ArticleProceedings of the National Academy of Sciences of the United States of America2017
Inactivation of CREBBP expands the germinal center B cell compartment, down-regulates MHCII expression and promotes DLBCL growth.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.
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Who cites it
74 citing papers in PubMed, 116 citations in OpenAlex.
- 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
- Sequential lymphoid neoplasms mimicking relapse of mediastinal grey zone lymphoma in a patient with germline variants in EP300 and PTPRK.Virchows Archiv : an international journal of pathology · 2026Article
- The Epigenetic Architecture of Classical Hodgkin Lymphoma: Lineage Erasure, Immune Escape, and Therapeutic Reprogramming.Medicina (Kaunas, Lithuania) · 2026Review
- Dissecting diffuse large B-cell lymphoma heterogeneity: New insights from a state-specific molecular characterisation.Clinical and translational medicine · 2026Article
- Consensus recommendations from the 2024 International Follicular Lymphoma Scientific Workshop.Blood advances · 2026Review
- Mouse models of B cell lymphomas on the basis of genetic features.Frontiers in immunology · 2026Review
- Case Report: FromFrontiers in immunology · 2026Article
- A proposed convergent molecular chain linking senescence, cancer, and chronic infection to a correctable failure of dendritic cell instruction.Frontiers in immunology · 2026Review
- Single-cell transcriptomics reveals dynamic reprogramming of testicular immunity inZoological research · 2025Article
- Biological mechanism and immune response of MHC-II expression in tumor cells.Cancer biology & medicine · 2025Review
- Unraveling the Epigenetic Landscape of Mature B Cell Neoplasia: Mechanisms, Biomarkers, and Therapeutic Opportunities.International journal of molecular sciences · 2025Review
- The epigenetic revolution in hematology: from benchside breakthroughs to clinical transformations.Clinical and experimental medicine · 2025Review
- Molecular mechanisms of viral oncogenesis in haematological malignancies: perspectives from metabolic reprogramming, epigenetic regulation and immune microenvironment remodeling.Experimental hematology & oncology · 2025Review
- Article
- Tumor microenvironment of Burkitt lymphoma: different immune signatures with different clinical behavior.Blood advances · 2024Article
- IRF8-mutant B cell lymphoma evades immunity through a CD74-dependent deregulation of antigen processing and presentation in MHCII complexes.Science advances · 2024Article
- Targeting AURKA to induce synthetic lethality in CREBBP-deficient B-cell malignancies via attenuation of MYC expression.Oncogene · 2024Article
- Molecular Subtypes and the Role of TP53 in Diffuse Large B-Cell Lymphoma and Richter Syndrome.Cancers · 2024Review
- Loss of CREBBP and KMT2D cooperate to accelerate lymphomagenesis and shape the lymphoma immune microenvironment.Nature communications · 2024Article
14 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The genes encoding the histone acetyl-transferases (HATs) CREB binding protein (CREBBP) and EP300 are recurrently mutated in the activated B cell-like and germinal center (GC) B cell-like subtypes of diffuse large B cell lymphoma (DLBCL). Here, we introduced a patient mutation into a human DLBCL cell line using CRISPR and deleted
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Registered trials
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.