Fukayama Masashi
Department of Pathology, University of Tokyo, Graduate School of Medicine.
Nihon Rinsho. 2012 Oct;70(10):1715-9.
Epstein-Barr virus (EBV)-associated gastric carcinoma (GC), comprising nearly 10% of all cases of GC, is the monoclonal growth of EBV-infected epithelial cells, which express a limited number of EBV-latent genes(latency I program). The primary molecular abnormality in EBV-associated GC is the epigenetic abnormality, that is, global CpG island methylation in the promoter region of many cancer-related genes. Experimental infection of EBV induced this EBV-specific epigenotype in addition to gastric cancer epigenotype in gastric cancer cells. Viral latent membrane protein 2A (LMP2A) is partly responsible for the promotion of DNA methylation, through STAT3-mediated up-regulation of DNMT1. Such a mechanism may be the overdrive of interaction between virus and infected cells.
爱泼斯坦-巴尔病毒(EBV)相关的胃癌(GC)占所有胃癌病例的近10%,是EBV感染的上皮细胞的单克隆生长,这些细胞表达有限数量的EBV潜伏基因(潜伏I程序)。EBV相关胃癌的主要分子异常是表观遗传异常,即许多癌症相关基因启动子区域的整体CpG岛甲基化。EBV的实验性感染除了在胃癌细胞中诱导胃癌表观基因型外,还诱导了这种EBV特异性表观基因型。病毒潜伏膜蛋白2A(LMP2A)部分负责通过STAT3介导的DNMT1上调促进DNA甲基化。这种机制可能是病毒与受感染细胞之间相互作用的过度驱动。