Open Accessβ‐Catenin ( Ctnnb1 ) Gene Mutations in Diethylnitrosamine (DEN)‐induced Liver Tumors in Male F344 Rats
Author(s) -
Yamada Yasuhiro,
Yoshimi Naoki,
Sugie Shigeyuki,
Suzui Masumi,
Matsunaga Kengo,
Kawabata Kunihiro,
Hara Akira,
Mori Hideki
Publication year - 1999
Publication title -
japanese journal of cancer research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.035
H-Index - 141
eISSN - 1349-7006
pISSN - 0910-5050
DOI - 10.1111/j.1349-7006.1999.tb00822.x
Subject(s) - exon , point mutation , mutation , biology , catenin , gene , cancer research , gene mutation , pathology , carcinogenesis , beta catenin , carcinogen , medicine , genetics , wnt signaling pathway
Alterations in multiple phosphorylation sites on exon 3 of the β‐catenin gene have recently been implicated in hepatocarcinogenesis in humans as well as mice. To identify genetic alterations which could be involved in the chemical‐induced hepatocarcinogenesis of rats, we analyzed the status of the sites in the β‐catenin gene (Ctnnb1) of liver neoplasms induced by diethylnitrosamine (DEN) in male F344 rats, using the polymerase chain reaction‐single strand conformation polymorphism method. In the present investigation, we examined 35 hepatocellular neoplasms (28 adenomas and 7 carcinomas) for the expression of mutations in the region of the β‐catenin gene. Point mutation at codon 32, 35, 37 or 41, which has been reported in human and mouse liver cell carcinomas and/or other cancers, was recognized in eleven (31%) out of 35 lesions (8 adenomas and 3 carcinomas). Our results indicate that Ctnnb1 mutations may contribute to hepatocarcinogenesis in rats. Our finding that Ctnnb1 mutation was present in adenomas as well as carcinomas also suggests that the mutation is a relatively early event in DEN‐induced hepatocarcinogenesis in rats.