ArticleGenes2026
Epigenetics and DNA Base Substitutions of Epstein-Barr Virus (EBV)-Related Gastric Cancers: Implications for Targeted Therapies.
Article in Genes, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundGastric adenocarcinomas constitute a histologically and genomically heterogeneous group of cancers. The genomic classification of gastric cancers in four groups by The Cancer Genome Atlas (TCGA) has defined a framework for pathogenic discoveries. One of the groups is associated with infection by the gamma herpes virus Epstein-Barr virus (EBV) and represents a distinct subset of gastric cancers with potential therapeutic opportunities.
methodsThe EBV-associated cancers from the TCGA gastric cancer cohort were analyzed to determine specific mutational and mRNA expression profiles that set these cancers apart from other gastric cancer subtypes. The cBioportal for Cancer Genomics site was used for downloading and analyzing the primary data.
resultsEBV-associated cancers represented about 7% of the cohort. Mutations in the catalytic alpha subunit of PI3K kinase,
conclusionsThe data presented here suggest that mutagenesis in the EBV-associated gastric cancers is not a direct consequence of the virus-derived hypermethylation. Up-regulation of kinase PI3K and its pathway is a prerequisite for EBV transformation, and epigenetic alterations are frequently present, suggesting therapeutic avenues.
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