Similar studies for GEO DataSets (Select 4169) - GEO DataSets

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Items: 20

Select item 41691.

Mixed lineage leukemia fusion protein induction of acute leukemia: bone marrow cells

Analysis of bone marrow of C57BL6 mice injected with AAF4.MLL-transduced or AF4.MLL/MLL.AF4-transduced leukemic cells. MLL fusion proteins initiate malignant transformation leading to the development of acute leukemia. Results provide insight into the leukemogenic properties of MLL fusion proteins.

Organism:: Mus musculus

Type:: Expression profiling by array, count, 2 disease state, 3 genotype/variation, 4 other sets

Platform:: GPL1261
Series:: GSE20519
4 Samples

Download data: CEL, CHP

DataSet

Accession:: GDS4169

ID:: 4169

Select item 2000205192.

Gene expression analysis of leukemic samples in C57BL6 mice

(Submitter supplied) [original title] Gene expression analysis of leukemic samples derived from AF4-MLL- or AF4-MLL/MLL-AF4-transduced and transplanted hematopoietic stem/precursor cells in C57BL6 mice. We used microarrays to analyze the global gene expression in leukemic cells with three distinct immunophenotypes.

Organism:: Mus musculus

Type:: Expression profiling by array

Dataset:: GDS4169
Platform:: GPL1261
4 Samples

Download data: CEL, CHP

Series

Accession:: GSE20519

ID:: 200020519

Select item 2000841163.

Instructive role of MLL fusion proteins revealed by a faithful model of t(4;11) proB acute lymphoblastic leukemia

(Submitter supplied) The t(4;11)(q21;q23) fuses MLL to AF4, the most common MLL fusion partner. Here we show that MLL fused to murine Af4, highly conserved with human AF4, produces high-titer retrovirus permitting efficient transduction of human CD34+ cells to generate a faithful model of t(4;11) proB ALL that fully recapitulates the immunophenotypic and molecular aspects of the disease. MLL-Af4 induces a distinct B-ALL from MLL-AF9 through differential DNA binding of the fusion proteins leading to specific gene expression patterns. more...

Organism:: Homo sapiens

Type:: Genome binding/occupancy profiling by high throughput sequencing

Platform:: GPL16791
1 Sample

Download data: BEDGRAPH

Series

Accession:: GSE84116

ID:: 200084116

PubMed Similar studies SRA Run Selector

Select item 2000769784.

A faithful in vivo model of human MLL-AF4 proB acute lymphoblastic leukemia

(Submitter supplied) Transcriptome analysis by RNAseq of leukemia model promoted by MLL-Af4 or MLL-AF9 fusion proteins. We find each fusion protein promotes a specific gene signature correlating to those identified in patients

Organism:: Homo sapiens

Type:: Expression profiling by high throughput sequencing

Platform:: GPL15433
20 Samples

Download data: TXT

Series

Accession:: GSE76978

ID:: 200076978

Select item 2000895605.

Inhibition of MEK and ATR induces synergistic killing of a Mll-Af4 B-ALL model harboring activated Ras mutation

(Submitter supplied) Infant B-acute lymphoblastic leukemias (B-ALL) that harbor MLL-AF4 rearrangements are associated with a poor prognosis. One important obstacle to progress for this patient population is the lack of models that faithfully recapitulate the short latency and aggressiveness of this disease. While current mouse models of Mll-Af4 can generate acute leukemia, not all are lymphoid, and the long latency to disease does not reflect what is seen in patients. more...

Organism:: Mus musculus

Type:: Expression profiling by high throughput sequencing

Platform:: GPL13112
6 Samples

Download data: TXT

Series

Accession:: GSE89560

ID:: 200089560

PubMed Full text in PMC Similar studies SRA Run Selector

Select item 2001684386.

