Abstract
Introduction: The Wnt/Beta-catenin signaling pathway has been identified as a critical molecular regulator of hepatic development, regeneration and carcinogenesis. Hepatic oval cells are a transiently amplifying progenitor population that proliferates in the liver during chronic injury. Hepatocarcinogenesis occurs with a prolonged latency in the setting of chronic liver stimulation by either hepatotoxins or viral hepatitis infection. We hypothesized therefore, that expansion of the liver stem cell compartment through Wnt signal transduction would cooperate with oncogenic MYC to shorten the latency of hepatic tumorigenesis in an established mouse model.
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