TY  - JOUR
A1  - Jiang, Zhaoshi
A1  - Jhunjhunwala, Suchit
A1  - Liu, Jinfeng
A1  - Haverty, Peter M.
A1  - Kennemer, Michael I.
A1  - Guan, Yinghui
A1  - Lee, William
A1  - Carnevali, Paolo
A1  - Stinson, Jeremy
A1  - Johnson, Stephanie
A1  - Diao, Jingyu
A1  - Yeung, Stacy
A1  - Jubb, Adrian
A1  - Ye, Weilan
A1  - Wu, Thomas D.
A1  - Kapadia, Sharookh B.
A1  - de Sauvage, Frederic J.
A1  - Gentleman, Robert C.
A1  - Stern, Howard M.
A1  - Seshagiri, Somasekar
A1  - Pant, Krishna P.
A1  - Modrusan, Zora
A1  - Ballinger, Dennis G.
A1  - Zhang, Zemin
T1  - The effects of hepatitis B virus integration into the genomes of hepatocellular carcinoma patients
Y1  - 2012/04/01 
JF  - Genome Research 
JO  - Genome Research 
SP  - 593 
EP  - 601 
DO  - 10.1101/gr.133926.111 
VL  - 22 
IS  - 4 
UR  - http://genome.cshlp.org/content/22/4/593.abstract 
N2  - Hepatitis B virus (HBV) infection is a leading risk factor for hepatocellular carcinoma (HCC). HBV integration into the host genome has been reported, but its scale, impact and contribution to HCC development is not clear. Here, we sequenced the tumor and nontumor genomes (>80× coverage) and transcriptomes of four HCC patients and identified 255 HBV integration sites. Increased sequencing to 240× coverage revealed a proportionally higher number of integration sites. Clonal expansion of HBV-integrated hepatocytes was found specifically in tumor samples. We observe a diverse collection of genomic perturbations near viral integration sites, including direct gene disruption, viral promoter-driven human transcription, viral-human transcript fusion, and DNA copy number alteration. Thus, we report the most comprehensive characterization of HBV integration in hepatocellular carcinoma patients. Such widespread random viral integration will likely increase carcinogenic opportunities in HBV-infected individuals. 
ER  -