Re-analysis of hepatitis B virus integration sites reveals potential new loci associated with oncogenesis in hepatocellular carcinoma

Figure 1 Hepatitis B virus integration breakpoints across the reference genomes. A: Integration breakpoints in the human reference genomes in tumor and non-tumor samples; B: Circos plot of integration breakpoints. Red represents tumor samples, and blue represents non-tumor samples; C: Hepatitis B virus genome integration breakpoints. T: Tumor; N: Non-tumor.

Figure 2 Integration breakpoints at chromosome 11. A: Circos plot of breakpoints at chromosome 11 in the human reference genomes; B: Integration breakpoints around 11q13.3 in relation to coding genes retrieved from Ensembl. Red represents tumor samples, and blue represents non-tumor samples; C: Comparison of integration breakpoints around 11q13.3 in the tumor samples. Actual represents actual number of integration breakpoints. Expected represents expected number of integration breakpoints assuming random distribution; D: Copy number of liver cancer samples from cBioPortal[18,19]. Red represents amplification, and blue represents deletion. E: Distribution of the number of fragments that provide breakend for the variant allele. T: Tumor; NT: Non-tumor.

Figure 3 Integration breakpoints in the mitochondrial genome. A: The upper panel displays integration breakpoints across mitochondrial genomes according to tumor and non-tumor samples, and the lower panel shows integration breakpoints along the human and hepatitis B virus genomes. Red represents tumor samples, and blue represents non-tumor samples; B: Integration breakpoints on the mitochondrial genome annotated using UCSC genome browser (NT: Non-tumor; T: Tumor)[22].