作者: Atsushi Kaneda , Keisuke Matsusaka , Hiroyuki Aburatani , Masashi Fukayama
DOI: 10.1158/0008-5472.CAN-11-3919
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摘要: Epstein-Barr virus (EBV) establishes latent infection and is associated with tumors, such as Burkitt lymphoma, nasopharyngeal carcinoma, gastric cancers. We recently reported that EBV(+) cancer shows an EBV(+)/extensively high-methylation epigenotype, in vitro EBV induces extensive DNA methylation gene repression within 18 weeks. On the basis of absence both accumulation surrounding mucosa cancer, it suggested EBV-infected cell acquires to silence multiple tumor suppressor genes a short time period transforms into cells, not forming precancerous field or accumulation. The mechanism induced by has been fully clarified. Differences genome are dependent on different latency status other epigenomic alterations, 3-dimensional conformation histone modification, may affect host methylation. Expressions viral proteins small RNAs also depending status, some might trigger inducing methyltransferase overexpression. In this review, we discuss these roles driving tumorigenesis their possible association aberrant