ArticleBlood2010
EZH2-mediated epigenetic silencing in germinal center B cells contributes to proliferation and lymphomagenesis.
Article in Blood, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 179 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
179 citing papers in PubMed, 295 citations in OpenAlex.
- A phase II study of belinostat (PXD101) in relapsed and refractory aggressive B-cell lymphomas: SWOG S0520.Leukemia & lymphoma · 2016Trial
- Genome-wide profiling identifies a DNA methylation signature that associates with TET2 mutations in diffuse large B-cell lymphoma.Haematologica · 2013Trial
- Epigenetic regulation of humoral immunity: molecular mechanisms, diseases and therapeutic targets.Signal transduction and targeted therapy · 2026Review
- Isotype-specific antibody secreting plasma cells harbor epigenetic and transcription factor architectures defining distinct cell lineages.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- EZH2 and intracellular CaCellular & molecular immunology · 2026Article
- T follicular helper cells transiently unlock a plasticity state in germinal centre B cells during the humoral immune response.Nature cell biology · 2026Article
- Chromatin Regulatory Targets for Anticancer Therapeutics.Chemical reviews · 2025Review
- G9a controls plasma cell differentiation through FOXO1 and ETS1 binding site regulatory networks.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- CFP1 promotes germinal center affinity maturation and restrains memory B cell differentiation through H3K4me3 modulation.Nature communications · 2025Article
- Unraveling the Epigenetic Landscape of Mature B Cell Neoplasia: Mechanisms, Biomarkers, and Therapeutic Opportunities.International journal of molecular sciences · 2025Review
- EZH2 loss promotes gastric squamous cell carcinoma.Nature communications · 2025Article
- EZH-2 expression and prognostic significance in patients with low-grade non-Hodgkin lymphoma.Scientific reports · 2025Article
- EZH2 mutations increase the heterogeneity of chromatin states in lymphoma.PLoS biology · 2025Article
- Mutant EZH2 alters the epigenetic network and increases epigenetic heterogeneity in B cell lymphoma.PLoS biology · 2025Article
- Subtyping Burkitt Lymphoma by DNA Methylation.Genes, chromosomes & cancer · 2025Article
- EZH1/EZH2 inhibition enhances adoptive T cell immunotherapy against multiple cancer models.Cancer cell · 2025Article
- The epigenetic hallmarks of immune cells in cancer.Molecular cancer · 2025Review
- EZH2 inhibition enhances T cell immunotherapies by inducing lymphoma immunogenicity and improving T cell function.Cancer cell · 2025Article
- Pharmacological Advancements of PRC2 in Cancer Therapy: A Narrative Review.Life (Basel, Switzerland) · 2024Review
- Exploring Senolytic and Senomorphic Properties of Medicinal Plants for Anti-Aging Therapies.International journal of molecular sciences · 2024Article
119 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
EZH2 is the catalytic subunit of the PRC2 Polycomb complex and mediates transcriptional repression through its histone methyltransferase activity. EZH2 is up-regulated in normal germinal center (GC) B cells and is implicated in lymphomagenesis. To explore the transcriptional programs controlled by EZH2, we performed chromatin immunoprecipitation (ChIP-on-chip) in GC cells and found that it binds approximately 1800 promoters, often associated with DNA sequences similar to Droso-phila Polycomb response elements. While EZH2 targets overlapped extensively between GC B cells and embryonic stem cells, we also observed a large GC-specific EZH2 regulatory program. These genes are preferentially histone 3 lysine 27-trimethylated and repressed in GC B cells and include several key cell cycle-related tumor suppressor genes. Accordingly, siRNA-mediated down-regulation of EZH2 in diffuse large B-cell lymphoma (DLBCL) cells resulted in acute cell cycle arrest at the G(1)/S transition and up-regulation of its tumor suppressor target genes. At the DNA level, EZH2-bound promoters are hypomethylated in GC B cells, but many of them are aberrantly hypermethylated in DLBCL, suggesting disruption of normal epigenetic processes in these cells. EZH2 is thus involved in regulating a specific epigenetic program in normal GCs, including silencing of antiproliferative genes, which may contribute to the malignant transformation of GC B cells into DLBCLs.
Indexed as
Identifiers
What OpenQuestion holds
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.