Abstract:
: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. HBV insertional sites are significantly enriched in the proximity of telomeres in tumours. Recurrent HBV target genes are identified with few that overlap. 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.
journal_name
Nat Communjournal_title
Nature communicationsauthors
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 TLdoi
10.1038/ncomms12992subject
Has Abstractpub_date
2016-10-05 00:00:00pages
12992issn
2041-1723pii
ncomms12992journal_volume
7pub_type
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