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Links from GEO DataSets

Items: 20

1.

Effect of PELI2 deficiency on the gene expression of bone marrow B220+ cells

(Submitter supplied) To investigate the effect of PELI2 in the regulation of bone marrow B220+ cells in PELI2 knockout mice. We then performed gene expression profiling analysis using data obtained from RNA-seq of 2 different cells.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
6 Samples
Download data: TXT
Series
Accession:
GSE228984
ID:
200228984
2.

Compare proB cells from WT, Tp53-/-, Lnk-/-, Tp53-/-Lnk-/- mice and Tp53-/-Lnk-/-B-ALL

(Submitter supplied) The adaptor protein LNK (SH2B3) has emerged as an important protein in regulating B cell development B cell leukemia. Loss-of-function mutations in LNK (SH2B3) are found in Philadelphia chromosome–like acute lymphoblastic leukemia (Ph-like ALL), but how LNK regulates normal B cell development or promotes leukemogenesis remains unclear. We found that combined loss of Lnk and tumor suppressors Tp53 in mice triggers a highly aggressive and transplantable precursor B-ALL. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL16570
15 Samples
Download data: CEL
Series
Accession:
GSE76940
ID:
200076940
3.

Assessment of ability of hTSLP to maintain primary CRLF2 B-ALL cells in a xenograft model in a state more similar to the parent leukemia

(Submitter supplied) Xenograft models represent an excellent method for expanding primary leukemias, but their ability to preserve the gene expression profile of the parent leukemia may also depend on providing microenvironmental factors that are not cross-reactive between human and mouse. Here we focused on leukemias with a CRLF2 mutation, and the ability of human TSLP to stimulate these cells.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL16791
5 Samples
Download data: XLSX
4.

TSLP-Induced Gene Expression Signature in Primary CRLF2 B-ALL

(Submitter supplied) The cytokine TSLP stimulates in vitro proliferation of human fetal B cell progenitors. Genetic alterations that cause overexpression of the TSLP receptor component, CRLF2, lead to B cell acute lymphoblastic leukemia (CRLF2 B-ALL) with poor outcome. The in vivo role of TSLP in normal human B cell development and its contribution to CRLF2 B-ALL are unknown. In classic xenograft models CRLF2-mediated signaling is unlikely to be activated by mouse TSLP, based on data from engineered cellular models. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL17077
18 Samples
Download data: TXT
Series
Accession:
GSE65274
ID:
200065274
5.

EBF1 and PAX5 control pro-B cell expansion via oppose regulation of the Myc gene

(Submitter supplied) Lineage restricted transcription factors are frequently found mutated in B-lymphoid leukemia, suggesting a close link between normal and malignant B-cell development. One of these transcription factors is EBF1, a protein of critical importance for specification but also survival of B-lymphoid progenitors. We here report that impaired EBF1 function in mouse B-cell progenitors results in reduced expression of Myc. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing; Other
Platform:
GPL19057
24 Samples
Download data: TXT
Series
Accession:
GSE159957
ID:
200159957
6.

Antitumor effect of FOXO1 inhibitor AS1842856 on B-cell precursor acute lymphoblastic leukemia (BCP-ALL).

(Submitter supplied) We found that small moleculal weight FOXO1 inhibitor has antitumor affect against BCP-ALL cell lines RS4;11 and UoCB6
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL6244
8 Samples
Download data: CEL
Series
Accession:
GSE86067
ID:
200086067
7.

An instructive role for Interleukin-7 receptor α in the development of human B-cell precursor leukemia

(Submitter supplied) Bulk RNAseq for transplanted transduced (CRLF2-IL7RAins or BB control)CB cells
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18573
11 Samples
Download data: XLSX
Series
Accession:
GSE190070
ID:
200190070
8.

 An instructive role for IL7RA in the development of human B-cell precursor leukemia 

(Submitter supplied) 10X single cell analysis of human leukemia, pre-leukemia and normal control. The leukemia was developed in xenograft mice that was serialy transplanted with cells from primary mouse that was transplanted with normal cord blood after transduction with virues encoding hyper activated mutant IL7RA. The preleukemic cells are from the primary engrafted mouse and the control is the same cord blood that was transduced with backbone virus expressing GFP.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18573
4 Samples
Download data: CSV
Series
Accession:
GSE151126
ID:
200151126
9.

