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Updated: May 2, 2026

Comprehensive DNA Methylation Analysis Using a Methyl-CpG-binding Domain Capture-based Method in Chronic Lymphocytic Leukemia Patients

Comprehensive DNA Methylation Analysis Using a Methyl-CpG-binding Domain Capture-based Method in Chronic Lymphocytic Leukemia Patients

Published on: June 16, 2017

The EBV-Positive Tumor Methylome Is Distinct from EBV-Negative in Diffuse Large B-Cell Lymphoma.

Ashley K Volaric¹, Ramiro Barrantes-Reynolds², Karine Sahakyan³

¹Department of Pathology and Laboratory Medicine, University of Vermont Larner College of Medicine, University of Vermont Cancer Center, Burlington, VT 05401, USA.

|September 27, 2025

Summary

Epstein-Barr virus (EBV) causes distinct DNA methylation changes in diffuse large B-cell lymphoma (DLBCL), differentiating EBV(+) from EBV(-) cases. These epigenetic alterations offer potential biomarkers for DLBCL classification and targeted therapies.

Keywords:

DLBCL EBV Epstein–Barr virus diffuse large B-cell lymphoma epigenetics methylation methylome

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Comprehensive DNA Methylation Analysis Using a Methyl-CpG-binding Domain Capture-based Method in Chronic Lymphocytic Leukemia Patients

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Published on: September 7, 2022

Area of Science:

Oncology
Virology
Epigenetics

Background:

Epstein-Barr virus (EBV) is linked to B-cell lymphomas, including diffuse large B-cell lymphoma (DLBCL), particularly in immunocompromised individuals.
The precise mechanisms of EBV-driven lymphomagenesis in DLBCL subtypes are not fully understood.
Global DNA methylation profiling offers insights into tumor heterogeneity and disease pathogenesis.

Purpose of the Study:

To investigate the global DNA methylome of EBV-positive (EBV(+)) versus EBV-negative (EBV(-)) DLBCL.
To identify epigenetic differences associated with EBV status in DLBCL.
To explore potential epigenetic biomarkers for DLBCL classification and treatment.

Main Methods:

Global methylome analysis using Illumina MethylationEPIC arrays on 43 DLBCL tissue samples with defined EBV status.
Differential methylation analysis employing linear mixed models to identify EBV-associated methylation changes.
Pathway enrichment analysis to determine biological processes affected by differential methylation.

Main Results:

EBV(+) DLBCL exhibits a distinct, globally hypermethylated DNA methylome compared to EBV(-) DLBCL.
A total of 117,334 differentially methylated probes were identified between EBV(+) and EBV(-) DLBCL, impacting 1557 cancer-associated genes.
Pathway analysis revealed hypermethylation in P53 feedback loops and hypomethylation in MAPK signaling in EBV(+) DLBCL.

Conclusions:

EBV(+) DLBCL is epigenetically distinct from EBV(-) DLBCL, characterized by significant DNA methylation alterations.
These epigenetic differences may contribute to the clinical heterogeneity observed in DLBCL subtypes.
Identified epigenetic alterations could serve as potential biomarkers for DLBCL classification and therapeutic targeting.