HBV VIS Detail Information

> This page shows VIS [1016105] detail information, including site information (chromosome, GRCh38 location, disease, sample, etc) and literature information.

Site Information

Literature Information

PubMed PMID	22634754
Year	2012 May 27;44(7):765-9
Journal	Nature genetics
Title	Genome-wide survey of recurrent HBV integration in hepatocellular carcinoma.
Author	Sung WK,Zheng H,Li S,Chen R,Liu X,Li Y,Lee NP,Lee WH,Ariyaratne PN,Tennakoon C,Mulawadi FH,Wong KF,Liu AM,Poon RT,Fan ST,Chan KL,Gong Z,Hu Y,Lin Z,Wang G,Zhang Q,Barber TD,Chou WC,Aggarwal A,Hao K,Zhou W,Zhang C,Hardwick J,Buser C,Xu J,Kan Z,Dai H,Mao M,Reinhard C,Wang J,Luk JM
Evidence	To survey hepatitis B virus (HBV) integration in liver cancer genomes, we conducted massively parallel sequencing of 81 HBV-positive and 7 HBV-negative hepatocellular carcinomas (HCCs) and adjacent normal tissues. We found that HBV integration is observed more frequently in the tumors (86.4%) than in adjacent liver tissues (30.7%). Copy-number variations (CNVs) were significantly increased at HBV breakpoint locations where chromosomal instability was likely induced. Approximately 40% of HBV breakpoints within the HBV genome were located within a 1,800-bp region where the viral enhancer, X gene and core gene are located. We also identified recurrent HBV integration events (in >/= 4 HCCs) that were validated by RNA sequencing (RNA-seq) and Sanger sequencing at the known and putative cancer-related TERT, MLL4 and CCNE1 genes, which showed upregulated gene expression in tumor versus normal tissue. We also report evidence that suggests that the number of HBV integrations is associated with patient survival.