GEO DataSets

Analysis of leukemic blasts from p53/Prkdc double-knockout mutants that spontaneously develop early B cell acute lymphoblastic leukemia (B-ALL). Results provide insight into molecular mechanisms underlying high-risk B-ALL.

Organism:

Mus musculus

Type:

Expression profiling by array, count, 3 cell type, 2 genotype/variation sets

Platform:

GPL1261

Series:

GSE56345

9 Samples

Download data: CEL, CHP

(Submitter supplied) This study revealed pathogenic role of pre-BCR-independent SYK activation in high-risk B-ALL. Intensified and central nervous system (CNS)-directed chemotherapy has significantly improved outcomes for pediatric B-acute lymphoblastic leukemia (B-ALL), but confers significant late-effect morbidities. Moreover, many patients suffer relapses, underscoring the need to develop novel, molecularly targeted B-ALL therapies. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Dataset:

GDS5640

Platform:

GPL1261

9 Samples

Download data: CEL, CHP

(Submitter supplied) We used ChIPseq in primary pre-B acute lymphomablastic leukemia (ALL) cells to identify target genes of the oncogenes TCF3-PBX1 and BCL6 that are involved in leukemogenesis of TCF3-PBX1 pre-B ALL.

Organism:

Homo sapiens

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL11154

6 Samples

Download data: BIGBED, BIGWIG

(Submitter supplied) BCL6fl/fl mouse bone marrow pre-B cells were transduced with an TCF3-PBX1 vector. The TCF3-PBX1 transduced BCL6fl/fl pre-B cells were then transduced with an empty vector (EV), or a Cre vector for Cre-mediated BCL6 deletion. Effect of BCL6 deletion in the TCF3-PBX1 pre-B cells were studied by Affymetrix GeneChip Mouse Genome 430 2.0 Arrays.

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL1261

6 Samples

Download data: CEL

(Submitter supplied) Induction of proximal components of the PI3-K/AKT pathway stimulates the expression of several genes, including several genes in the JAK/STAT pathway, documenting a crosstalk between these two important pathways. These changes were accompnied by nuclear translocation of certain transcription factors as well.

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL8300

6 Samples

Download data: CEL, CHP

(Submitter supplied) Deregulated RTK activity has been implicated as a causal leukemogenic factor in the context of molecular aberrations that perturb differentiation in the hematopoietic lineage such as in childhood ALL. A deeper understanding of RTK signaling processes on a system-wide scale will be key in defining critical components of signaling networks. To link RTK activity with in vivo output in primary ALL we took a functional approach, which combined SH2 domain binding, mass spectrometry, and transcriptome analyses. more...

Organism:

Homo sapiens

Type:

Genome variation profiling by SNP array

Platform:

GPL6801

12 Samples

Download data: CEL, TXT

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

Organism:

Homo sapiens

Type:

Expression profiling by array; Genome variation profiling by SNP array

Platforms:

GPL6801 GPL570

115 Samples

Download data: CEL, CHP

(Submitter supplied) The purpose of this study was the principal investigation and frequency of RTK expression in primary T-ALLs. Primary initial T-ALLs were assessed regarding their transcriptome-wide expression profiles and screend for prominent RTK expression.

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL570

79 Samples

Download data: CEL

(Submitter supplied) Deregulated RTK activity has been implicated as a causal leukemogenic factor in the context of molecular aberrations that perturb differentiation in the hematopoietic lineage such as in childhood ALL. A deeper understanding of RTK signaling processes on a system-wide scale will be key in defining critical components of signaling networks. To link RTK activity with in vivo output in primary ALL we took a functional approach, which combined SH2 domain binding, mass spectrometry, and transcriptome analyses. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL570

24 Samples

Download data: CEL, CHP

(Submitter supplied) Gene expression data from CD22+B220+ FACS-purified splenocytes of adult Sca1-HGAL knock-in CBAxC57BL/6J mice or wild-type littermates.

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL6246

8 Samples

Download data: CEL

(Submitter supplied) CNS leukemia is still the major obstacle in treating childhood acute lymphoblastic leukemia (ALL). We have used our NOD/SCID/huALL xenotransplantation model to identify molecular pathways leading to the infiltration of leukemic cells into the CNS compartment. We analysed gene expression differences of leukemic cells isolated from CNS and BM of CNS-positive samples using a microarray approach to detect expression differences between different infiltrated compartments.

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL570

18 Samples

Download data: CEL

(Submitter supplied) we identified for the first time that the phosphorylation state of SRSF1 is linked to different phases in ALL. Our results underscore the phosphorylation of SRSF1 at the Tyr-19 residue disrupts subcellular localization of SRSF1 and promotes cell proliferation in leukemic cells by accelerating cell-cycle progression. Targeting Tie2 kinase is able to catalyze Tyr-19 phosphorylation of SRSF1, and offer a promising therapeutic target for the treatment of pediatric ALL. more...

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL20301

4 Samples

Download data: XLS

(Submitter supplied) Targeted therapy of cancer typically focuses on the development of agents that will inactivate a transforming oncogene. In this study, we tested the concept that besides the oncogene itself, factors that enable permissiveness of a normal cell to oncogenic signaling represent a novel class of therapeutic targets. This hypothesis was based on our finding that acute activation of oncogenes in normal pre-B cells typically results in immediate cell death, unless pre-B cells were capable of adapting quickly enough to a high level of signaling output in Erk and Stat5 pathways. more...

Organism:

Homo sapiens

Type:

Genome variation profiling by high throughput sequencing

Platform:

GPL11154

2 Samples

Download data: TXT

(Submitter supplied) Human B cell lineage acute lymphoblastic leukemia (ALL) cells carrying MLL-AF4 (SEM; BEL) and E2A-PBX1 (697) gene rearrangements were transduced with the mouse ecotropic receptor to permit subsequent entry of retroviral BCR-ABL1 GFP and GFP empty vectors (EV) pseudotyped with murine ecotropic envelope. GFP expression was measured by flow cytometry. Transductions with BCR-ABL1 GFP and GFP empty vectors (EV) were performed in the presence and absence of 2 mmol/l Imatinib (TKI). more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL570

12 Samples

Download data: CEL

(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:

GPL16791

10 Samples

Download data: NARROWPEAK

(Submitter supplied) Here we report both TET1-WT and catalytically dead mutant TET1 (TET1-MUT) directly interact with STAT5B in PDX2 B-ALL cells. To study the landscape of TET1 and STAT5B binding in whole genomic DNA and test if the STAT5B binding signal is affected by TET1, we conduct the ChIP-seq assay with flag antibody (TET1-WT, TET1-MUT) and STAT5B antibody (sgNS or sgTET1) respectively. The results showed that TET1 bound peaks overlap with STAT5B very well and the tag density of STAT5B on target genes decreases in TET1-impeded cells. more...

Organism:

Homo sapiens

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL16791

6 Samples

Download data: BW, NARROWPEAK

(Submitter supplied) Here we report that TET1 has a critical role in B-ALL development. TET1-depleted cells delayed the onset of B-ALL. To investigate the mechanisms, we first generate the patient-derived xenograft cells (PDX2) and transduce with inducible-Cas9 and sgRNA targeting TET1. After treatment with doxycycline, we observe the expression of Cas9 and a depletion of TET1 protein. By using the high throughput sequencing RNA-seq, we check the potential targets of TET1 in B-ALL cells. more...

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL16791

4 Samples

Download data: TXT