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Toxicologic Pathology
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Articles

Absence of β-Catenin Alteration in Hepatic Tumors Induced by p-Nitroanisole in Crj:BDF1 Mice

Masahiko Kushida1, Sigetoshi Aiso2, Keiichirou Morimura1, Min Wei1, Hideki Wanibuchi1, Kasuke Nagano2 and Shoji Fukushima1

1 Department of Pathology, Osaka City University Medical School, Abeno-ku, Osaka 545-8585, Japan
2 Division of Pathology, Japan Bioassay Research Center, Hadano, Kanagawa 257-0015, Japan

Correspondence: Address correspondence to: Shoji Fukushima, Department of Pathology, Osaka City University Medical School, 1-4-3, Asahi-machi, Abeno-ku, Osaka, Japan, 545-8585; e-mail:fukuchan{at}med.osaka-cu.ac.jp

In the present study, β-catenin localization in hepatocellular neoplasms and hepatoblastomas, induced by oral administration of p-Nitroanisole (pNA) in Crj:BDF1 for 2 years, was evaluated by immunohistochemistry along with genetic alterations in exon 2 of β-catenin by the polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP) approach. Genomic DNA was isolated from paraffin sections of a total of 53 liver tumors. Immunohistochemical analysis revealed no abnormal accumulation of the β-catenin protein in any of the cases. No mutations (0/13), 20% silent mutations (3/15) and 8% silent plus 12% functional mutations (2 + 3/25), not in the multiple phosphorylation sites of β-catenin, were observed in hepatocellular adenomas, carcinomas and hepatoblastomas, respectively. The results indicate that β-catenin does not play an important role in development of hepatic tumors induced by pNA in Crj:BDF1 mice.

Key Words: β-Catenin alteration • p-Nitroanisol carcinogenicity • mouse liver tumors

Abbreviations: pNA, p-Nitroanisole • HCA, hepatocellular adenoma • HCC, hepatocellular carcinoma • HB, hepatoblastoma • PCR-SSCP, polymerase chain reaction-single strand conformation polymorphism

Toxicologic Pathology, Vol. 34, No. 3, 237-242 (2006)
DOI: 10.1080/01926230600695474
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