Table 1. Selection of mouse models of hepatocellular carcinoma*.
| Inflammatory models (Tumors arise in chronically inflamed liver) |
Non-inflammatory models (Tumors induction provokes inflammation) |
|---|---|
| NemoΔLPC (hepatocyte-specific deletion of NFκB mediated signaling: steatosis, fibrosis, slow-progressing tumors) | DEN** (alkylating DNA structures: slow-progressing tumors; different application and dosing schedules published) |
| Tak1ΔLPC (hepatocyte-specific deletion of the upstream kinase Tak1: cholestasis, fibrosis, fast-progressing tumors) | (Liver-specific) overexpression of oncogenes: MYC; MET; β catenin, NrasG12V… |
| AlbLTαβ (hepatocyte-specific overexpression of lymphotoxin: hepatitis, slow-progressing tumors) | (Liver-specific) overexpression of growth factors: EGF; FGF19; TGFα/β, epidermal growth factor… |
| Mdr2−/− (lack of biliary transporter Mdr2: cholestatic hepatitis, slow-progressing tumors) |
Abbreviations: DEN, diethylnitrosamine; EGF, epidermal growth factor; FGF19, fibroblast growth factor 19; TAK1, TGFβ-activated kinase 1; TGF, transforming growth factor. *Rough classification with respect to the origin of the cancer-associated inflammatory response; **DEN can be combined with additional inflammatory stimuli such as chronic carbon tetrachloride (CCl4) injections in order to address the impact of an inflammatory microenvironment.