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Links from GEO DataSets

Items: 20

1.

Runx1 targets in early B-cell progenitors

(Submitter supplied) The t(12;21) chromosomal translocation, targeting the gene encoding the RUNX1 transcription factor, is observed in 25% of pediatric acute lymphoblastic leukemia (ALL) and is an initiating event in the disease. To elucidate the mechanism by which RUNX1 disruption initiates leukemogenesis, we investigated its normal role in murine B-cell development. Gene expression analysis and genome-wide Runx1-occupancy studies support the hypothesis that Runx1 reinforces the transcription factor network in B-cell progenitors governing early B-cell survival and development .
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by array
Platforms:
GPL11002 GPL11202 GPL7202
10 Samples
Download data: TXT
Series
Accession:
GSE45425
ID:
200045425
2.

Gene expression analysis to identify Runx1 target genes in B-cell progenitors

(Submitter supplied) The t(12;21) chromosomal translocation, targeting the gene encoding the RUNX1 transcription factor, is observed in 25% of pediatric acute lymphoblastic leukemia (ALL) and is an initiating event in the disease. To elucidate the mechanism by which RUNX1 disruption initiates leukemogenesis, we investigated its normal role in murine B-cell development. Gene expression analysis and genome-wide Runx1-occupancy studies support the hypothesis that Runx1 reinforces the transcription factor network in B-cell progenitors governing early B-cell survival and development .
Organism:
Mus musculus
Type:
Expression profiling by array
Platforms:
GPL7202 GPL11202
8 Samples
Download data: TXT
Series
Accession:
GSE45424
ID:
200045424
3.

Genome-wide mapping of Runx1-bound sites in early B-cell progenitors

(Submitter supplied) The t(12;21) chromosomal translocation, targeting the gene encoding the RUNX1 transcription factor, is observed in 25% of pediatric acute lymphoblastic leukemia (ALL) and is an initiating event in the disease. To elucidate the mechanism by which RUNX1 disruption initiates leukemogenesis, we investigated its normal role in murine B-cell development. Gene expression analysis and genome-wide Runx1-occupancy studies support the hypothesis that Runx1 reinforces the transcription factor network in B-cell progenitors governing early B-cell survival and development .
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL11002
2 Samples
Download data: BED
Series
Accession:
GSE45377
ID:
200045377
4.

The transcriptional cofactor TRIM33 prevents apoptosis in B lymphoblastic leukemia by deactivating a single enhancer

(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
23 Samples
Download data: BIGWIG
Series
Accession:
GSE66234
ID:
200066234
5.

The transcriptional cofactor TRIM33 prevents apoptosis in B lymphoblastic leukemia by deactivating a single enhancer [ChIP-Seq]

(Submitter supplied) Most mammalian transcription factors and cofactors occupy thousands of genomic sites and modulate the expression of large gene networks to implement their biological functions. In this study, we describe an exception to this paradigm. TRIM33 is identified here as a lineage dependency in B cell neoplasms and is shown to perform this essential function by associating with a single cis element. ChIP-seq analysis of TRIM33 in murine B cell leukemia revealed a preferential association with two lineage-specific enhancers that harbor an exceptional density of motifs recognized by the PU.1 transcription factor. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL13112
19 Samples
Download data: BIGWIG
Series
Accession:
GSE66233
ID:
200066233
6.

The transcriptional cofactor TRIM33 prevents apoptosis in B lymphoblastic leukemia by deactivating a single enhancer [RNA-Seq]

(Submitter supplied) Most mammalian transcription factors and cofactors occupy thousands of genomic sites and modulate the expression of large gene networks to implement their biological functions. In this study, we describe an exception to this paradigm. TRIM33 is identified here as a lineage dependency in B cell neoplasms and is shown to perform this essential function by associating with a single cis element. ChIP-seq analysis of TRIM33 in murine B cell leukemia revealed a preferential association with two lineage-specific enhancers that harbor an exceptional density of motifs recognized by the PU.1 transcription factor. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL13112
4 Samples
Download data: TXT
Series
Accession:
GSE66232
ID:
200066232
7.