ATAC-Seq of foetal blood progenitors

(Submitter supplied) Chromatin accessibility was assessed by ATAC-Seq in lymphoid-primed multipotent progenitors (LMPPs) from human foetal livers (FLs) and mouse wild-type FLs as well as FLs from mouse embryos that express the oncofusion Mll-AF4 in the definitive blood system. The aim of this study was to establish whether overall chromatin accessibility at key haematopoietic sites and loci that have been linked to leukaemia are differentially accessible in human vs mouse LMPPs and whether this is altered by the expression of the Mll-AF4 oncofusion.

Organism:: Homo sapiens; Mus musculus

Type:: Genome binding/occupancy profiling by high throughput sequencing

Platforms:: GPL21273 GPL20795
10 Samples

Download data: BW

Series

Accession:: GSE168438

ID:: 200168438

PubMed Similar studies SRA Run Selector

Select item 2001620417.

A novel human fetal model of infant ALL reveals a link between MLL-AF4, PAF1 and increased H3K79me2/3

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.

Organism:: Homo sapiens

Type:: Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing

Platform:: GPL18573
24 Samples

Download data: BIGWIG

Series

Accession:: GSE162041

ID:: 200162041

PubMed Full text in PMC Similar studies

Select item 2001620348.

A novel human fetal liver-derived model reveals that MLL-AF4 drives fetal gene expression programs in infant ALL [ChIP-seq]

(Submitter supplied) Although 90% of children with acute lymphoblastic leukemia (ALL) are now cured, the prognosis of infant-ALL (diagnosis within the first year of life) remains dismal. Infant-ALL is usually caused by a single genetic hit that arises in utero: rearrangement of the MLL/KMT2A gene (MLL-r). This is sufficient to give rise to a uniquely aggressive and treatment-refractory leukemia compared to older children with the same MLL-r. more...

Organism:: Homo sapiens

Type:: Genome binding/occupancy profiling by high throughput sequencing

Platform:: GPL18573
7 Samples

Download data: BED, BIGWIG

Series

Accession:: GSE162034

ID:: 200162034

PubMed Full text in PMC Similar studies SRA Run Selector

Select item 2001620329.

A novel human fetal model of infant ALL reveals a link between MLL-AF4, PAF1 and increased H3K79me2/3 [RNA-seq]

(Submitter supplied) Acute Lymphoblastic Leukemia (ALL) caused by chromosomal translocation involving the Mixed Lineage Leukemia (MLL) gene remains a poor prognosis disease, especially in infants. The most common MLL-rearrangement in infant ALL (iALL), MLL-AF4, originates in utero where the properties of fetal target cells likely provide a permissive landscape for transformation. We describe the first faithful MLL-AF4 iALL model derived by CRISPR-Cas9 genome editing of primary human fetal liver (FL) cells. more...

Organism:: Homo sapiens

Type:: Expression profiling by high throughput sequencing

Platform:: GPL18573
17 Samples

Download data: TXT

Series

Accession:: GSE162032

ID:: 200162032

PubMed Full text in PMC Similar studies Analyze with GEO2R SRA Run Selector

Select item 20008598810.

MLL-AF4 binds directly to a BCL-2 specific enhancer and impacts H3K27 acetylation

(Submitter supplied) Survival rates for children diagnosed with acute lymphoblastic leukemia (ALL) have drastically improved, but those carrying mutations in the Mixed Lineage Leukemia (MLL) gene continue to have a very poor prognosis. The most common MLL mutation in ALL is the t(4;11)(q21;q23) chromosome translocation that fuses MLL in frame with the AF4 gene producing MLL-AF4 and AF4-MLL fusion proteins. Previously, we showed that MLL-AF4 binds to the BCL-2 gene and directly activates it through DOT1L recruitment and increased H3K79me2/3 levels. more...

Organism:: Homo sapiens

Type:: Expression profiling by high throughput sequencing; Other; Genome binding/occupancy profiling by high throughput sequencing

Platforms:: GPL18573 GPL16791
21 Samples

Download data: BW, TXT

Series

Accession:: GSE85988

ID:: 200085988

PubMed Full text in PMC Similar studies Analyze with GEO2R SRA Run Selector

Select item 20001236311.

