B-cell lymphoma/leukaemia 11B (BCL11B) is an essential transcription factor for T-cell lineage commitment and maturation. We investigated BCL11B expression by immunohistochemistry in T-lymphoblastic leukaemia/lymphoma (T-ALL/LBL) (n = 115). The majority (83%) of early T-cell precursor T-ALL/LBL (ETP-ALL) cases showed negative BCL11B expression, while most (84%) of non-ETP-ALL/LBL were positive for BCL11B. A simplified three-marker [BCL11B, cluster of differentiation 5 (CD5), CD13] immunophenotypic score discriminated reliably between ETP-ALL and non-ETP-ALL/LBL. In ETP-ALL, patients with positive BCL11B expression had a better overall survival than those with negative BCL11B (P = 0·009). In summary, BCL11B is a valuable marker for T-ALL/LBL subtyping and serves as a potential prognostic marker in patients with ETP-ALL.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1111/bjh.17681 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Background: Human pluripotent stem cell (hPSC)-derived brain organoids patterned towards the cerebral cortex are valuable models of interactions occurring in vivo in cortical tissue. We and others have used these cortical organoids to model dominantly inherited FTD-tau. While these studies have provided essential insights, cortical organoid models have yet to reach their full potential.
View Article and Find Full Text PDFA timed epigenetic switch balances T and ILC lineage proportions in the thymus.
Development
December 2024
Department of Bioengineering, University of Washington, Seattle, WA 98105, USA.
How multipotent progenitors give rise to multiple cell types in defined numbers is a central question in developmental biology. Epigenetic switches, acting at single gene loci, can generate extended delays in the activation of lineage-specifying genes and impact lineage decisions and cell type output. Here, we analyzed a timed epigenetic switch controlling expression of mouse Bcl11b, a transcription factor that drives T-cell commitment, but only after a multi-day delay.
View Article and Find Full Text PDFIn utero human cytomegalovirus infection expands NK-like FcγRIII+CD8+ T cells that mediate Fc antibody functions.
J Clin Invest
November 2024
Children's Health and Discovery Initiative.
Human cytomegalovirus (HCMV) profoundly impacts host T and NK cells across the lifespan, yet how this common congenital infection modulates developing fetal immune cell compartments remains underexplored. Using cord blood from neonates with and without congenital HCMV (cCMV) infection, we identify an expansion of Fcγ receptor III-expressing (FcγRIII-expressing) CD8+ T cells following HCMV exposure in utero. Most FcγRIII+CD8+ T cells express the canonical αβ T cell receptor (TCR), but a proportion express noncanonical γδ TCR.
View Article and Find Full Text PDFMutations at Exon 4 Associated with T Cell Acute Lymphoblastic Leukemia Are Facilitated by AID and Formation of Non-B DNA Conformations.
Mol Cell Biol
November 2024
Department of Biochemistry, Indian Institute of Science, Bangalore, India.
Article Synopsis
- The deregulation of a specific transcription factor is key in the development of T cell acute lymphoblastic leukemia (T-ALL), mainly due to mutations in exon 4 that disrupt its DNA-binding ability.
- The study highlights the role of Activation-induced cytidine deaminase (AID) in mutagenesis, showing that AID is present in T-ALL cells and creates distinct mutation patterns by binding to fragile regions in the DNA.
- AID's binding leads to the formation of complex DNA structures that can cause errors during replication, ultimately resulting in harmful mutations that impair the transcription factor's function and contribute to the onset of T-ALL.
BCL11b interacts with RNA and proteins involved in RNA processing and developmental diseases.
Biochim Biophys Acta Gene Regul Mech
December 2024
University of Strasbourg, UPR CNRS 9002, ARN, IUT Louis Pasteur, Schiltigheim, France. Electronic address:
BCL11b is a transcription regulator and a tumor suppressor involved in lymphomagenesis, central nervous system (CNS) and immune system developments. BCL11b favors persistence of HIV latency and contributes to control cell cycle, differentiation and apoptosis in multiple organisms and cell models. Although BCL11b recruits the non-coding RNA 7SK and epigenetic enzymes to regulate gene expression, BCL11b-associated ribonucleoprotein complexes are unknown.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!