Mouse hepatoblastoma models with expression of mutant β-catenin and/or c-Myc for therapeutic target identification of childhood liver cancer. Mus musculus

Hepatoblastoma (HB), the most common type of pediatric liver cancer, is associated with aberrant wnt/β-catenin activation and Myc amplification/overexpression. Mice expressing both alleles developed HBs and HCCs with incomplete penetrance by 5-6 weeks of age with fetal and mixed fetal/embryonal HBs, the most prevalent histologic HB subtypes seen in children being the predominant tumor types. To address the roles of mutant wnt/β-catenin activation and Myc over-expression in the pathogenesis of HB, c-Myc and mutant dominant-stable β-catenin were co-targeted to immature cells of the developing mouse liver. Overall design: Whole genome gene expression profiling with Agilent 1 color protocol were performed to total of 11 samples (4 Wild types, 3 with mutant beta-catenin expression, and 4 with c-Myc expression) derived from tumor-bearing livers.