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:: Homo sapiens; Mus musculus

Type:: Expression profiling by array; Genome binding/occupancy profiling by genome tiling array

Platforms:: GPL5082 GPL5811 GPL8321
49 Samples

Download data: BAR, BED, CEL

Series

Accession:: GSE12363

ID:: 200012363

PubMed Full text in PMC Similar studies Analyze with GEO2R

Select item 20001236212.

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

PubMed Full text in PMC Similar studies

Select item 20001236113.

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

PubMed Full text in PMC Similar studies

Select item 20001236014.

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

PubMed Full text in PMC Similar studies

Select item 20001231315.

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

Organism:: Mus musculus

Type:: Expression profiling by array

Platform:: GPL8321
4 Samples

Download data: CEL

Series

Accession:: GSE12313

ID:: 200012313

PubMed Full text in PMC Similar studies Analyze with GEO2R

Select item 20001231016.

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

Organism:: Mus musculus

Type:: Expression profiling by array

Platform:: GPL8321
39 Samples

Download data: CEL

Series

Accession:: GSE12310

ID:: 200012310

PubMed Full text in PMC Similar studies Analyze with GEO2R

Select item 20004207517.

RUNX1 is a key target gene in t(4;11) leukemias and contributes to gene activation by interacting with the AF4-MLL complex

(Submitter supplied) The Mixed Lineage Leukemia 1 protein (MLL1) is an important epigenetic regulator required for the maintenance of gene activation during development. MLL1 chromosome translocations produce novel fusion proteins that cause aggressive leukemias in humans. Individual MLL1 fusion proteins have distinct leukemic phenotypes even when expressed in the same cell type, but how this distinction is delineated on a molecular level is poorly understood. more...

Organism:: Homo sapiens

Type:: Genome binding/occupancy profiling by high throughput sequencing

Platform:: GPL11154
2 Samples

Download data: BIGBED, BIGWIG

Series

Accession:: GSE42075

ID:: 200042075

PubMed Full text in PMC Similar studies SRA Run Selector

Select item 20017856918.

Changes in chromatin accessibility over time in cells expressing t(4;11) fusion proteins

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.

Organism:: Homo sapiens

Type:: Genome binding/occupancy profiling by high throughput sequencing

Platform:: GPL18573
30 Samples

Download data

Series

Accession:: GSE178569

ID:: 200178569

PubMed Full text in PMC Similar studies

Select item 20017856819.

Changes in chromatin accessibility over time in cells expressing t(4;11) fusion proteins [II]

(Submitter supplied) We have used a combination of constitutive and inducible MLL-AF4 and AF4-MLL fusion genes to investigate the power of theses fusion proteins. All transgenes were stably or transiently transfected. Here, we compared 48 induction of MLL-AF4 or AF4-MLL (day 3) and looked for persistance at days 28. This was compared to the situation with constitutive MLL-AF4 with 48 inductionn of AF4-MLL at day 3 and day 28.

Organism:: Homo sapiens

Type:: Genome binding/occupancy profiling by high throughput sequencing

Platform:: GPL18573
18 Samples

Download data: TSV

Series

Accession:: GSE178568

ID:: 200178568

PubMed Full text in PMC Similar studies SRA Run Selector

Select item 20017856720.

Changes in chromatin accessibility over time in cells expressing t(4;11) fusion proteins [I]

(Submitter supplied) We have used a constitutive MLL-AF4 fusion gene together with a inducible AF4-MLL fusion gene to investigate the power of theses fusion proteins. All transgenes were stably or transiently transfected.

Organism:: Homo sapiens

Type:: Genome binding/occupancy profiling by high throughput sequencing

Platform:: GPL18573
12 Samples

Download data: TSV

Series

Accession:: GSE178567

ID:: 200178567

PubMed Full text in PMC Similar studies SRA Run Selector

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