ArticleScience translational medicine2023
TP63 fusions drive multicomplex enhancer rewiring, lymphomagenesis, and EZH2 dependence.
Article in Science translational medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 11 citations in OpenAlex.
- Non-Haematologica · 2026Article
- TBL1XR1 mutations promoted tumor progression in diffuse large B-cell lymphoma through impairing nature killer cytotoxicity via the MYC-CD47/PD-L1 axis.Molecular cancer · 2026Article
- Molecular characterization of HPV integrations in high-risk HPV-positive women and development of a prognostic signature based on integration-associated genes for cervical cancer.Infectious agents and cancer · 2026Article
- Hi-C for genome-wide detection of enhancer-hijacking rearrangements in routine lymphoid cancer biopsies.Cell genomics · 2026Article
- PRMT5 encourages cell migration and metastasis of tongue squamous cell carcinoma through methylating ΔNp63α.Cell death and differentiation · 2026Article
- ALK-negative anaplastic large cell lymphoma in pediatric and adolescent patients: a mini-review.Frontiers in oncology · 2026Review
- Molecular Insights into the Diagnosis of Anaplastic Large Cell Lymphoma: Beyond Morphology and Immunophenotype.International journal of molecular sciences · 2025Review
- Nuclear Control of Mitochondrial Homeostasis and Venetoclax Efficacy in AML via COX4I1.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Crosstalk between paralogs and isoforms influences p63-dependent regulatory element activity.Nucleic acids research · 2024Article
- Epigenetics-targeted drugs: current paradigms and future challenges.Signal transduction and targeted therapy · 2024Review
- Context dependent activity of p63-bound gene regulatory elements.bioRxiv : the preprint server for biology · 2024Article
- The Role of Epigenetic Modifier Mutations in Peripheral T-Cell Lymphomas.Current issues in molecular biology · 2023Review
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Authors and funding
39 authors at 9 institutions in 1 country.
Funding
Abstract
Gene fusions involving tumor protein p63 gene (TP63) occur in multiple T and B cell lymphomas and portend a dismal prognosis for patients. The function and mechanisms of TP63 fusions remain unclear, and there is no target therapy for patients with lymphoma harboring TP63 fusions. Here, we show that TP63 fusions act as bona fide oncogenes and are essential for fusion-positive lymphomas. Transgenic mice expressing TBL1XR1::TP63, the most common TP63 fusion, develop diverse lymphomas that recapitulate multiple human T and B cell lymphomas. Here, we identify that TP63 fusions coordinate the recruitment of two epigenetic modifying complexes, the nuclear receptor corepressor (NCoR)-histone deacetylase 3 (HDAC3) by the N-terminal TP63 fusion partner and the lysine methyltransferase 2D (KMT2D) by the C-terminal TP63 component, which are both required for fusion-dependent survival. TBL1XR1::TP63 localization at enhancers drives a unique cell state that involves up-regulation of MYC and the polycomb repressor complex 2 (PRC2) components EED and EZH2. Inhibiting EZH2 with the therapeutic agent valemetostat is highly effective at treating transgenic lymphoma murine models, xenografts, and patient-derived xenografts harboring TP63 fusions. One patient with
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