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Self-enforcing Feedback Activation between BCL6 and Pre-B Cell Receptor Signaling Defines a Distinct Subtype of Acute Lymphoblastic Leukemia

ABSTRACT: 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(S): Homo sapiens

PROVIDER: GSE59538 | GEO | 2015/02/08

SECONDARY ACCESSION(S): PRJNA255521

REPOSITORIES: GEO

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Self-enforcing Feedback Activation between BCL6 and Pre-B Cell Receptor Signaling Defines a Distinct Subtype of Acute Lymphoblastic Leukemia

Project description: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. ChIP-seq using E2A (TCF3), PBX1, p300 and BCL6 antibodies in ICN12 cells (primary pre-B acute lymphomablastic leukemia)

2015-02-08 | E-GEOD-59538 | biostudies-arrayexpress

Self-Enforcing Feedback Activation between BCL6 and Pre-B Cell Receptor Signaling Defines a Distinct Subtype of Acute Lymphoblastic Leukemia

Project description: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.

2015-02-08 | GSE59332 | GEO

Chronic active pre-B cell receptor signaling drives BCL6 expression and represents a therapeutic target in a distinct subtype of acute lymphoblastic leukemia

2015-02-08 | E-GEOD-59332 | biostudies-arrayexpress

BCL6 represents a therapeutic target in E2A-PBX1 and MLL-rearranged acute lymphoblastic leukemia

Project description:We used ChIPseq to identify target genes of BCL6 that are involved in leukemogenesis of E2A-PBX1 and MLL-AF4 pre-B ALL.

2019-12-31 | GSE59541 | GEO

CircRNAome of childhood B-ALL: Deciphering subtype-specific expression profiles and functional involvement

Project description:Childhood acute lymphoblastic leukemia (ALL) is a heterogeneous disease comprising multiple molecular subgroups with subtype-specific expression profiles. Recently, a new type of ncRNA, termed circular RNA (circRNA), has emerged as a promising biomarker in cancer, but little is known about their role in childhood B-ALL. Here, through RNA-seq analysis in 105 childhood B-ALL patients comprising 6 genetic subtypes and 7 B-cell controls from two independent cohorts, we demonstrated that circRNAs properly stratified B-ALL subtypes. By differential expression analysis, 110 overexpressed and 134 underexpressed circRNAs were identified consistently for each subtype in both cohorts. Focusing on overexpressed circRNAs, most of them had a subtype-specific expression, with 73 circRNA (66%) only expressed in one subgroup. Interestingly, TCF3/PBX1 subtype was the one with the highest number of unique circRNAs, as well as overexpressed circRNAs. Our results indicated that NUDT21, an RNA-binding protein (RBP) involved in circRNA biogenesis, contributes to this circRNA enrichment in TCF3-PBX1 ALL. Further functional characterization using CRISPR-Cas13d system demonstrated that circBARD1 (hsa_circ_0001098), overexpressed in TCF3/PBX1 subtype, was involved in cancer phenotypes. Our results suggest that circRNAs could have a role in the pathogenesis of childhood B-ALL, adding a new layer of complexity in leukemogenesis.

2024-02-15 | GSE206336 | GEO

Self-enforcing feedback activation between BCL6 and pre-B cell receptor signaling defines a distinct subtype of acute lymphoblastic leukemia.

Project description: Not available

| S-EPMC4618684 | biostudies-literature

Gene expression data of BCR-ABL1 transformed B cell precursors from BCL6 wild-type and BCL6 knockout mice

Project description:To elucidate the mechanism of BCL6-mediated pre-B cell survival signaling, we investigated the gene expression pattern in BCR-ABL1-transformed BCL6+/+ and BCL6-/- B cell precursors. Pharmacological inhibition of BCR-ABL1 was performed with the BCR-ABL1 kinase inhibitor STI571 (Imatinib). BCR-ABL1 transformed B cell precursors of BCL6 wildtype and BCL6 knockout mice were either treated with 10ÂµM STI571 (Imatinib) for 16 hours or cultured in absence of STI571. Three samples for each condition were processed.

2010-05-27 | E-GEOD-20987 | biostudies-arrayexpress

Gene expression data of BCR-ABL1 transformed B cell precursors from BCL6 wild-type and BCL6 knockout mice

2010-05-10 | GSE20987 | GEO

Genome-wide maps of factors and gene expression in pre-B leukemic 697 line

Project description:E2A, a basic helix-loop-helix (bHLH) transcription factor, plays a crucial role in determining tissue-specific cell fate, including differentiation of B cell lineages. In 5% of childhood acute lymphoblastic leukemia (ALL), the t(1,19) chromosomal translocation specifically targets the E2A gene and produces an oncogenic E2A-PBX1 fusion protein. While previous studies have demonstrated oncogenic functions of E2A-PBX1 in cell and animal models, the E2A-PBX1-enforced cistrome, the E2A-PBX1 interactome, and related mechanisms underlying leukemogenesis remain unclear. Here, by unbiased genomic profiling approaches, we identify the direct target sites of E2A-PBX1 in t(1,19)-positive pre-B ALL cells and show that, compared to normal E2A, E2A-PBX1 preferentially binds to a subset of gene loci co-bound by RUNX1 and gene-activating machineries (p300, MED1, and H3K27 acetylation). Using biochemical analyses, we further document a direct interaction between E2A-PBX1 and RUNX1 and show that E2A-PBX1 binding to gene enhancers is dependent on RUNX1, but not the DNA-binding activity harbored within the PBX1 homeodomain of E2A-PBX1. Transcriptome analyses and cell transformation assays further establish a significant RUNX1 requirement for E2A-PBX1-mediated target gene activation and leukemogenesis. Notably, the RUNX1 locus itself is also directly activated by E2A-PBX1, indicating a multilayered interplay between E2A-PBX1 and RUNX1. Collectively, our study provides the first unbiased profiling of the E2A-PBX1 cistrome in pre-B ALL cells and reveals a previously unappreciated pathway in which E2A-PBX1 acts in concert with RUNX1 to enforce transcriptome alterations for the development of pre-B ALL.

2020-03-06 | GSE138031 | GEO

Effect of Bach2 overexpression in BCL6+/+ and -/- BCR-ABL1 transformed pre-B cells

Project description:The aim was to investigate how BCL6 genotype affects Bach2 dependent gene expression changes. We compared gene expression profiles of BCL6+/+ and BCL6-/- BCR-ABL1 transformed pre-B cells after inducible overexpression of Bach2.

2013-07-11 | E-GEOD-41042 | biostudies-arrayexpress

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