GEO DataSets

(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

(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

(Submitter supplied) The gene expression profile of E/R KO clones versus REH cells and controls clones, analysed by total RNA-sequencing, showed a total of 342 genes differentially expressed (q<0.05), 182 upregulated and 160 downregulated. The heatmap of the top50 of the most deregulated genes according to fold change (FC) values showed a distinct expression signature of E/R KO clones as compared with REH cells and control clones

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL21697

6 Samples

Download data: CSV, XLSX

(Submitter supplied) Background: ETV6/RUNX1 (E/R) (also known as TEL/AML1) is the most frequent gene fusion in childhood acute lymphoblastic leukemia (ALL) and also most likely the crucial factor for disease initiation, whereas its role in leukemia propagation and maintenance remains largely elusive. To address this issue we performed a shRNA-mediated knock-down (KD) of the E/R fusion gene and investigated the ensuing consequences on genome-wide gene expression patterns and deducible regulatory functions in two E/R-positive leukemic cell lines. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Dataset:

GDS4298

Platform:

GPL570

10 Samples

Download data: CEL

Analysis of ETV6/RUNX1 (E/R) fusion gene-positive, BCP ALL cell lines (AT2 and REH) following E/R knockdown. E/R (also known as TEL/AML1) is the most frequent gene fusion in childhood ALL. Results provide insight into role of E/R gene fusion in leukemia propagation and maintenance.

Organism:

Homo sapiens

Type:

Expression profiling by array, transformed count, 2 cell line, 2 protocol sets

Platform:

GPL570

Series:

GSE29639

10 Samples

Download data: CEL

(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

(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

(Submitter supplied) Around 20-25% of childhood acute lymphoblastic leukemias carry the TEL-AML1 (TA) fusion gene. It is a fusion of two central hematopoietic transcription factors, TEL (ETV6) and AML1 (RUNX1). Despite its prevalence, the exact genomic targets of TA have remained elusive. We evaluated gene loci and enhancers targeted by TA genome-wide in precursor B acute leukemia cells using global nuclear run-on sequencing (GRO-seq).

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL11154

12 Samples

Download data: BEDGRAPH

(Submitter supplied) The t(8;21) translocation fuses the DNA binding domain of the hematopoietic master regulator RUNX1 to the ETO protein. The resultant RUNX1/ETO fusion protein is a leukemia-initiating transcription factor that interferes with RUNX1 function. The result of this interference is a block in differentiation and, finally, the development of acute myeloid leukemia (AML). To obtain insights into RUNX1/ETO-dependant alterations of the epigenetic landscape we measured genome-wide RUNX1- and RUNX1/ETO bound regions in t(8;21) cells and assessed to what extent the effects of RUNX1/ETO on the epigenome depend on its continued expression in established leukemic cells. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL10558

10 Samples

Download data: TXT

(Submitter supplied) The t(8;21) translocation fuses the DNA binding domain of the hematopoietic master regulator RUNX1 to the ETO protein. The resultant RUNX1/ETO fusion protein is a leukemia-initiating transcription factor that interferes with RUNX1 function. The result of this interference is a block in differentiation and, finally, the development of acute myeloid leukemia (AML). To obtain insights into RUNX1/ETO-dependant alterations of the epigenetic landscape we measured genome-wide RUNX1- and RUNX1/ETO bound regions in t(8;21) cells and assessed to what extent the effects of RUNX1/ETO on the epigenome depend on its continued expression in established leukemic cells. more...

Organism:

Homo sapiens

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL9052

6 Samples

Download data: TXT

(Submitter supplied) The t(8;21) translocation fuses the DNA binding domain of the hematopoietic master regulator RUNX1 to the ETO protein. The resultant RUNX1/ETO fusion protein is a leukemia-initiating transcription factor that interferes with RUNX1 function. The result of this interference is a block in differentiation and, finally, the development of acute myeloid leukemia (AML). To obtain insights into RUNX1/ETO-dependant alterations of the epigenetic landscape we measured genome-wide RUNX1- and RUNX1/ETO bound regions in t(8;21) cells and assessed to what extent the effects of RUNX1/ETO on the epigenome depend on its continued expression in established leukemic cells. more...