B cell development requires discrete regulation by PTEN-PI3K and mTOR pathways and the intricate interplay with IL-7 r-Stat5 signaling

(Submitter supplied) IL-7 r and Stat5 signaling drives early B lymphopoiesis, but it remains poorly understood how Stat5-dependent and independent pathways contribute to this process. We report the discrete effects of PI3K and mTOR signaling on Stat5 signaling and B cell development. PI3K was not engaged by IL-7 in pro-B cells but was actively suppressed by PTEN to ensure proper IL-7 r expression, Stat5 signaling and pro-B cell survival. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL16570
12 Samples
Download data: CEL
Series
Accession:
GSE81844
ID:
200081844
10.

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
11.

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
12.

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
13.

Myc regulates chromatin decompaction and nuclear architecture during B cell activation

(Submitter supplied) 50 years ago, Vincent Allfrey and colleagues discovered that lymphocyte activation triggers massive acetylation of chromatin. However, the molecular mechanisms driving epigeneticaccessibility are still unknown. We here show that stimulated lymphocytes decondense chromatin by three differentially regulated steps. First, chromatin is repositioned away from the nuclear periphery in response to global acetylation. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing; Other; Expression profiling by high throughput sequencing
Platforms:
GPL21273 GPL17021 GPL13112
258 Samples
Download data: BW, HIC, TXT
Series
Accession:
GSE82144
ID:
200082144
14.

IL-7 receptor signaling drives human B-cell precursor differentiation and expansion

(Submitter supplied) Whereas absence of interleukin 7 (IL-7) signaling completely abrogates T and B lymphopoiesis in mice, severe combined immunodeficiency patients with mutations in the IL-7 receptor α chain still generate peripheral blood B cells. Consequently, human B lymphopoiesis has been thought to be independent of IL-7 signaling. Using flow cytometric analysis and single-cell RNA sequencing of bone marrow samples of IL-7 receptor α chain-deficient patients and healthy controls in combination with in vitro modeling of human B-cell differentiation, we demonstrate that IL-7 receptor signaling has a crucial role in human B lymphopoiesis. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24676
8 Samples
Download data: MTX, TSV
Series
Accession:
GSE214693
ID:
200214693
15.

Replication timing alterations in leukemia reflect stable clinically-relevant changes in genome architecture

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Other; Genome variation profiling by genome tiling array; Genome variation profiling by high throughput sequencing
4 related Platforms
111 Samples
Download data: PAIR
Series
Accession:
GSE130374
ID:
200130374
16.

Replication timing alterations in leukemia reflect stable clinically-relevant changes in genome architecture [Repli-Seq]

(Submitter supplied) Human B-lineage precursor acute lymphoid leukemias (BCP-ALLs) comprise a group of genetically and clinically distinct disease entities with features of differentiation arrest at known stages of normal B-lineage differentiation. We previously showed BCP-ALL cells display unique and clonally heritable DNA-replication timing (RT) programs; i.e., programs describing the variable order of replication and sub-nuclear 3D architecture of megabase-scale chromosomal units of DNA in different cell types. more...
Organism:
Homo sapiens
Type:
Other; Third-party reanalysis; Genome variation profiling by high throughput sequencing
Platform:
GPL16791
48 Samples
Download data: TXT
Series
Accession:
GSE130373
ID:
200130373
17.

Replication timing alterations in leukemia reflect stable clinically-relevant changes in genome architecture [Repli-Chip]

(Submitter supplied) Human B-lineage precursor acute lymphoid leukemias (BCP-ALLs) comprise a group of genetically and clinically distinct disease entities with features of differentiation arrest at known stages of normal B-lineage differentiation. We previously showed BCP-ALL cells display unique and clonally heritable DNA-replication timing (RT) programs; i.e., programs describing the variable order of replication and sub-nuclear 3D architecture of megabase-scale chromosomal units of DNA in different cell types. more...
Organism:
Homo sapiens
Type:
Other; Third-party reanalysis; Genome variation profiling by genome tiling array
Platforms:
GPL14965 GPL18318 GPL14120
63 Samples
Download data: PAIR, TXT
Series
Accession:
GSE130372
ID:
200130372
18.

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
19.

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
20.

Reprogramming of primary human Philadelphia chromosome-positive B cell acute lymphoblastic leukemia cells into nonleukemic macrophages

(Submitter supplied) BCR–ABL1+ precursor B-cell acute lymphoblastic leukemia (BCR– ABL1+ B-ALL) is an aggressive hematopoietic neoplasm characterized by a block in differentiation due in part to the somatic loss of transcription factors required for B-cell development. We hypothesized that overcoming this differentiation block by forcing cells to reprogram to the myeloid lineage would reduce the leukemogenicity of these cells. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL19883
15 Samples
Download data: CEL
Series
Accession:
GSE66792
ID:
200066792
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