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Links from GEO DataSets

Items: 20

1.

MLL-AF6 leukemia

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens; Mus musculus
Type:
Expression profiling by array; Genome binding/occupancy profiling by high throughput sequencing
4 related Platforms
10 Samples
Download data: CEL, WIG
Series
Accession:
GSE43069
ID:
200043069
2.

Expression data from a human MLL-AF6 positive AML cell line

(Submitter supplied) The MLL gene on chromosome 11 fuses to the AF6 gene on chromosome 6 in a balanced chromosomal translocation that is characetristic of certain adult and pediatric human leukemias. We established a murine leukemia model of MLL-AF6 using the retroviral MLL-AF6 contruct in a bone marrow transplantation system. The ML2 human MLL-AF6 positive leukemia cell line was used for gene expression profiling to assess the transctiptional profile in MLL-AF6 leukemias.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
1 Sample
Download data: CEL
Series
Accession:
GSE43068
ID:
200043068
3.

Expression data from MLL-AF6 positive leukemia cells

(Submitter supplied) The MLL gene on chromosome 11 fuses to the AF6 gene on chromosome 6 in a balanced chromosomal translocation that is characetristic of certain adult and pediatric human leukemias. We established a murine leukemia model of MLL-AF6 using the retroviral MLL-AF6 contruct in a bone marrow transplantation system.
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL1261
3 Samples
Download data: CEL
Series
Accession:
GSE43067
ID:
200043067
4.

Genome wide mapping of histone 3 lysine 79 dimethylation in MLL rearranged and control human leukemia cell lines

(Submitter supplied) We report the genome wide distribution of H3K79 dimethylation in the human MLL-AF6 rearranged cell line ML2 as well as the human MOLM13 and HL60 cell lines
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL11154
3 Samples
Download data: WIG
Series
Accession:
GSE43063
ID:
200043063
5.

Genome wide mapping of histone 3 lysine 79 dimethylation in MLL-AF6 murine leukemias

(Submitter supplied) We report the genome wide distribution of H3K79 dimethylation in mouse MLL-AF6 positive leukemias to assess whether this epigenetic mark drives MLL-target gene expression.
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL13112
3 Samples
Download data: WIG
Series
Accession:
GSE43062
ID:
200043062
6.

Gene expression induced by DOT1L and Menin inhibition in cell line models of leukemia

(Submitter supplied) Gene expression upon DOT1L inhibition, or Menin inhibition, or a combination of DOT1L and Menin inhibiting agents, was assessed in several MLL-rearranged human cell lines and a mouse model of MLL-AF9 leukemia. The goal of the study was to explore the mechanisms by which the EPZ0004777 and MI-2-2 chemicals collaborate to induce differentiation and cell death in MLL-AF4 and MLL-AF9 leukemias.
Organism:
Homo sapiens; Mus musculus
Type:
Expression profiling by array
Platforms:
GPL1261 GPL570
56 Samples
Download data: CEL
Series
Accession:
GSE63664
ID:
200063664
7.

DOT1L Inhibits SIRT1 and SUV39H1-Mediated H3K9 Modification to Maintain Gene Expression

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens; Mus musculus
Type:
Expression profiling by array; Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL14761 GPL13112 GPL1261
44 Samples
Download data: BW, CEL, TDF
Series
Accession:
GSE61022
ID:
200061022
8.

H3K79 methylation profiles define murine and human MLL-AF4 leukemias

(Submitter supplied) We created a mouse model where conditional expression of physiologic levels of an Mll-AF4 fusion oncogene induces development of acute lymphoblastic (ALL) or acute myeloid leukemias (AML). Immunophenotypic and gene expression analysis of the ALL cells demonstrated bone marrow replacement with B-precursor cells which express a gene expression profile that has significant overlap with profiles in human MLL-rearranged ALL. more...
Organism:
Mus musculus; Homo sapiens
Type:
Expression profiling by array; Genome binding/occupancy profiling by genome tiling array
Platforms:
GPL5082 GPL8321 GPL5811
49 Samples
Download data: BAR, BED, CEL
Series
Accession:
GSE12363
ID:
200012363
9.

Genome-wide analysis of H3K79 dimethylation in MLL-AF4 leukemic bone marrow

(Submitter supplied) We created a mouse model where conditional expression of physiologic levels of an Mll-AF4 fusion oncogene induces development of acute lymphoblastic (ALL) or acute myeloid leukemias (AML). ChIP-chip analysis demonstrated increased histone H3 Lysine 79 (H3K79) dimethylation that correlated with Mll-AF4 associated gene expression profiles in murine ALLs, and in human MLL-rearranged leukemias. In addition, human MLL-rearranged ALLs can be distinguished from other ALLs by their genome-wide H3K79 methylation profiles. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by genome tiling array
Platform:
GPL5811
1 Sample
Download data: BAR, BED, BPMAP, CEL
Series
Accession:
GSE12362
ID:
200012362
10.

