Erratum: Genomic and oncogenic preference of HBV integration in hepatocellular carcinoma

نویسندگان

  • Ling-Hao Zhao
  • Xiao Liu
  • He-Xin Yan
  • Wei-Yang Li
  • Xi Zeng
  • Yuan Yang
  • Jie Zhao
  • Shi-Ping Liu
  • Xue-Han Zhuang
  • Chuan Lin
  • Chen-Jie Qin
  • Yi Zhao
  • Ze-Ya Pan
  • Gang Huang
  • Hui Liu
  • Jin Zhang
  • Ruo-Yu Wang
  • Yun Yang
  • Wen Wen
  • Gui-Shuai Lv
  • Hui-Lu Zhang
  • Han Wu
  • Shuai Huang
  • Ming-Da Wang
  • Liang Tang
  • Hong-Zhi Cao
  • Ling Wang
  • T P Lee
  • Hui Jiang
  • Ye-Xiong Tan
  • Sheng-Xian Yuan
  • Guo-Jun Hou
  • Qi-Fei Tao
  • Qin-Guo Xu
  • Xiu-Qing Zhang
  • Meng-Chao Wu
  • Xun Xu
  • Jun Wang
  • Huan-Ming Yang
  • Wei-Ping Zhou
  • Hong-Yang Wang
چکیده

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.

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عنوان ژورنال:

دوره 7  شماره 

صفحات  -

تاریخ انتشار 2016