ArticleNature immunology2015
Mechanisms of clonal evolution in childhood acute lymphoblastic leukemia.
Article in Nature immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 125 papers, 3 of them syntheses that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
125 citing papers in PubMed, 3 syntheses or guidelines pooled it, 197 citations in OpenAlex.
- Evolutionary Comparative Analyses of DNA-Editing Enzymes of the Immune System: From 5-Dimensional Description of Protein Structures to Immunological Insights and Applications to Protein Engineering.Frontiers in immunology · 2021Pooled it
- Vaccination and the Risk of Childhood Cancer-A Systematic Review and Meta-Analysis.Frontiers in oncology · 2020Pooled it
- A systematic review and meta-analysis of the association between childhood infections and the risk of childhood acute lymphoblastic leukaemia.British journal of cancer · 2018Pooled it
- Beyond the Classical View: Early Emergence of Class Switch Recombination-Associated Molecular Features During B-Cell Development in the Bone Marrow.International journal of molecular sciences · 2026Review
- A genomic and epigenomic lens into the biology of acute lymphoblastic leukaemia.Nature reviews. Cancer · 2026Review
- The gastrointestinal microbiome and constituent short-chain fatty acids: a narrative review of an underexplored axis in acute lymphoblastic leukemia.Gut pathogens · 2026Review
- RAG-mediated structural variation and its impact on relapse risk in acute lymphoblastic leukemia.medRxiv : the preprint server for health sciences · 2026Article
- The nonamer code for RAG-mediated recombination in vivo.Nucleic acids research · 2025Article
- The IL7 receptor and the RAG complex are required for the onset of B-cell acute lymphoblastic leukemia.Blood advances · 2025Article
- FoxO1 signaling in B cell malignancies and its therapeutic targeting.FEBS letters · 2025Review
- Common origins of autoimmune diseases and lymphoid malignancies.Trends in immunology · 2025Review
- Article
- Single-cell sequencing reveals the expansion and diversity of T cell subsets in the bone marrow microenvironment of chronic myeloid leukemia.Genes & diseases · 2025Article
- IGH::IL3-Rearranged B-Cell Precursor Acute Lymphoblastic Leukemia With Hypereosinophilia in a Child With a Novel PAX5 Germline Variant.Genes, chromosomes & cancer · 2025Article
- High levels of circular DNA made as immune cells develop increases the risk of leukaemia relapse.Nature · 2025Article
- Article
- The rewired immune microenvironment in leukemia.Nature immunology · 2025Review
- B lymphoproliferative diseases: Effective treatment, inhibited progression, and potential cures through isoform-specific targeting of the prolactin receptor.Vitamins and hormones · 2025Review
- Toward a Unified Theory of Why Young People Develop Cancer.Cold Spring Harbor perspectives in medicine · 2024Review
- Childhood B cell leukemia: Intercepting the paths to progression.BioEssays : news and reviews in molecular, cellular and developmental biology · 2024Review
65 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
18 authors at 8 institutions in 4 countries.
Funding
Abstract
Childhood acute lymphoblastic leukemia (ALL) can often be traced to a pre-leukemic clone carrying a prenatal genetic lesion. Postnatally acquired mutations then drive clonal evolution toward overt leukemia. The enzymes RAG1-RAG2 and AID, which diversify immunoglobulin-encoding genes, are strictly segregated in developing cells during B lymphopoiesis and peripheral mature B cells, respectively. Here we identified small pre-BII cells as a natural subset with increased genetic vulnerability owing to concurrent activation of these enzymes. Consistent with epidemiological findings on childhood ALL etiology, susceptibility to genetic lesions during B lymphopoiesis at the transition from the large pre-BII cell stage to the small pre-BII cell stage was exacerbated by abnormal cytokine signaling and repetitive inflammatory stimuli. We demonstrated that AID and RAG1-RAG2 drove leukemic clonal evolution with repeated exposure to inflammatory stimuli, paralleling chronic infections in childhood.
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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.