EBV VIS Detail Information

> This page shows VIS [3001104] detail information, including site information (chromosome, GRCh38 location, disease, sample, etc) and literature information.

Site Information

Literature Information

PubMed PMID	30867819
Published year	2019
Journal	Theranostics
Title	Genome-wide profiling of Epstein-Barr virus integration by targeted sequencing in Epstein-Barr virus associated malignancies.
Author	Xu M,Zhang WL,Zhu Q,Zhang S,Yao YY,Xiang T,Feng QS,Zhang Z,Peng RJ,Jia WH,He GP,Feng L,Zeng ZL,Luo B,Xu RH,Zeng MS,Zhao WL,Chen SJ,Zeng YX,Jiao Y
Evidence	A less well-studied mechanism is the integration of EBV into the human genome possibly at sites which may disrupt gene expression or genome stability. Bioinformatic analysis was used to detect the breakpoints of EBV integrations in the genome of cancer cells. EBV integrations were enriched at vulnerable regions of the human genome and were close to tumor suppressor and inflammation-related genes. We found that EBV integrations into the introns could decrease the expression of the inflammation-related genes, TNFAIP3, PARK2, and CDK15, in NPC tumors. These breakpoints were surrounded by microhomology sequences, consistent with a mechanism for integration involving viral genome replication and microhomology-mediated recombination. Conclusion: Our finding provides insight into the potential of EBV integration as an additional mechanism mediating tumorigenesis in EBV associated malignancies.