ArticleLeukemia2016
Loss of a chromosomal region with synteny to human 13q14 occurs in mouse chronic lymphocytic leukemia that originates from early-generated B-1 B cells.
Article in Leukemia, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 26 citations in OpenAlex.
- B-1 derived anti-Thy-1 B cells in old aged mice develop lymphoma/leukemia with high expression of CD11b and Hamp2 that different from TCL1 transgenic mice.Immunity & ageing : I & A · 2024Article
- Homeostatic role of B-1 cells in tissue immunity.Frontiers in immunology · 2023Review
- Old and New Facts and Speculations on the Role of the B Cell Receptor in the Origin of Chronic Lymphocytic Leukemia.International journal of molecular sciences · 2022Review
- Pla2g2a promotes innate Th2-type immunity lymphocytes to increase B1a cells.Scientific reports · 2022Article
- CXCR4+ Treg cells control serum IgM levels and natural IgM autoantibody production by B-1 cells in the bone marrow.The Journal of experimental medicine · 2022Article
- Single-cell genomics identifies distinct B1 cell developmental pathways and reveals aging-related changes in the B-cell receptor repertoire.Cell & bioscience · 2022Article
- Chronic Lymphocytic Leukemia.Cold Spring Harbor perspectives in medicine · 2021Review
- CTLA-4 expression by B-1a B cells is essential for immune tolerance.Nature communications · 2021Article
- TheFrontiers in immunology · 2021Article
- Pathophysiology of chronic lymphocytic leukemia and human B1 cell development.International journal of hematology · 2020Review
- Nfkbie-deficiency leads to increased susceptibility to develop B-cell lymphoproliferative disorders in aged mice.Blood cancer journal · 2020Article
- Hematopoietic stem cell-independent hematopoiesis and the origins of innate-like B lymphocytes.Development (Cambridge, England) · 2019Review
- Crucial Role of Increased Arid3a at the Pre-B and Immature B Cell Stages for B1a Cell Generation.Frontiers in immunology · 2019Article
- Early Generated B-1-Derived B Cells Have the Capacity To Progress To Become Mantle Cell Lymphoma-like Neoplasia in Aged Mice.Journal of immunology (Baltimore, Md. : 1950) · 2018Article
- Control of B-1a cell development by instructive BCR signaling.Current opinion in immunology · 2018Review
- Role of Bruton's tyrosine kinase in B cells and malignancies.Molecular cancer · 2018Review
- Identification of Distinct Unmutated Chronic Lymphocytic Leukemia Subsets in Mice Based on Their T Cell Dependency.Frontiers in immunology · 2018Article
- circEPSTI1 as a Prognostic Marker and Mediator of Triple-Negative Breast Cancer Progression.Theranostics · 2018Article
- A Hard(y) Look at B-1 Cell Development and Function.Journal of immunology (Baltimore, Md. : 1950) · 2017Review
- Early generated B1 B cells with restricted BCRs become chronic lymphocytic leukemia with continued c-Myc and low Bmf expression.The Journal of experimental medicine · 2016Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
A common feature of B-cell chronic lymphocytic leukemia (CLL) is chromosomal loss of 13q14, containing the miR15a/16-1 locus controlling B-cell proliferation. However, CLL etiology remains unclear. CLL is an adult leukemia with an incidence that increases with advancing age. A unique feature of CLL is biased B-cell antigen receptor (BCR) usage, autoreactivity with polyreactivity and CD5 expression, all suggest a role for the BCR in driving CLL pathogenesis. Among human CLLs, BCRs autoreactive with non-muscle myosin IIA (AMyIIA) are recurrent. Here we identify an unmutated AMyIIA BCR in mouse, with distinctive CDR3 segments capable of promoting leukemogenesis. B cells with this AMyIIA BCR are generated by BCR-dependent signaling during B-1 fetal/neonatal development with CD5 induction, but not in adults. These early-generated AMyIIA B-1 B cells self-renew, increase during aging and can progress to become monoclonal B-cell lymphocytosis, followed by aggressive CLL in aged mice, often with the loss of a chromosomal region containing the miR15a/16-1 locus of varying length, as in human CLL. Thus, the ability to generate this defined autoreactive BCR by B-1 B cells is a key predisposing step in mice, promoting progression to chronic leukemia.
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