Genome-wide analysis of H3K79 dimethylation in normal and MLL-AF4 leukemic pre-B cells

(Submitter supplied) We created a mouse model where conditional expression of physiologic levels of an Mll-AF4 fusion oncogene induces development of acute lymphoblastic (ALL) or acute myeloid leukemias (AML). ChIP-chip analysis demonstrated increased histone H3 Lysine 79 (H3K79) dimethylation that correlated with Mll-AF4 associated gene expression profiles in murine ALLs, and in human MLL-rearranged leukemias. In addition, human MLL-rearranged ALLs can be distinguished from other ALLs by their genome-wide H3K79 methylation profiles. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by genome tiling array
Platform:
GPL5811
2 Samples
Download data: BAR, BED, BPMAP, CEL
Series
Accession:
GSE12361
ID:
200012361
11.

Genome-wide analysis of H3K79 methylation in CD34+ CD19+ cells from normal marrow, MLL-rearranged or MLL-germline ALL

(Submitter supplied) We created a mouse model where conditional expression of physiologic levels of an Mll-AF4 fusion oncogene induces development of acute lymphoblastic (ALL) or acute myeloid leukemias (AML). ChIP-chip analysis demonstrated increased histone H3 Lysine 79 (H3K79) dimethylation that correlated with Mll-AF4 associated gene expression profiles in murine ALLs, and in human MLL-rearranged leukemias. In addition, human MLL-rearranged ALLs can be distinguished from other ALLs by their genome-wide H3K79 methylation profiles. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by genome tiling array
Platform:
GPL5082
3 Samples
Download data: BAR, BED, BPMAP, CEL
Series
Accession:
GSE12360
ID:
200012360
12.

Expression profiling of activated or control 5-FU bone marrow from MLL-AF4stop knockin mice

(Submitter supplied) We created a mouse model where conditional expression of physiologic levels of an Mll-AF4 fusion oncogene induces development of acute lymphoblastic (ALL) or acute myeloid leukemias (AML). Immunophenotypic and gene expression analysis of the ALL cells demonstrated bone marrow replacement with B-precursor cells which express a gene expression profile that has significant overlap with profiles in human MLL-rearranged ALL. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL8321
4 Samples
Download data: CEL
Series
Accession:
GSE12313
ID:
200012313
13.

Expression profiling of normal murine lymphoid progenitors and MLL-AF4 leukemic lymphoblasts

(Submitter supplied) We created a mouse model where conditional expression of physiologic levels of an Mll-AF4 fusion oncogene induces development of acute lymphoblastic (ALL) or acute myeloid leukemias (AML). Immunophenotypic and gene expression analysis of the ALL cells demonstrated bone marrow replacement with B-precursor cells which express a gene expression profile that has significant overlap with profiles in human MLL-rearranged ALL. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL8321
39 Samples
Download data: CEL
Series
Accession:
GSE12310
ID:
200012310
14.

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
15.

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
16.
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
17.

Expression Profiling of Mixed Lineage Leukemia Cells Treated with a Potent Small-Molecule DOT1L Inhibitor

(Submitter supplied) Cell lines bearing MLL translocations (MV4-11 and MOLM-13) were treated with a potent, selective inhibitor of the DOT1L histone methyl transferase. Treatment of MLL-rearranged cell lines with the DOT1L inhibitor selectively inhibits H3K79 methylation and blocks expression of leukemogenic genes. Here we provide expression profiling data of cells treated with DOT1L inhibitor or vehicle control.
Organism:
Homo sapiens
Type:
Expression profiling by array
Dataset:
GDS4290
Platform:
GPL570
24 Samples
Download data: CEL
Series
Accession:
GSE29828
ID:
200029828
18.
Full record GDS4290

Small-molecule DOT1L inhibitor EPZ004777 effect on mixed lineage leukemia cells: time course

Temporal analysis of mixed lineage leukemia (MLL)-rearranged cell lines MV4-11 and MOLM-13 treated with EPZ004777, a potent inhibitor of DOT1L histone methyl transferase. EPZ004777 induces differentiation and apoptosis in MLL-rearranged cells. Results provide insight into role of DOT1L in MLL cells.
Organism:
Homo sapiens
Type:
Expression profiling by array, count, 2 agent, 2 cell line, 3 time sets
Platform:
GPL570
Series:
GSE29828
24 Samples
Download data: CEL
19.

Functional diversity of inhibitors tackling the differentiation arrest of MLL-rearranged leukemia

(Submitter supplied) Purpose: The chromosomal rearrangements of the mixed-lineage leukemia (MLL) gene have been extensively characterized as a potent oncogenic driver on the molecular and mechanistic level in acute lymphoblastic (ALL) and acute myeloid (AML) leukemia. For its oncogenic function the MLL fusion protein is hijacking the the multi enzyme super elongation complex (SEC) leading to elevated expression of MLL target genes (e.g. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL16791
305 Samples
Download data: TSV
20.

The histone H2B ubiquitin ligase RNF20 is required for MLL-rearranged leukemia

(Submitter supplied) MLL-fusions are potent oncogenes that initiate aggressive forms of acute leukemia. As aberrant transcriptional regulators, MLL-fusion proteins alter gene expression in hematopoietic cells through interactions with the histone H3 lysine 79 (H3K79) methyltransferase DOT1L. Notably, interference with MLL-fusion cofactors like DOT1L is an emerging therapeutic strategy in this disease. Here we identify the histone H2B E3 ubiquitin ligase RNF20 as an additional requirement for MLL-fusion-mediated leukemogenesis. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL13112
3 Samples
Download data: TXT
Series
Accession:
GSE43725
ID:
200043725
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