HBV VIS Detail Information

> This page shows VIS [1009699] detail information, including site information (chromosome, GRCh38 location, disease, sample, etc) and literature information.

Site Information

DVID	1009699
VISID	TVIS10018424
Chromosome	chr3
GRCh38 Location	81724579
Disease	Hepatocellular carcinoma
Sample	Nontumor
Virus Reference Genome	NC_003977
Target Gene	GBE1

Literature Information

PubMed PMID	29212479
Published year	2017
Journal	BMC medicine
Title	A pilot systematic genomic comparison of recurrence risks of hepatitis B virus-associated hepatocellular carcinoma with low- and high-degree liver fibrosis.
Author	Yoo S,Wang W,Wang Q,Fiel MI,Lee E,Hiotis SP,Zhu J
Evidence	However, how HBV integration and other genomic changes contribute to the risk of tumor recurrence with regards to the different degree of liver fibrosis is not clearly understood. RESULTS: We developed a robust pipeline for sensitively identifying HBV integration sites based on sequencing data. When applying it to other RNA sequencing datasets, consistently more HBV integrations were identified in non-neoplastic liver than in tumor tissues. More significant enrichment of tumor suppressor genes was observed among HBV host genes identified from patients with tumor recurrence, indicating the potential risk of tumor recurrence driven by HBV integration in non-neoplastic liver tissues. Additionally, HBV host genes identified in non-neoplastic liver tissues significantly overlapped with pathogenic somatic mutations, suggesting that HBV integration and somatic mutations targeting the same set of genes are important to tumorigenesis. HBV integrations and pathogenic mutations showed distinct patterns between low and high liver fibrosis patients with regards to tumor recurrence. CONCLUSIONS: The results suggest that HBV integrations and pathogenic SNPs in non-neoplastic tissues are important for tumorigenesis and different recurrence risk models are needed for patients with low and high degrees of liver fibrosis.