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SHR Neuro Krebs Kardio Lipid Stoffw Microb

Vucur, M; Roderburg, C; Bettermann, K; Tacke, F; Heikenwalder, M; Trautwein, C; Luedde, T.
Mouse models of hepatocarcinogenesis: what can we learn for the prevention of human hepatocellular carcinoma?
Oncotarget. 2010; 1(5):373-378 Doi: 10.18632/oncotarget.170 [OPEN ACCESS]
Web of Science PubMed PUBMED Central FullText FullText_MUG

 

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Bettermann Kira
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Abstract:
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.
Find related publications in this database (using NLM MeSH Indexing)
Animals -
Anti-Inflammatory Agents - therapeutic use
Carcinoma, Hepatocellular - enzymology
Cell Transformation, Neoplastic - drug effects
Disease Models, Animal -
Hepatitis - drug therapy
Humans -
Inflammation Mediators - metabolism
Liver - drug effects
Liver Neoplasms - enzymology
MAP Kinase Kinase Kinases - deficiency
Mice -
Mice, Knockout -
NF-kappa B - metabolism
Signal Transduction - drug effects

Find related publications in this database (Keywords)
HCC
mouse models
TAK1
DEN
inflammation
signaling
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