Fig. 1
Most HBV DNA integration occurs before HBeAg seroconversion and contributes to carcinogenesis in half of HBCV-HCC cases through similar insertional mutagenesis mechanisms as in HBV-HCC. A Detection rate of clonal HBV DNA integration in virus-related HCCs. B Distribution of HBV breakpoints of integrated HBV in int(+) HBV-HCCs and int(+) HBCV-HCCs. The height of the bar indicates the frequency of junction breakpoint detected at each nucleotide in the HBV genome. C Distribution of HBV-human junction in the human chromosome in int(+) HBV-HCCs and int(+) HBCV-HCCs. The height of the bar indicates the frequency of junction detected in the window of 106 nucleotides in the human genome. D, E Detection rates of (D) HBV-TERT and (E) HBV-MLL4 in int(+) HBV-HCCs and int(+) HBCV-HCCs (left panel) and the distribution of junction breakpoints within the indicated genes (right panel). The X-axis represents the gene position, with exon regions shaded in gray. F, G (F) The PC mutation rate and (G) BCP mutation rate for integrated HBV in int(+) HBV-HCCs and int(+) HBCV-HCCs. (***, P < 0.001; ns, no significant difference.)