ArticleCancer discovery2017
CREBBP Inactivation Promotes the Development of HDAC3-Dependent Lymphomas.
Article in Cancer discovery, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 169 papers, 1 of them a synthesis that pooled it.
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Who cites it
169 citing papers in PubMed, 1 synthesis or guideline pooled it, 265 citations in OpenAlex.
- The role of chidamide in the treatment of B-cell non-Hodgkin lymphoma: An updated systematic review.Biomolecules & biomedicine · 2023Pooled it
- Chidamide, a Histone Deacetylase Inhibitor, Combined With R-GemOx in Relapsed/Refractory Diffuse Large B-Cell Lymphoma (TRUST): A Multicenter, Single-Arm, Phase 2 Trial.Cancer medicine · 2025Trial
- A 5-Genomic Mutation Signature Can Predict the Survival for Patients With NSCLC Receiving Atezolizumab.Frontiers in immunology · 2021Trial
- Clinical efficacy and molecular biomarkers in a phase II study of tucidinostat plus R-CHOP in elderly patients with newly diagnosed diffuse large B-cell lymphoma.Clinical epigenetics · 2020Trial
- Genetic polymorphism and transcriptional regulation ofBioscience reports · 2019Trial
- CREBBP loss drives immune evasion by epigenetically silencing STING and MHC-I in small cell lung cancer.Science advances · 2026Article
- Epigenetic regulation of humoral immunity: molecular mechanisms, diseases and therapeutic targets.Signal transduction and targeted therapy · 2026Review
- Structural and functional divergence of cancer hotspot mutations in CREBBP.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Review
- The Epigenetic Architecture of Classical Hodgkin Lymphoma: Lineage Erasure, Immune Escape, and Therapeutic Reprogramming.Medicina (Kaunas, Lithuania) · 2026Review
- A bivalent molecular glue linking lysine acetyltransferases to oncogene-induced cell death.Cell · 2026Article
- Article
- Novel therapeutic targets at the crossroad between epigenetics and signal transduction pathways in B-cell lymphomas.Clinical and experimental medicine · 2026Review
- Article
- Enhanced efficacy of a specific HDAC3 inhibitor in combination with 5-azacitidine against diffuse large B-cell lymphoma.Blood neoplasia · 2026Article
- Review
- Molecular Pathogenesis and Therapeutic Response of Diffuse Large B Cell Lymphoma Genetic Subtypes.Annual review of cancer biology · 2026Article
- Consensus recommendations from the 2024 International Follicular Lymphoma Scientific Workshop.Blood advances · 2026Review
- Epigenetic dysregulation of B‑cells in autoimmune diseases and lymphomas (Review).International journal of molecular medicine · 2026Review
- Exploring the toxic mechanism of cypermethrin-induced neurodegeneration diseases via network toxicology and molecular docking.Scientific reports · 2026Article
109 more citing papers are in PubMed but not listed here.
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31 authors at 8 institutions in 4 countries.
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Abstract
Somatic mutations in CREBBP occur frequently in B-cell lymphoma. Here, we show that loss of CREBBP facilitates the development of germinal center (GC)-derived lymphomas in mice. In both human and murine lymphomas, CREBBP loss-of-function resulted in focal depletion of enhancer H3K27 acetylation and aberrant transcriptional silencing of genes that regulate B-cell signaling and immune responses, including class II MHC. Mechanistically, CREBBP-regulated enhancers are counter-regulated by the BCL6 transcriptional repressor in a complex with SMRT and HDAC3, which we found to bind extensively to MHC class II loci. HDAC3 loss-of-function rescued repression of these enhancers and corresponding genes, including MHC class II, and more profoundly suppressed CREBBP-mutant lymphomas in vitro and in vivo Hence, CREBBP loss-of-function contributes to lymphomagenesis by enabling unopposed suppression of enhancers by BCL6/SMRT/HDAC3 complexes, suggesting HDAC3-targeted therapy as a precision approach for CREBBP-mutant lymphomas. SIGNIFICANCE: Our findings establish the tumor suppressor function of CREBBP in GC lymphomas in which CREBBP mutations disable acetylation and result in unopposed deacetylation by BCL6/SMRT/HDAC3 complexes at enhancers of B-cell signaling and immune response genes. Hence, inhibition of HDAC3 can restore the enhancer histone acetylation and may serve as a targeted therapy for CREBBP-mutant lymphomas. Cancer Discov; 7(1); 38-53. ©2016 AACR.See related commentary by Höpken, p. 14This article is highlighted in the In This Issue feature, p. 1.
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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.