HBV VIS Detail Information

> This page shows VIS [1001007] detail information, including site information (chromosome, GRCh38 location, disease, sample, etc) and literature information.

Site Information

DVID	1001007
VISID	TVIS10010683
Chromosome	chr17
GRCh38 Location	31269955
Disease	Hepatocellular carcinoma
Sample	Nontumor
Virus Reference Genome	NC_003977
Target Gene	NF1

Literature Information

PubMed PMID	30271481
Published year	2018
Journal	Journal of Cancer
Title	Molecular Characterization of HBV DNA Integration in Patients with Hepatitis and Hepatocellular Carcinoma.
Author	Yang L,Ye S,Zhao X,Ji L,Zhang Y,Zhou P,Sun J,Guan Y,Han Y,Ni C,Hu X,Liu W,Wang H,Zhou B,Huang J
Evidence	Viral DNA integration into the host cell genome is a key mechanism of hepatocarcinogenesis. However, the molecular characterization and the potential clinical implications of HBV DNA integration into patients suffering from different hepatitis and HCC remain unclear. In this study, we analyzed HBV integrations in patients with hepatitis B and HCC using HBV probe-based capturing and next-generation sequencing. The results revealed that the sizes of the HBV integrations ranged from 28 bp to 3215 bp, including the full-length HBV DNA sequence. The integration breakpoints were preferentially distributed in the viral enhancer, X protein, and core protein regions of the HBV genome. The number of HBV integrations followed an increasing trend from hepatitis to HCC, which was positively correlated with the HBV virus load in patients with hepatitis. The number of HBV integrations in the HBeAg positive chronic hepatitis B group was significantly greater than that in the other hepatitis B groups (P < 0. However, the relative abundance of HBV integrations was significantly higher in HCC tissues than in the adjacent liver tissues.6% (8/13) of HBV-human DNA integration fragments could be detected at the RNA level. Our results also showed that HBV integration-targeted genes (ITGs) were significantly enriched in many cancer-related pathways, such as MAPK, extracellular matrix (ECM)-receptor interaction, and the hedgehog signaling pathway. Individuals with HBV integrations exhibited shorter disease-free survival (DFS) and overall survival (OS) than those without HBV integrations in some ITGs including LINC00293 (long intergenic non-protein coding RNA 293; DFS P = 0. This study determined the underlying mechanism of HBV DNA integration in liver diseases and laid the foundation for future studies on the pathogenesis of liver cancer.