Comparative intraindividual transcriptome analysis of B-precursor ALL of childhood

(Submitter supplied) The objective of this study was the assessment of transcriptional dysregulation in particular with regard to B-cell differentiation factors. Most studies focus on cross-section analyses of various leukemia subtypes to identify differentially regulated genes lacking suitable reference models. Here we applied comparative intraindividual transcriptome analysis of B-precursor ALL of childhood, which introduces a side-by-side analysis of leukemic cells and matched normal lymphoblasts from the same individual in complete continuous remission after the end of re-induction therapy. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL96
11 Samples
Download data: CEL, CHP
Series
Accession:
GSE42221
ID:
200042221
8.

Affymetrix SNP array data for acute lymphoblastic leukemia samples

(Submitter supplied) Development of B-acute lymphoblastic leukemia accompanies with multiple variable mutations. Beside the structural and chromosomal alterations, especially mutations in the regulators of B cell differentiation are common. Around 60% of the B-ALL show deletions of these genes.
Organism:
Homo sapiens
Type:
Genome variation profiling by SNP array
Platform:
GPL6801
40 Samples
Download data: CEL, TXT
Series
Accession:
GSE42056
ID:
200042056
9.

Whole-genome mapping of RUNX1, FUBP1, H3K4me1, H3K4me3, H3K27me3 and H3K27ac in human pre-B lymphoblasts, and B cell precursor leukemia (BCP-ALL)

(Submitter supplied) Genome binding/occupancy profiling of human Runt-related transcription factor 1 (RUNX1), Far Upstream Binding Protein 1 (FUBP1) and histone marks by high throughput sequencing. RUNX1 and FUBP1 are two key transcriptional regulators implicated in hematopoiesis, from the maintenance of HSC to lineage-specific differentiation. We hypothesized that both proteins could play a joint role in transcription regulation of hematologic lineages. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL16791 GPL18460
13 Samples
Download data: WIG
Series
Accession:
GSE109377
ID:
200109377
10.

Epigenetic regulation of the apoptosis program in t(8;21) AMLs by an AML1-ETO, ERG and RUNX1 triad

(Submitter supplied) The t(8;21) acute myeloid leukemia associated oncoprotein AML1-ETO is a transcription factor that aberrantly regulates the pathways that lead to myeloid differentiation. Here, we set out to investigate the effects of AML1-ETO on gene expression and the epigenome in patient blast cells. We identify two modules, one in which AML1-ETO binds promoter regions of active genes and one represented by non-promoter binding to accessible, yet inactive chromatin regions. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing
Platforms:
GPL10999 GPL11154
16 Samples
Download data: WIG
Series
Accession:
GSE76464
ID:
200076464
11.

Single cell characterization of arrested B-lymphoid differentiation and leukemic cell states in ETV6-RUNX1-positive pediatric leukemia

(Submitter supplied) Arrested bone marrow (BM) lymphoid cell differentiation underlies the emergence of the most common childhood cancer, acute lymphoblastic leukemia (ALL). Recurrent genetic lesions often directly involve transcription factors (TFs), such as ETV6 and RUNX1 found in the most common ALL translocation. Here, we studied differential gene expression in ETV6-RUNX1 primary ALL samples and the REH cell line using single cell RNA-seq (scRNA-seq). more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
4 related Platforms
15 Samples
Download data: BIGWIG, MTX, TSV
Series
Accession:
GSE148218
ID:
200148218
12.

RNA polymerase in pre-B-ALL cell lines

(Submitter supplied) [Gro-seq] Precursor B acute leukemia cells measured using global nuclear run-on sequencing [ChIP-Seq] The genome-wide occupancy of ser2 and ser5 phosphorylated RNA pol2 and H3K4me3 was measured in precursor B acute leukemia cells measured using chip-seq.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Third-party reanalysis; Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL11154
21 Samples
Download data: BEDGRAPH, TXT
13.

Whole-genome mapping of RUNX1, CBFA2T3, H3K4me1, H3K4me3, H3k27me3 and H3K27ac in pre-B lymphoblast models

(Submitter supplied) Genome binding/occupancy profiling of Runt Related Transcription Factor 1 (RUNX1), CBFA2T3 (ETO2, MRG16) and histone marks by high throughput sequencing. RUNX1 and CBFA2T3 are found overexpressed in pediatric t(12;21) ETV6-RUNX1 B cell precursor acute lymphoblastic leukemia. As CBFA2T3 is a transcription regulator, we hypothesized a potential collaboration between the transcription factor RUNX1 and CBFA2T3. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL18460 GPL16791
8 Samples
Download data: WIG
Series
Accession:
GSE117684
ID:
200117684
14.

