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Historically, sporadic, endemic, and immunodeficiency\u2010associated variants were distinguished, which differ in the frequency of Epstein\u2013Barr 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\u2010transformed lymphoblastoid cell lines using Illumina BeadChip arrays. DNA methylation analyses clustered the cases into four subgroups: two containing mostly EBV\u2010positive cases (BL\u2010mC1, BL\u2010mC2) and two containing mostly EBV\u2010negative cases (BL\u2010mC3, BL\u2010mC4). The subgroups BL\u2010mC1\/2, enriched for EBV\u2010positive cases, showed increased DNA methylation, epigenetic age, and, in part, proliferation history compared to BL\u2010mC3\/4. CpGs hypermethylated in EBV\u2010positive BLs were enriched for polycomb repressive complex 2 marks, while the CpGs hypomethylated in EBV\u2010negative BLs were linked to, for example, B\u2010cell receptor signaling. EBV\u2010associated hypermethylation affected regulatory regions of genes frequently mutated in BL (e.g., <jats:italic>CCND3<\/jats:italic>, <jats:italic>TP53<\/jats:italic>) and impacted superenhancers. This finding suggests that hypermethylation may compensate for the lower mutational burden of pathogenic drivers in EBV\u2010positive BLs. Though minor, significant differences were also observed between EBV\u2010positive endemic and sporadic cases (e.g., at the <jats:italic>SOX11<\/jats:italic> and <jats:italic>RUNX1<\/jats:italic> loci). Our findings suggest that EBV status, rather than epidemiological variants, drives the DNA methylation\u2010based subgrouping of BL.<\/jats:p>","DOI":"10.1002\/gcc.70042","type":"journal-article","created":{"date-parts":[[2025,4,7]],"date-time":"2025-04-07T18:28:33Z","timestamp":1744050513000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":13,"title":["Subtyping Burkitt Lymphoma by <scp>DNA<\/scp> Methylation"],"prefix":"10.1002","volume":"64","author":[{"ORCID":"https:\/\/orcid.org\/0009-0008-2923-1829","authenticated-orcid":false,"given":"Selina","family":"Glaser","sequence":"first","affiliation":[{"name":"Institute of Human Genetics Ulm University and Ulm University Medical Center  Ulm Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rabea","family":"Wagener","sequence":"additional","affiliation":[{"name":"Institute of Human Genetics Ulm University and Ulm University Medical Center  Ulm 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