HBV VIS Detail Information

> This page shows VIS [1014953] detail information, including site information (chromosome, GRCh38 location, disease, sample, etc) and literature information.

Site Information

DVID	1014953
VISID	TVIS10014863
Chromosome	chr8
GRCh38 Location	39342931
Disease	Carcinoma, Hepatocellular
Sample	Tumor
Virus Reference Genome	NC_003977.1
Target Gene	ADAM5

Literature Information

PubMed PMID	22634756
Year	2012 May 27;44(7):760-4
Journal	Nature genetics
Title	Whole-genome sequencing of liver cancers identifies etiological influences on mutation patterns and recurrent mutations in chromatin regulators.
Author	Fujimoto A,Totoki Y,Abe T,Boroevich KA,Hosoda F,Nguyen HH,Aoki M,Hosono N,Kubo M,Miya F,Arai Y,Takahashi H,Shirakihara T,Nagasaki M,Shibuya T,Nakano K,Watanabe-Makino K,Tanaka H,Nakamura H,Kusuda J,Ojima H,Shimada K,Okusaka T,Ueno M,Shigekawa Y,Kawakami Y,Arihiro K,Ohdan H,Gotoh K,Ishikawa O,Ariizumi S,Yamamoto M,Yamada T,Chayama K,Kosuge T,Yamaue H,Kamatani N,Miyano S,Nakagama H,Nakamura Y,Tsunoda T,Shibata T,Nakagawa H
Evidence	Hepatocellular carcinoma (HCC) is the third leading cause of cancer-related death worldwide. We sequenced and analyzed the whole genomes of 27 HCCs, 25 of which were associated with hepatitis B or C virus infections, including two sets of multicentric tumors. Although no common somatic mutations were identified in the multicentric tumor pairs, their whole-genome substitution patterns were similar, suggesting that these tumors developed from independent mutations, although their shared etiological backgrounds may have strongly influenced their somatic mutation patterns. Statistical and functional analyses yielded a list of recurrently mutated genes. Multiple chromatin regulators, including ARID1A, ARID1B, ARID2, MLL and MLL3, were mutated in approximately 50% of the tumors. Hepatitis B virus genome integration in the TERT locus was frequently observed in a high clonal proportion. Our whole-genome sequencing analysis of HCCs identified the influence of etiological background on somatic mutation patterns and subsequent carcinogenesis, as well as recurrent mutations in chromatin regulators in HCCs.