@article{Jiang01042012,
author = {Jiang, Zhaoshi and Jhunjhunwala, Suchit and Liu, Jinfeng and Haverty, Peter M. and Kennemer, Michael I. and Guan, Yinghui and Lee, William and Carnevali, Paolo and Stinson, Jeremy and Johnson, Stephanie and Diao, Jingyu and Yeung, Stacy and Jubb, Adrian and Ye, Weilan and Wu, Thomas D. and Kapadia, Sharookh B. and de Sauvage, Frederic J. and Gentleman, Robert C. and Stern, Howard M. and Seshagiri, Somasekar and Pant, Krishna P. and Modrusan, Zora and Ballinger, Dennis G. and Zhang, Zemin}, 
title = {The effects of hepatitis B virus integration into the genomes of hepatocellular carcinoma patients},
volume = {22}, 
number = {4}, 
pages = {593-601}, 
year = {2012}, 
doi = {10.1101/gr.133926.111}, 
abstract ={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.}, 
URL = {http://genome.cshlp.org/content/22/4/593.abstract}, 
eprint = {http://genome.cshlp.org/content/22/4/593.full.pdf+html}, 
journal = {Genome Research} 
}