ArticleGenes, chromosomes & cancer2025
Subtyping Burkitt Lymphoma by DNA Methylation.
Article in Genes, chromosomes & cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- DNA methylation-based classification of hematolymphoid neoplasms.Blood advances · 2026Article
- Review
- Immune disparities in the TME of EBV+ and EBV- BL: role of reactive oxygen species generation pathways and platelet activation.Blood advances · 2026Article
- Burkitt Lymphoma-A Guide to Biological Features, Diagnosis and Differential Diagnosis.Cancers · 2026Review
- miRNA profiling in pediatric and young adult Burkitt leukemia and lymphoma.Virchows Archiv : an international journal of pathology · 2026Article
- Proteomic analysis of Burkitt lymphoma tissues: insights into the impact of age and EBV infection on protein expression and molecular characteristics.Discover oncology · 2025Article
- Article
- Epigenetic Regulation of Aging and its Rejuvenation.MedComm · 2025Review
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Authors and funding
41 authors.
Funding
Abstract
Burkitt lymphoma (BL) is an aggressive germinal center B-cell-derived malignancy. Historically, sporadic, endemic, and immunodeficiency-associated variants were distinguished, which differ in the frequency of Epstein-Barr virus (EBV) positivity. Aiming to identify subgroups based on DNA methylation patterns, we here profiled 96 BL cases, 17 BL cell lines, and six EBV-transformed lymphoblastoid cell lines using Illumina BeadChip arrays. DNA methylation analyses clustered the cases into four subgroups: two containing mostly EBV-positive cases (BL-mC1, BL-mC2) and two containing mostly EBV-negative cases (BL-mC3, BL-mC4). The subgroups BL-mC1/2, enriched for EBV-positive cases, showed increased DNA methylation, epigenetic age, and, in part, proliferation history compared to BL-mC3/4. CpGs hypermethylated in EBV-positive BLs were enriched for polycomb repressive complex 2 marks, while the CpGs hypomethylated in EBV-negative BLs were linked to, for example, B-cell receptor signaling. EBV-associated hypermethylation affected regulatory regions of genes frequently mutated in BL (e.g., CCND3, TP53) and impacted superenhancers. This finding suggests that hypermethylation may compensate for the lower mutational burden of pathogenic drivers in EBV-positive BLs. Though minor, significant differences were also observed between EBV-positive endemic and sporadic cases (e.g., at the SOX11 and RUNX1 loci). Our findings suggest that EBV status, rather than epidemiological variants, drives the DNA methylation-based subgrouping of BL.
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