML Methods: We sequenced mRNA from murine LSK-cells transformed using forced expression of MN1 (MSCV-MN1-IRES-GFP), and transduced with Cre-vector to inactivate either Dot1l or Mll1. Cells were sorted for Cre-expression (pTomato fluorescent marker) or expression of an inert control vector. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL13112
6 Samples
Download data: TXT
Series
Accession:
GSE76748
ID:
200076748
16.

The Histone Methyltransferases MLL1 and DOT1L Cooperate with Meningioma-1 to Induce AML [Human RNA-seq]

(Submitter supplied) Purpose: To characterize transcriptional changes associated with inhibition of Dot1l in 2 inv(16) patient AML samples Methods: We sequenced mRNA from patient samples that were exposed to 5 uM EPZ004777 or DMSO control for 7 days. Results: Inhibition of Dot1l leads to gene expression changes in genes related to cell growth and cell cycle.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11154
4 Samples
Download data: TXT
17.

The Histone Methyltransferases MLL1 and DOT1L Cooperate with Meningioma-1 to Induce AML [Mouse ChIP-seq]

(Submitter supplied) Purpose: To characterize the genome-wide distribution of H3K79me2 in murine MN1 driven myeloid leukemia Methods: We performed Chip-seq for the H3K79me2 in leukemias isolated from moribund mice that had been injected with common myeloid progenitors (CMPs) transduced with MSCV-MN1-GFP Results: H3K79me2 is enriched at key loci that 1. are bound by MN1 in the data set of Heuser et al, (Cancer Cell. 2011 Jul 12;20(1):39-52.), 2. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL13112
6 Samples
Download data: BW, XLSX
Series
Accession:
GSE76746
ID:
200076746
18.

The Histone Methyltransferases MLL1 and DOT1L Cooperate with Meningioma-1 to Induce AML [Human ChIP-seq]

(Submitter supplied) Purpose: To characterize the genome-wide distribution of H3K79me2 in human leukemia cell lines treated with the Dot1l inhibitor EPZ004777 or control Methods: We performed Chip-seq for the H3K79me2 on the leukemia cell lines Mutz3, Loucy and Molm14 after 6 days in culture in the presence of 3uM EPZ004777 or DMSO control Results: H3K79me2 is completely erased from key target genes such as the HOXA cluster. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL11154
6 Samples
Download data: BW
Series
Accession:
GSE76745
ID:
200076745
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