Anti-platelet therapy in the prevention of hepatitis B virus-associated hepatocellular carcinoma

Research output: Contribution to journalArticlepeer-review


Previous studies in mouse models of self-limited viral hepatitis showed that platelets contribute to acute liver damage by promoting the intrahepatic accumulation of virus-specific CD8 T cells and, secondarily, virus-non-specific inflammatory cells. Built on these observations, a recent preclinical study took advantage of a previously established hepatitis B virus (HBV) transgenic mouse model of immune-mediated chronic hepatitis that progresses to hepatocellular carcinoma (HCC), to demonstrate that clinically achievable doses of the anti-platelet drugs aspirin and clopidogrel - administered continuously after the onset of liver disease - can prevent hepatocarcinogenesis and greatly improve overall survival. These outcomes were preceded by and associated with reduced hepatic accumulation of virus-specific CD8 T cells and virus-non-specific inflammatory cells, reduced hepatocellular injury and hepatocellular proliferation, and reduced severity of liver fibrosis. The observation that anti-platelet therapy inhibits HCC development identifies platelets as key players in the pathogenesis of HBV-associated liver cancer and supports the notion that a sustained immune-mediated necroinflammatory liver disease is sufficient to trigger HCC. The results abovementioned and their clinical implications are discussed in this report.

Original languageEnglish
Pages (from-to)1135-1138
Number of pages4
JournalJournal of Hepatology
Issue number5
Publication statusPublished - Nov 2013


  • Anti-platelet drugs
  • CD8 T cells
  • Hepatitis B virus
  • Hepatocellular carcinoma
  • Platelets
  • Viral hepatitis

ASJC Scopus subject areas

  • Hepatology


Dive into the research topics of 'Anti-platelet therapy in the prevention of hepatitis B virus-associated hepatocellular carcinoma'. Together they form a unique fingerprint.

Cite this