ArticleNature communications2022
IRF4 drives clonal evolution and lineage choice in a zebrafish model of T-cell lymphoma.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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Who cites it
9 citing papers in PubMed, 15 citations in OpenAlex.
- Genetic Background Predicts Uveal Melanoma Patients' Outcomes.Ophthalmology science · 2026Article
- Multi-trait analysis of pigmentation traits in relation to skin and ocular cancers: Relevance for evolutionary medicine.Evolution, medicine, and public health · 2026Article
- The axillary lymphoid organ is an external, experimentally accessible immune organ in the zebrafish.The Journal of experimental medicine · 2025Article
- Article
- Advances in biology, diagnosis and treatment of DLBCL.Annals of hematology · 2024Review
- Fishing Innate Immune System Properties through the Transcriptomic Single-Cell Data ofBiology · 2023Review
- Larval T Cells Are Functionally Distinct from Adult T Cells in Xenopus laevis.ImmunoHorizons · 2023Article
- Advances in single-cell RNA sequencing and its applications in cancer research.Journal of hematology & oncology · 2023Review
- IRF4 as an Oncogenic Master Transcription Factor.Cancers · 2022Review
Corrections and comments
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Authors and funding
15 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
IRF4 is a master regulator of immunity and is also frequently overexpressed in mature lymphoid neoplasms. Here, we demonstrate the oncogenicity of IRF4 in vivo, its potential effects on T-cell development and clonal evolution using a zebrafish model. IRF4-transgenic zebrafish develop aggressive tumors with massive infiltration of abnormal lymphocytes that spread to distal organs. Many late-stage tumors are mono- or oligoclonal, and tumor cells can expand in recipient animals after transplantation, demonstrating their malignancy. Mutation of p53 accelerates tumor onset, increases penetrance, and results in tumor heterogeneity. Surprisingly, single-cell RNA-sequencing reveals that the majority of tumor cells are double-negative T-cells, many of which express tcr-γ that became dominant as the tumors progress, whereas double-positive T-cells are largely diminished. Gene expression and epigenetic profiling demonstrates that gata3, mycb, lrrn1, patl1 and psip1 are specifically activated in tumors, while genes responsible for T-cell differentiation including id3 are repressed. IRF4-driven tumors are sensitive to the BRD inhibitor.
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Registered trials
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