ArticleCancer cell2021
A hotspot mutation in transcription factor IKZF3 drives B cell neoplasia via transcriptional dysregulation.
Article in Cancer cell, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 57 citations in OpenAlex.
- Malignant B-cell States Orchestrate Spatially Organized Immune Ecosystems in B-cell Lymphomas.Research square · 2026Article
- Mutational profiling of HIV+ diffuse large B-cell lymphoma reveals distinct mutational features with evidence of genomic instability.AIDS (London, England) · 2026Article
- Archaic Introgression Shapes Genetic Variation at Loci Associated With DNA Virus Load in Modern Humans.Genome biology and evolution · 2026Article
- Mutant ribosomal protein RPS15 drives B cell malignancy through oxidative stress and genomic instability.Nature communications · 2026Article
- Targeting β-catenin degradation with GSK3β inhibitors induces cell death in acute lymphoblastic leukemia.Nature cancer · 2026Article
- Host Genetic Architecture between Epstein-Barr Virus Activity and Multiple Sclerosis Reveals Shared Pathways.medRxiv : the preprint server for health sciences · 2025Article
- [IKZF3/Aiolos and tumors].Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2025Review
- SF3B1 mutation accelerates the development of CLL via activation of the mTOR pathway.JCI insight · 2025Article
- FmH2ST: foundation model-based spatial transcriptomics generation from histological images.Nucleic acids research · 2025Article
- Genomic landscape of multiple myeloma and its precursor conditions.Nature genetics · 2025Article
- Supercharging CAR-T cells through transcriptional and epigenetic armoring.Theranostics · 2025Review
- A question of TiME: how microenvironmental interactions shape response to immunotherapy in CLL and Richter Transformation.Frontiers in immunology · 2025Review
- Identifying methamphetamine use predictors in HIV infection: Immune-dopaminergic signatures in peripheral leukocytes and the role of COMT genotype.Brain, behavior, & immunity - health · 2024Article
- Improving prediction performance of general protein language model by domain-adaptive pretraining on DNA-binding protein.Nature communications · 2024Article
- Integrative Analysis of Multi-Omics Data to Identify Deregulated Molecular Pathways and Druggable Targets in Chronic Lymphocytic Leukemia.Journal of personalized medicine · 2024Article
- Gapped-kmer sequence modeling robustly identifies regulatory vocabularies and distal enhancers conserved between evolutionarily distant mammals.Nature communications · 2024Article
- IKZF3 amplification predicts worse prognosis especially in intestinal-type gastric cancer.Journal of cancer research and clinical oncology · 2024Article
- AIOLOS-Associated Inborn Errors of Immunity.Journal of clinical immunology · 2024Review
- Identification and Functional Analysis of a de novo IKZF3 Mutation in a Pediatric Patient with Combined Immunodeficiency.Journal of clinical immunology · 2024Article
- Bifunctional Inhibitor Reveals NEK2 as a Therapeutic Target and Regulator of Oncogenic Pathways in Lymphoma.Molecular cancer therapeutics · 2024Article
Corrections and comments
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Authors and funding
29 authors at 11 institutions in 4 countries.
Funding
Abstract
Hotspot mutation of IKZF3 (IKZF3-L162R) has been identified as a putative driver of chronic lymphocytic leukemia (CLL), but its function remains unknown. Here, we demonstrate its driving role in CLL through a B cell-restricted conditional knockin mouse model. Mutant Ikzf3 alters DNA binding specificity and target selection, leading to hyperactivation of B cell receptor (BCR) signaling, overexpression of nuclear factor κB (NF-κB) target genes, and development of CLL-like disease in elderly mice with a penetrance of ~40%. Human CLL carrying either IKZF3 mutation or high IKZF3 expression was associated with overexpression of BCR/NF-κB pathway members and reduced sensitivity to BCR signaling inhibition by ibrutinib. Our results thus highlight IKZF3 oncogenic function in CLL via transcriptional dysregulation and demonstrate that this pro-survival function can be achieved by either somatic mutation or overexpression of this CLL driver. This emphasizes the need for combinatorial approaches to overcome IKZF3-mediated BCR inhibitor resistance.
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