抄録
Abnormal β-catenin protein accumulation in cytoplasm or nucleus with somatic mutation of β-catenin has been reported to be very frequent in hepatoblastomas (HBs) both in humans and in experimental animals. Recently we noted HBs developing in an evaluation of the carcinogenicity of N, N-dimethylformamide (DMF) in a 104 week mouse inhalation study1 performed by the Japan Bioassay Research Center. In the present study we evaluated β-catenin mutations in mouse HBs induced by DMF, which is considered to be a non-genotoxic carcinogen. Immunohistochemistry and polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP) analyses were performed using formalin-fixed and paraffin-embedded sections. No abnormal β-catenin accumulation or no apparent mutation was detected, and these findings point to functional normality of the Wnt signal pathway in these HBs induced by DMF. Our results raise questions as to the general nature of any relationship between HB and abnormal β-catenin accumulation.