| Literature DB >> 22634754 |
Wing-Kin Sung1, Hancheng Zheng, Shuyu Li, Ronghua Chen, Xiao Liu, Yingrui Li, Nikki P Lee, Wah H Lee, Pramila N Ariyaratne, Chandana Tennakoon, Fabianus H Mulawadi, Kwong F Wong, Angela M Liu, Ronnie T Poon, Sheung Tat Fan, Kwong L Chan, Zhuolin Gong, Yujie Hu, Zhao Lin, Guan Wang, Qinghui Zhang, Thomas D Barber, Wen-Chi Chou, Amit Aggarwal, Ke Hao, Wei Zhou, Chunsheng Zhang, James Hardwick, Carolyn Buser, Jiangchun Xu, Zhengyan Kan, Hongyue Dai, Mao Mao, Christoph Reinhard, Jun Wang, John M Luk.
Abstract
To survey hepatitis B virus (HBV) integration in liver cancer genomes, we conducted massively parallel sequencing of 81 HBV-positive and 7 HBV-negative hepatocellular carcinomas (HCCs) and adjacent normal tissues. We found that HBV integration is observed more frequently in the tumors (86.4%) than in adjacent liver tissues (30.7%). Copy-number variations (CNVs) were significantly increased at HBV breakpoint locations where chromosomal instability was likely induced. Approximately 40% of HBV breakpoints within the HBV genome were located within a 1,800-bp region where the viral enhancer, X gene and core gene are located. We also identified recurrent HBV integration events (in ≥ 4 HCCs) that were validated by RNA sequencing (RNA-seq) and Sanger sequencing at the known and putative cancer-related TERT, MLL4 and CCNE1 genes, which showed upregulated gene expression in tumor versus normal tissue. We also report evidence that suggests that the number of HBV integrations is associated with patient survival.Entities:
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Year: 2012 PMID： 22634754 DOI： 10.1038/ng.2295
Source DB: PubMed Journal: Nat Genet ISSN： 1061-4036 Impact factor: 38.330