Open AccessMouse models of hepatocarcinogenesis: what can we learn for the prevention of human hepatocellular carcinoma?
Author(s) -
Mihael Vucur,
Christoph Roderburg,
Kira Bettermann,
Frank Tacke,
Mathias Heikenwälder,
Christian Trautwein,
Tom Luedde
Publication year - 2010
Publication title -
pubmed
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.373
H-Index - 127
eISSN - 1949-2553
DOI - 10.18632/oncotarget.100906
Subject(s) - hepatocellular carcinoma , liver cancer , knockout mouse , medicine , cancer research , inflammation , cancer , fibrosis , biology , pathology , immunology , receptor
There is growing evidence that chronic inflammatory processes are involved in triggering the sequence from chronic liver injury to liver fibrosis, ultimately leading to liver cancer. In the last years this process has been recapitulated in a growing number of different mouse models. However, it has remained unclear whether and how these mouse models reflect the clinical reality of human hepatocellular carcinoma (HCC). Research with animal models but also human liver specimens has indicated that the NF-κB signaling pathway might withhold a crucial function in the mediation of chronic hepatic inflammation and the transition to HCC in humans. However, previous studies led to divergent and partly conflicting results with regards to the functional role of NF-κB in hepatocarcinogenesis. Here, we discuss a new genetic mouse model for HCC, the liver-specific TAK1 knockout mouse, which lacks the NF-κB activating kinase TAK1 specifically in parenchymal liver cells. Molecular findings in this mouse model and their possible significance for chemopreventive strategies against HCC are compared to other murine HCC models.