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  • Writer's pictureKirk T. Hartley

New Evidence of Virus Induced Cancers - EBV and Gastric Cancers

Over time, litigators dealing with cancer issues will need to become more attuned to asking plaintiffs and their doctors more questions about their history of viral diseases. Why? As we are slowly learning with Covid 19, there can be many adverse effects from a virus. Indeed, researchers have known for decades that the Epstein-Barr virus (EBV) triggers many Burkitt's lymphomas in children in hot and humid countries in Africa, as explained in this open access 2019 medical article

Now, with better scientific tools, more cancers are being traced back to an EBV trigger. In this instance, a July 27, 2020 article in Nature Genetics suggests EBV also is triggering 8-10% of gastric/stomach cancers. Interestingly, the research findings show the triggers are not DNA alternations, and instead are epigenetic events. A July 27, 2020 article at Science Daily provides a less technical summary based on the press release.

The abstract for the Nature Genetics article explains as follows the epigenetic assay method and findings:


Epstein–Barr virus (EBV) is associated with several human malignancies including 8–10% of gastric cancers (GCs). Genome-wide analysis of 3D chromatin topologies across GC lines, primary tissue and normal gastric samples revealed chromatin domains specific to EBV-positive GC, exhibiting heterochromatin-to-euchromatin transitions and long-range human–viral interactions with non-integrated EBV episomes. EBV infection in vitro suffices to remodel chromatin topology and function at EBV-interacting host genomic loci, converting H3K9me3+ heterochromatin to H3K4me1+/H3K27ac+ bivalency and unleashing latent enhancers to engage and activate nearby GC-related genes (for example TGFBR2 and MZT1). Higher-order epigenotypes of EBV-positive GC thus signify a novel oncogenic paradigm whereby non-integrative viral genomes can directly alter host epigenetic landscapes (‘enhancer infestation’), facilitating proto-oncogene activation and tumorigenesis."

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