ArticleNature communications2019
Infectious stimuli promote malignant B-cell acute lymphoblastic leukemia in the absence of AID.
Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 31 citations in OpenAlex.
- Deletion of 9p drives B-ALL through heterozygous inactivation of Pax5 and Cd72 in preleukemic cells.JCI insight · 2026Article
- Childhood acute leukemia and type 1 diabetes in children: A nationwide case-control study.International journal of cancer · 2026Article
- Pediatric leukemia: origins, pathogenesis, the role of microenvironment and immunological modulation.Frontiers in immunology · 2026Review
- PD-1 Expression Promotes Immune Evasion in B-ALL.Hematology reports · 2025Article
- The rewired immune microenvironment in leukemia.Nature immunology · 2025Review
- Childhood B cell leukemia: Intercepting the paths to progression.BioEssays : news and reviews in molecular, cellular and developmental biology · 2024Review
- Article
- Concepts in B cell acute lymphoblastic leukemia pathogenesis.Journal of leukocyte biology · 2024Review
- The Diverse Roles of ETV6 Alterations in B-Lymphoblastic Leukemia and Other Hematopoietic Cancers.Advances in experimental medicine and biology · 2024Review
- Noncoding mutations cause super-enhancer retargeting resulting in protein synthesis dysregulation during B cell lymphoma progression.Nature genetics · 2023Article
- Immune stress suppresses innate immune signaling in preleukemic precursor B-cells to provoke leukemia in predisposed mice.Nature communications · 2023Article
- Lessons from mouse models in the impact of risk factors on the genesis of childhood B-cell leukemia.Frontiers in immunology · 2023Review
- The role of microenvironment in the initiation and evolution of B-cell precursor acute lymphoblastic leukemia.Frontiers in oncology · 2023Review
- Inflammation accelerates BCR-ABL1+ B-ALL development through upregulation of AID.Blood advances · 2022Article
- Childhood B-Cell Preleukemia Mouse Modeling.International journal of molecular sciences · 2022Review
- Transient Inhibition of the JAK/STAT Pathway Prevents B-ALL Development in Genetically Predisposed Mice.Cancer research · 2022Article
- Oncogene-Induced Reprogramming in Acute Lymphoblastic Leukemia: Towards Targeted Therapy of Leukemia-Initiating Cells.Cancers · 2021Review
- Article
- Infectious triggers and novel therapeutic opportunities in childhood B cell leukaemia.Nature reviews. Immunology · 2021Review
- Support of BCP-ALL-cells by autologous bone marrow Th-cells involves induction of AID expression but not widespread AID off-target mutagenesis.Cancer immunology, immunotherapy : CII · 2021Article
Corrections and comments
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Authors and funding
26 authors at 8 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The prerequisite to prevent childhood B-cell acute lymphoblastic leukemia (B-ALL) is to decipher its etiology. The current model suggests that infection triggers B-ALL development through induction of activation-induced cytidine deaminase (AID; also known as AICDA) in precursor B-cells. This evidence has been largely acquired through the use of ex vivo functional studies. However, whether this mechanism governs native non-transplant B-ALL development is unknown. Here we show that, surprisingly, AID genetic deletion does not affect B-ALL development in Pax5-haploinsufficient mice prone to B-ALL upon natural infection exposure. We next test the effect of premature AID expression from earliest pro-B-cell stages in B-cell transformation. The generation of AID off-target mutagenic activity in precursor B-cells does not promote B-ALL. Likewise, known drivers of human B-ALL are not preferentially targeted by AID. Overall these results suggest that infections promote B-ALL through AID-independent mechanisms, providing evidence for a new model of childhood B-ALL development.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.