Additional file 1: of Viral integration drives multifocal HCC during the occult HBV infection
- Resource Type
- Authors
- Chen, Xiao-Ping; Long, Xin; Jia, Wen-Long; Han-Jie Wu; Zhao, Jing; Liang, Hui-Fang; Laurence, Arian; Zhu, Jun; Dong, Dong; Chen, Yan; Lin, Long; Xia, Yu-Dong; Li, Wei-Yang; Gui-Bo Li; Zhao, Zhi-Kun; Wu, Kui; Hou, Yong; Yu, Jing-Jing; Xiao, Wei; Wang, Guo-Ping; Zhu, Peng-Cheng; Chen, Wei; Bai, Ming-Zhou; Jian, Yi-Xing; Kristiansen, Karsten; Chen, Qian
- Source
- Subject
- digestive system diseases
- Language
Figure S1. HBV breakpoint detection workflow from sequencing reads in FuseSV. Figure S2. HBV sub-genotype tree in host by VCS analysis. Figure S3. Constructing HBV genomes in tumors by VCS analysis. Figure S4. Comparison of genome-wide somatic SNVs among the six tumor specimens. Figure S5. Comparison of genome-wide copy number in six tumor specimens. Figure S6. EXT1 expression in hepatic or HCC cell lines by western blot. Figure S7. EXT1 affects HCC growth in vitro. Figure S8. EXT1 does not affect HCC cell migration in vitro. Table S1. Clinicopathologic features of the HBV patient with multiple HCC. Table S2. Sequencing data summary and HBV genome details of ten specimens. Table S3. VCS data summary and constructed HBV genome details of 264 single cells. Table S4. Alterations on HBV_B2 genome in ten specimens. Table S5. Homologous sequences at the junction sites of minor viral integration and HBV rearrangement cases. Table S6. Copy number alterations of six tumor specimens. Table S7. Somatic structure variations of six tumor specimens. (PDF 5584 kb)