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14q32 recombinations deregulating BCL11B mark a distinct Mixed Phenotype Leukemia

ABSTRACT: 14q32 recombinations deregulating BCL11B mark a distinct Mixed Phenotype Leukemia

PROVIDER: PRJNA681239 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13160442_1.fastq.gz	Fastqsanger.gz
	SRR13160442_2.fastq.gz	Fastqsanger.gz
	SRR13160443_1.fastq.gz	Fastqsanger.gz
	SRR13160443_2.fastq.gz	Fastqsanger.gz
	SRR13160444_1.fastq.gz	Fastqsanger.gz

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14q32 recombinations deregulating BCL11B mark a distinct Mixed Phenotype Leukemia

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-09-05 | GSE162283 | GEO

Affymetrix SNP array data for acute leukemias with a 14q32/BCL11B rearrangement

Project description:This study identified a cytogenetic-molecular entity, we named BCL11B-R, that showed a typical constellation of genomic features, namely BCL11B activation via chromosome translocations at 14q32, a distinct transcriptome profile, and FLT3 mutations.

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14q32 rearrangements deregulating BCL11B mark a distinct subgroup of T-lymphoid and myeloid immature acute leukemia.

Project description:Acute leukemias (ALs) of ambiguous lineage are a heterogeneous group of high-risk leukemias characterized by coexpression of myeloid and lymphoid markers. In this study, we identified a distinct subgroup of immature acute leukemias characterized by a broadly variable phenotype, covering acute myeloid leukemia (AML, M0 or M1), T/myeloid mixed-phenotype acute leukemia (T/M MPAL), and early T-cell precursor acute lymphoblastic leukemia (ETP-ALL). Rearrangements at 14q32/BCL11B are the cytogenetic hallmark of this entity. In our screening of 915 hematological malignancies, there were 202 AML and 333 T-cell acute lymphoblastic leukemias (T-ALL: 58, ETP; 178, non-ETP; 8, T/M MPAL; 89, not otherwise specified). We identified 20 cases of immature leukemias (4% of AML and 3.6% of T-ALL), harboring 4 types of 14q32/BCL11B translocations: t(2,14)(q22.3;q32) (n = 7), t(6;14)(q25.3;q32) (n = 9), t(7;14)(q21.2;q32) (n = 2), and t(8;14)(q24.2;q32) (n = 2). The t(2;14) produced a ZEB2-BCL11B fusion transcript, whereas the other 3 rearrangements displaced transcriptionally active enhancer sequences close to BCL11B without producing fusion genes. All translocations resulted in the activation of BCL11B, a regulator of T-cell differentiation associated with transcriptional corepressor complexes in mammalian cells. The expression of BCL11B behaved as a disease biomarker that was present at diagnosis, but not in remission. Deregulation of BCL11B co-occurred with variants at FLT3 and at epigenetic modulators, most frequently the DNMT3A, TET2, and/or WT1 genes. Transcriptome analysis identified a specific expression signature, with significant downregulation of BCL11B targets, and clearly separating BCL11B AL from AML, T-ALL, and ETP-ALL. Remarkably, an ex vivo drug-sensitivity profile identified a panel of compounds with effective antileukemic activity.

| S-EPMC8513670 | biostudies-literature

Targeted Sequencing of BCL11B-R patients

2021-09-05 | GSE162282 | GEO

RNA-seq analysis of 12 cases with BCL11B rearrangement

2021-09-05 | GSE162280 | GEO

Affymetrix SNP array data for acute leukemias with a 14q32/BCL11B rearrangement

Project description:Affymetrix SNP array data for acute leukemias with a 14q32/BCL11B rearrangement

| PRJNA680304 | ENA

Molecular characterization of t(2;14)(q22;q32) and t(6;14)(q25;q32) translocations in mixed myeloid/T lymphoid leukemia patients.

Project description:We characterized two recurrent translocations, i.e. t(2;14)(q22.3;q32) and t(6;14)(q25;q32), in FLT3 positive mixed myeloid/T-cell lymphoid leukemias (MLPA). Both translocations involved BCL11B at 14q32. In cases with t(2;14), the 2q22.3 breakpoint disrupted ZEB2 and produced a ZEB2-BCL11B fusion, a significant ZEB2-BCL11B over-expression with concomitant BCL11B wild type (wt) down-regulation. In cases with t(6;14), the 6q25 breakpoints fell in a 100Kb region where no genes have been mapped thus it not appeared to produce a fusion transcript. As long and short BCL11B isoforms were overexpressed in cases with t(6;14), this could be linked to loss of negative regulatory elements or juxtaposition to strong enhancers/promoters to the intact gene. As BCL11B and ZEB2-BCL11B have identical motifs for DNA and protein interactions, we hypothresized that common downstream target genes might be deregulated. Indeed, gene expression profiling analysis identified a specific signature that characterized this subgroup of MLPA and was unlike any known AML and T-ALL. Exome sequencing did no revealed common variations, thus it was used to investigate 252 candidate genes known to be involved in solid cancer or leukemias. Recurrent mutations in 13 genes, 5 of which were new somatic mutations of DNMT3A, EP300, GNAS, FAT4, and PRRX1 were identified.

2021-12-21 | GSE43417 | GEO

BCL11B

Project description:BCL11B

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Genome-wide identification of Bcl11b gene targets

Project description:B-cell leukemia/lymphoma 11B (Bcl11b) is a transcription factor showing predominant expression in the striatum. To date, there are no known gene targets of Bcl11b in the nervous system. Here, we define targets for Bcl11b in striatal cells by performing genome-wide expression profiling. Transcriptome-wide analysis revealed that 694 genes were significantly altered in striatal cells over-expressing Bcl11b, including genes showing striatal-enriched expression similar to Bcl11b. Functional analysis on the gene target list identified significant association of Bcl11b to brain-derived neurotrophic factor/neurotrophin signaling. These data implicate Bcl11b as a novel regulator of the BDNF signaling pathway, which is disrupted in many neurological disorders. n=4 wt STHdh striatal cells and n=4 Bcl11b-transfected STHdh striatal cells

2011-08-01 | E-GEOD-31096 | biostudies-arrayexpress

Mouse iNKT cell: Wild type Vs Bcl11b deficient

Project description:Transcriptional profiling of mouse iNKT cells comparing wild type and Bcl11b deficient cell. The mice were treated with 4 Î¼g of Î±-galactosylceramide. Goal was to determine the effects of transcription factor Bcl11b removal in iNKT cells. Intraperitoneal treatment with 4 Î¼g of Î±-Galactosylceramide. Two pair of wild type (BCL11b F/F VÎ±14 transgenic) and Knock out (BCL11b F/F PLZF-Cre VÎ±14 transgenic)) mice were treated. Lymphocytes from spleen and liver were enriched and stain with PBS-57 Loaded CD1d tetramer. Pure iNKT cells were collected through cell sorter.

2016-08-10 | E-GEOD-73679 | biostudies-arrayexpress

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