HBV VIS Detail Information

> This page shows VIS [1017852] detail information, including site information (chromosome, GRCh38 location, disease, sample, etc) and literature information.

Site Information

Literature Information

PubMed PMID	27703150
Published year	2016
Journal	Nature communications
Title	Genomic and oncogenic preference of HBV integration in hepatocellular carcinoma.
Author	Zhao LH,Liu X,Yan HX,Li WY,Zeng X,Yang Y,Zhao J,Liu SP,Zhuang XH,Lin C,Qin CJ,Zhao Y,Pan ZY,Huang G,Liu H,Zhang J,Wang RY,Yang Y,Wen W,Lv GS,Zhang HL,Wu H,Huang S,Wang MD,Tang L,Cao HZ,Wang L,Lee TL,Jiang H,Tan YX,Yuan SX,Hou GJ,Tao QF,Xu QG,Zhang XQ,Wu MC,Xu X,Wang J,Yang HM,Zhou WP,Wang HY
Evidence	Hepatitis B virus (HBV) can integrate into the human genome, contributing to genomic instability and hepatocarcinogenesis. Here by conducting high-throughput viral integration detection and RNA sequencing, we identify 4,225 HBV integration events in tumour and adjacent non-tumour samples from 426 patients with HCC. We show that HBV is prone to integrate into rare fragile sites and functional genomic regions including CpG islands. We observe a distinct pattern in the preferential sites of HBV integration between tumour and non-tumour tissues. The overall HBV integration frequency is much higher in tumour genomes of males than in females, with a significant enrichment of integration into chromosome 17. Furthermore, a cirrhosis-dependent HBV integration pattern is observed, affecting distinct targeted genes. Our data suggest that HBV integration has a high potential to drive oncogenic transformation.