Table 1.

Genetic background and phenotypic presentation of mouse models

ModelGenetic backgroundModePhenotype of tumors as originally documentedPhenotype of surrounding liver tissue as originally documentedAverage age at tumor developmentReference
DEN wtC57BL/6/129Chemically induced DNA damage (DEN)Incidence lower in female animals and younger animals, typical liver histologyLiver injury and cell death, proliferative response8–10 monthsMaeda et al. 2005
c-MycC57BL/6J-CBA/JTransgenic model with oncogene overexpression leading to genomic instabilitySolid or trabecular histologic type, atypia, polymorphism, hemorrhagic necrosisTransition of mild to severe dysplasia in hepatocytes, benign lesion ("adenoma")12–15 monthsThorgeirsson et al. 1996
TAK1LPC-KOC57BL/6-SV129OlaKnockout model with TAK1 deficiency, enhanced liver cell proliferationDuctopenia, fibrosis, liver cell apoptosis, necrosis, hyperproliferationExpansive growth, high cellularity, anisokaryosis of hepatocytes4 monthsBettermann et al. 2010 Vucur et al. 2013
AlbLTαβCL57BL/6Transgenic model with overexpression of cytokines, indirectly leading to cell damageMulticentric nodules in tg 1223 mice, high proliferation, loss of collagen IV networkInfiltration of lymphocytes and macrophages, increased proliferation (A6+ cells)12 monthsHaybaeck et al. 2009
Mcl-1ΔhepC57BL/6Deficiency of antiapoptotic Mcl-1 with enhanced liver cell apoptosis and hyperproliferationAltered liver architecture, cellular atypia, loss of collagen IV, immunoreactivity for glutamine synthetaseApoptosis, pericellular fibrosis, enhanced proliferation12 monthsVick et al. 2009 Weber et al. 2010 Boege et al. 2017