Organism:

Homo sapiens

Type:

Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by array; Methylation profiling by array

Platforms:

GPL9052 GPL10558

38 Samples

Download data: TXT

(Submitter supplied) The t(8;21) translocation fuses the DNA binding domain of the hematopoietic master regulator RUNX1 to the ETO protein. The resultant RUNX1/ETO fusion protein is a leukemia-initiating transcription factor that interferes with RUNX1 function. The result of this interference is a block in differentiation and, finally, the development of acute myeloid leukemia (AML). To obtain insights into RUNX1/ETO-dependant alterations of the epigenetic landscape we measured genome-wide RUNX1- and RUNX1/ETO bound regions in t(8;21) cells and assessed to what extent the effects of RUNX1/ETO on the epigenome depend on its continued expression in established leukemic cells. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL10558

8 Samples

Download data: TXT

(Submitter supplied) The t(8;21) translocation fuses the DNA binding domain of the hematopoietic master regulator RUNX1 to the ETO protein. The resultant RUNX1/ETO fusion protein is a leukemia-initiating transcription factor that interferes with RUNX1 function. The result of this interference is a block in differentiation and, finally, the development of acute myeloid leukemia (AML). To obtain insights into RUNX1/ETO-dependant alterations of the epigenetic landscape we measured genome-wide RUNX1- and RUNX1/ETO bound regions in t(8;21) cells and assessed to what extent the effects of RUNX1/ETO on the epigenome depend on its continued expression in established leukemic cells. more...

Organism:

Homo sapiens

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL9052

14 Samples

Download data: TXT

(Submitter supplied) Transcription factors regulate gene networks controlling normal hematopoiesis and are frequently deregulated in acute myeloid leukemia (AML). Critical to our understanding of the mechanism of cellular transformation by oncogenic transcription factors is the ability to define their direct gene targets. However, gene network cascades can change within minutes to hours, making it difficult to distinguish direct from secondary or compensatory transcriptional changes by traditional methodologies. more...

Organism:

Homo sapiens

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL24676

31 Samples

Download data: BW, CSV, XLS

(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

Platforms:

GPL24676 GPL18573

74 Samples

Download data: BEDGRAPH, BW, CSV, XLS

(Submitter supplied) Transcription factors regulate gene networks controlling normal hematopoiesis and are frequently deregulated in acute myeloid leukemia (AML). Critical to our understanding of the mechanism of cellular transformation by oncogenic transcription factors is the ability to define their direct gene targets. However, gene network cascades can change within minutes to hours, making it difficult to distinguish direct from secondary or compensatory transcriptional changes by traditional methodologies. more...

Organism:

Homo sapiens

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL24676

9 Samples

Download data: BEDGRAPH, BW, CSV, TXT

(Submitter supplied) Transcription factors regulate gene networks controlling normal hematopoiesis and are frequently deregulated in acute myeloid leukemia (AML). Critical to our understanding of the mechanism of cellular transformation by oncogenic transcription factors is the ability to define their direct gene targets. However, gene network cascades can change within minutes to hours, making it difficult to distinguish direct from secondary or compensatory transcriptional changes by traditional methodologies. more...

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL18573

18 Samples

Download data: BEDGRAPH, TXT

(Submitter supplied) Transcription factors regulate gene networks controlling normal hematopoiesis and are frequently deregulated in acute myeloid leukemia (AML). Critical to our understanding of the mechanism of cellular transformation by oncogenic transcription factors is the ability to define their direct gene targets. However, gene network cascades can change within minutes to hours, making it difficult to distinguish direct from secondary or compensatory transcriptional changes by traditional methodologies. more...

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platforms:

GPL18573 GPL24676

16 Samples

Download data: DIFF

(Submitter supplied) Background: The most common rearrangement in childhood precursor B-cell acute lymphoblastic leukemia (pre-B ALL) is the t(12;21)(p13;q22) translocation resulting in the ETV6-AML1 fusion gene. A frequent concomitant event is the loss of the residual ETV6 allele suggesting a critical role for the ETV6 transcriptional repressor in the etiology of pre-B ALL. However, the precise mechanism through which loss of functional ETV6 contributes to disease pathogenesis is still unclear Results: To investigate the impact of ETV6 loss on the transcriptional network and identify new transcriptional targets of ETV6, we used whole transcriptome analysis of both pre-B leukemic cell lines and pre-B ALL patients combined with chromatin immunoprecipitation. more...

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platforms:

GPL16558 GPL16791

25 Samples

Download data: TXT

(Submitter supplied) B-cell precursor acute lymphoblastic leukemia (pre-B ALL) is the most common pediatric cancer. Although the genetic origin of the disease remains unclear, epigenetic modifications including DNA methylation are suggested to contribute significantly to leukemogenesis. We assessed the DNA methylation status of 402,842 CpG-sites across the genome (Illumina 450k array) in tumor and remission samples of 46 pre-B ALL patients, thus generating the most comprehensive single CpG-site resolution pre-B ALL methylomes so far. more...

Organism:

Homo sapiens

Type:

Methylation profiling by genome tiling array

Platform:

GPL13534

92 Samples

Download data: TXT