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HBV integrations reshaping genomic structures promote hepatocellular carcinoma.

Zhaoyang Qian1,2, Junbo Liang3, Rong Huang3,4

  • 1Department of Hepatobiliary Surgery, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.

Gut
|February 23, 2024
PubMed
Summary

Hepatitis B virus (HBV) integrations extensively alter cancer genomes, driving hepatocellular carcinoma (HCC) development. These HBV DNA integrations can lead to early-onset tumors, highlighting their critical role in hepatocarcinogenesis.

Keywords:
CARCINOGENESISGENE MUTATIONHEPATOCELLULAR CARCINOMA

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Area of Science:

  • Genomics
  • Oncology
  • Hepatology

Background:

  • Hepatocellular carcinoma (HCC) is frequently associated with Hepatitis B virus (HBV) integrations.
  • Previous research focused on limited HBV integration hotspots, leaving the oncogenic role of other integrations unclear.

Purpose of the Study:

  • To investigate the comprehensive impact of HBV integrations on hepatocellular carcinoma (HCC) development.
  • To elucidate the mechanisms by which HBV integrations contribute to tumourigenesis.

Main Methods:

  • Whole genome sequencing and Nanopore long reads were used to analyze HBV integrations in 124 HCCs.
  • A CRISPR-based genetic screen in mouse hepatocytes identified candidate genes involved in HBV integration-mediated oncogenesis.
  • CRISPR/Cas9 editing was employed to validate the oncogenic potential of specific amplified genes.

Main Results:

  • HBV integrations exhibit complex genomic rearrangements, including bridge-fusion-bridge patterns and translocations.
  • These rearrangements are linked to copy number variations in key cancer driver genes (e.g., TERT, CDKN2A/B, TP53, RB1) and early amplifications in chr8q.
  • HBV integrations correlate with younger age, higher HBV DNA levels, TP53 mutations, and are less common after antiviral therapy.
  • Amplification of TONSL and TMEM65 in chr8q, driven by HBV integration, demonstrated tumourigenic potential in mouse models.

Conclusions:

  • HBV integrations significantly reshape host genomes, promoting hepatocarcinogenesis.
  • These genomic alterations can occur early in the development of HCC.
  • Understanding HBV integration patterns provides insights into HCC pathogenesis and potential therapeutic targets.