ArticleNature communications2021
Interleukin-7 receptor α mutational activation can initiate precursor B-cell acute lymphoblastic leukemia.
Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 50 citations in OpenAlex.
- Signals from the bone marrow B cell niches shape pre-leukemic fate in a murine model of B cell acute lymphoblastic leukemia.Oncogene · 2026Article
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- IL-7 promotes naïve T cell motility to enable T cell scanning of dendritic cells in the LN.Cytokine · 2026Article
- Integrative Multi-Omics Analysis Reveals Molecular Signatures of Recurrence in Paired Primary and Recurrent High-Grade Serous Ovarian Cancer.International journal of molecular sciences · 2026Article
- ICU-acquired infections and mortality in community-acquired pneumonia-induced sepsis: Insights from a transcriptomic analysis.PloS one · 2026Article
- Identification of Molecular Subtypes of B-Cell Acute Lymphoblastic Leukemia in Mexican Children by Whole-Transcriptome Analysis.International journal of molecular sciences · 2025Article
- CD79A and IL7R mRNA Levels in the Cerebrospinal Fluid of Adults with Acute B-Cell Lymphoblastic Leukemia: A Pilot Study.Diseases (Basel, Switzerland) · 2025Article
- Construction of enhanced MRI-based radiomics models using machine learning algorithms for non-invasive prediction of IL7R expression in high-grade gliomas and its prognostic value in clinical practice.Journal of translational medicine · 2025Article
- Single nucleotide polymorphism-based analysis of linkage disequilibrium and runs of homozygosity patterns of indigenous sheep in the southern Taklamakan desert.BMC genomics · 2025Article
- Unveiling the omics tapestry of B-acute lymphoblastic leukemia: bridging genomics, metabolomics, and immunomics.Scientific reports · 2025Article
- Differential activation of basal and IL-7-induced PI3K/Akt/ mTOR and JAK/STAT5 signaling distinguishes pediatric from adult acute lymphoblastic leukemia.Haematologica · 2024Article
- Concepts in B cell acute lymphoblastic leukemia pathogenesis.Journal of leukocyte biology · 2024Review
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- Rare Drivers at Low Prevalence with High Cancer Effects in T-Cell and B-Cell Pediatric Acute Lymphoblastic Leukemia.International journal of molecular sciences · 2024Article
- Rare SH2B3 coding variants in lupus patients impair B cell tolerance and predispose to autoimmunity.The Journal of experimental medicine · 2024Article
- CD161Oncoimmunology · 2024Article
- XBP1 promotes NRASJournal of cellular and molecular medicine · 2023Article
- Article
- Defining the Basal and Immunomodulatory Mediator-Induced Phosphoprotein Signature in Pediatric B Cell Acute Lymphoblastic Leukemia (B-ALL) Diagnostic Samples.International journal of molecular sciences · 2023Article
- Histone acetylation by HBO1 (KAT7) activates Wnt/β-catenin signaling to promote leukemogenesis in B-cell acute lymphoblastic leukemia.Cell death & disease · 2023Article
Corrections and comments
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Authors and funding
29 authors at 7 institutions in 6 countries.
Funding
Abstract
Interleukin-7 receptor α (encoded by IL7R) is essential for lymphoid development. Whether acute lymphoblastic leukemia (ALL)-related IL7R gain-of-function mutations can trigger leukemogenesis remains unclear. Here, we demonstrate that lymphoid-restricted mutant IL7R, expressed at physiological levels in conditional knock-in mice, establishes a pre-leukemic stage in which B-cell precursors display self-renewal ability, initiating leukemia resembling PAX5 P80R or Ph-like human B-ALL. Full transformation associates with transcriptional upregulation of oncogenes such as Myc or Bcl2, downregulation of tumor suppressors such as Ikzf1 or Arid2, and major IL-7R signaling upregulation (involving JAK/STAT5 and PI3K/mTOR), required for leukemia cell viability. Accordingly, maximal signaling drives full penetrance and early leukemia onset in homozygous IL7R mutant animals. Notably, we identify 2 transcriptional subgroups in mouse and human Ph-like ALL, and show that dactolisib and sphingosine-kinase inhibitors are potential treatment avenues for IL-7R-related cases. Our model, a resource to explore the pathophysiology and therapeutic vulnerabilities of B-ALL, demonstrates that IL7R can initiate this malignancy.
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Registered trials
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