Abstract
Introduction: In most patients, hepatocellular carcinoma (HCC) develops as a consequence of advanced fibrosis but the mechanisms are still incompletely understood. Recently it has been shown that initiation of HCC can be modelled by a single dose of the hepatocarcinogen diethylnitrosamine (DEN) in mice (Naugler et al. Science 2007). ABCB4-deficient mice develop biliary liver fibrosis and can be used as a spontaneous model to dissect profibrotic pathways. To investigate the early events in hepatocarcinogenesis, our aim now was to examine tumour initiation in ABCB4-deficient mice.
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