ArticlePloS one2013
Reduced level of the BCL11B protein is associated with adult T-cell leukemia/lymphoma.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 24 citations in OpenAlex.
- The transcription factor BCL11B drives NK cell cytotoxicity and antitumor activity.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- Targeting BCL11B in CAR-engineered lymphoid progenitors drives NK-like cell development with prolonged anti-leukemic activity.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Analysis of the Transcriptional Control ofAnimals : an open access journal from MDPI · 2025Article
- Screening of potential immune-related genes expressed during sepsis using gene sequencing technology.Scientific reports · 2023Article
- A survival prediction model and nomogram based on immune-related gene expression in chronic lymphocytic leukemia cells.Frontiers in medicine · 2022Article
- Article
- From Anti-EBV Immune Responses to the EBV Diseasome via Cross-reactivity.Global medical genetics · 2020Article
- Bcl11b-A Critical Neurodevelopmental Transcription Factor-Roles in Health and Disease.Frontiers in cellular neuroscience · 2017Review
- Human T-cell leukemia virus type 1 Tax oncoprotein represses the expression of the BCL11B tumor suppressor in T-cells.Cancer science · 2015Article
- Kinetic analysis of BCL11B multisite phosphorylation-dephosphorylation and coupled sumoylation in primary thymocytes by multiple reaction monitoring mass spectroscopy.Journal of proteome research · 2014Article
- SWI/SNF chromatin remodeling complexes and cancer.American journal of medical genetics. Part C, Seminars in medical genetics · 2014Review
- Low expression of T-cell transcription factor BCL11b predicts inferior survival in adult standard risk T-cell acute lymphoblastic leukemia patients.Journal of hematology & oncology · 2014Article
- Illegitimate V(D)J recombination-mediated deletions in Notch1 and Bcl11b are not sufficient for extensive clonal expansion and show minimal age or sex bias in frequency or junctional processing.Mutation research · 2014Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAdult T-cell leukemia/lymphoma (ATLL) develops in a small proportion of human T-cell leukemia virus type I (HTLV-I)-infected individuals. However, the mechanism by which HTLV-I causes ATLL has not been fully elucidated. To provide fundamental insights into the multistep process of leukemogenesis, we have mapped the chromosomal abnormalities in 50 ATLL cases to identify potential key regulators of ATLL.
resultsThe analysis of breakpoints in one ATLL case with the translocations t(14;17)(q32;q22-23) resulted in the identification of a Kruppel zinc finger gene, BCL11B, which plays a crucial role in T-cell development. Among the 7 ATLL cases that we examined by immunofluorescence analysis, 4 displayed low and one displayed moderate BCL11B signal intensities. A dramatically reduced level of the BCL11B protein was also found in HTLV-I-positive T-cell lines. The ectopic expression of BCL11B resulted in significant growth suppression in ATLL-derived cell lines but not in Jurkat cells.
conclusionsOur genetic and functional data provide the first evidence that a reduction in the level of the BCL11B protein is a key event in the multistep progression of ATLL leukemogenesis.
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