ArticleLeukemia2005
Disruption of the BCL11B gene through inv(14)(q11.2q32.31) results in the expression of BCL11B-TRDC fusion transcripts and is associated with the absence of wild-type BCL11B transcripts in T-ALL.
Article in Leukemia, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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57 citing papers in PubMed, 122 citations in OpenAlex.
- Trial
- Frequent TCR rearrangements in pediatric B-cell lymphoblastic acute leukemia: genomic and phenotypic features.Annals of hematology · 2025Article
- Dual role ofBlood science (Baltimore, Md.) · 2024Review
- Pivotal role of BCL11B in the immune, hematopoietic and nervous systems: a review of the BCL11B-associated phenotypes from the genetic perspective.Genes and immunity · 2024Review
- The function of BCL11B in base excision repair contributes to its dual role as an oncogene and a haplo-insufficient tumor suppressor gene.Nucleic acids research · 2024Article
- TNFAIP3 mutation is an independent poor overall survival factor for patients with T-cell acute lymphoblastic leukemia.Cancer medicine · 2023Article
- Analysis of rare driving events in pediatric acute myeloid leukemia.Haematologica · 2023Article
- Generation of InducibleInternational journal of molecular sciences · 2022Article
- Human induced-T-to-natural killer cells have potent anti-tumour activities.Biomarker research · 2022Article
- BCL11B depletion induces the development of highly cytotoxic innate T cells out of IL-15 stimulated peripheral blood αβ CD8+ T cells.Oncoimmunology · 2022Article
- Novel targeted therapies of T cell lymphomas.Journal of hematology & oncology · 2020Review
- First Case of Double T-Cell Receptor Alpha/Delta Rearrangements of t(11;14) and inv(14) and SubsequentAnnals of laboratory medicine · 2020Article
- Bcl11b/Ctip2 in Skin, Tooth, and Craniofacial System.Frontiers in cell and developmental biology · 2020Review
- Characterization of novel, recurrent genomic rearrangements as sensitive MRD targets in childhood B-cell precursor ALL.Blood cancer journal · 2019Article
- Article
- The N-Terminal CCHC Zinc Finger Motif Mediates Homodimerization of Transcription Factor BCL11B.Molecular and cellular biology · 2018Article
- Comprehensive translocation and clonality detection in lymphoproliferative disorders by next-generation sequencing.Haematologica · 2017Article
- Depletion of B cell CLL/Lymphoma 11B Gene Expression Represses Glioma Cell Growth.Molecular neurobiology · 2016Article
- The complex translocation (9;14;14) involving IGH and CEBPE genes suggests a new subgroup in B-lineage acute lymphoblastic leukemia.Genetics and molecular biology · 2016Article
- Age-related profiling of DNA methylation in CD8+ T cells reveals changes in immune response and transcriptional regulator genes.Scientific reports · 2015Article
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Authors and funding
13 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
T-cell acute lymphoblastic leukemia (T-ALL) is associated with chromosomal aberrations characterized by juxtaposition of proto-oncogenes to T-cell receptor gene loci (TCR), resulting in the deregulated transcription of these proto-oncogenes. Here, we describe the molecular characterization of a novel chromosomal aberration, inv(14)(q11.2q32.31), in a T-ALL sample, involving the recently described BCL11B gene and the TCRD locus. The inversion joined the 5' part of BCL11B, including exons 1-3, to the TRDD3 gene segment of the TCRD locus, whereas the reciprocal breakpoint fused the TRDV1 gene segment to the fourth exon of BCL11B. The TRDV1-BCL11B joining region was 1344 bp long and contained fragments derived from 20q11.22, 3p21.33 and from 11p12, indicating the complex character of this aberration. A strong expression of in-frame transcripts with truncated BCL11B and TCRD constant region (TRDC) were observed, but in contrast to normal T cells and other T-ALL samples, no wild-type BCL11B transcripts were detected in the T-ALL sample. Screening of 37 other T-ALLs revealed one additional case with expression of the BCL11B-TRDC fusion transcript. As BCL11B appears to play a key role in T-cell differentiation, BCL11B disruption and disturbed expression may contribute to the development of T-cell malignancies in man.
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