Autophagy driving ETV6-RUNX1 positive leukaemia

(Submitter supplied) This file contains the gene expression data for 654 pediatric acute lymphoblastic leukemia samples
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
654 Samples
Download data: CEL
Series
Accession:
GSE87070
ID:
200087070
15.

Genetic analysis of Ikaros target genes and tumor suppressor function in BCR-ABL1+ pre-B ALL

(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:
GPL11154
28 Samples
Download data: BED, BEDGRAPH, BIGWIG
Series
Accession:
GSE90670
ID:
200090670
16.

Genetic analysis of Ikaros target genes and tumor suppressor function in BCR-ABL1+ pre-B ALL [ATAC-Seq]

(Submitter supplied) Using patient-derived Ph+ pre-B ALL cells that harbor deletions of the IKZF1 DNA binding domain (Ik6), we performed ATAC-sequencing in cells that inducibly express wild-type Ikaros (Ik1) or an empty vector control.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL11154
2 Samples
Download data: BEDGRAPH
Series
Accession:
GSE90666
ID:
200090666
17.

Genetic analysis of Ikaros target genes and tumor suppressor function in BCR-ABL1+ pre-B ALL [RNA-seq]

(Submitter supplied) RNA-seq was performed in human Ph+ pre-B ALL cells that harbor a deletion of the Ikaros DNA binding domain (Ik6) after doxycycline induction of exogenous expression of wild-type Ikaros (Ik1) or control empty vector over 0, 12, 24 and 48 hours. Biological replicates (n=2) using independent cultures and inductions were performed.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11154
16 Samples
Download data: TXT
Series
Accession:
GSE90659
ID:
200090659
18.

Genetic analysis of Ikaros target genes and tumor suppressor function in BCR-ABL1+ pre-B ALL [ChIP-seq]

(Submitter supplied) ChIP-seq was performed in patient-derived BCR-ABL1+ (Ph+) pre-B ALL cells that harbor heterozygote deletions of the IKZF1 DNA binding domain (Ik6), using cells that inducibly express wild-type Ikaros (Ik1) or an empty vector control.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL11154
10 Samples
Download data: BED, BIGWIG
Series
Accession:
GSE90656
ID:
200090656
19.

Genome wide mapping of IKAROS binding (ChIP-Seq) in human patient-derived BCR-ABL1+ (Ph+) pre-B ALL xenograft cells

(Submitter supplied) IKAROS is an important tumor suppressor in human pre-B ALL and is mutated or deleted in a high percentage of human BCR-ABL1+ (Ph+) pre-B ALL. We here report the genome-wide binding of IKAROS in two independent patient-derived BCR-ABL1+ (Ph+) pre-B ALL xenograft cells that express wild type full-length IKAROS.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL11154
8 Samples
Download data: BEDGRAPH, TXT
Series
Accession:
GSE58825
ID:
200058825
20.

Loss of Ikaros tumor suppressor function in a mouse model of BCR-ABL1-induced B-ALL correlates with a developmental block at a highly proliferative stage

(Submitter supplied) Deletions within the human IKZF1 gene, which encodes Ikaros, a zinc finger transcription factor critical for lymphopoiesis, appear to be the most prominent recurring lesion in human BCR-ABL1+ (Ph+) B-ALL. Furthermore, IKZF1 mutations correlate with poor prognosis of progenitor B-ALL, further strengthening the notion that IKZF1 is a critical tumor suppressor gene in human B-lineage malignancies. To better understand the relationship between Ikzf1 mutations, BCR-ABL, and B-lineage leukemia, we examined the effect of two newly generated Ikzf1 germline mutation on BCR-ABL-induced proliferation and leukemogenesis in vitro and in vivo. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL13112
6 Samples
Download data: BIGWIG, TXT
Series
Accession:
GSE39160
ID:
200039160
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