Rare mutations of p53, Ki-ras, and beta-catenin genes and absence of K-samand c-erbB-2 amplification in N-methyl-N '-nitro-N-nitrosoguanidine-induced rat stomach cancers

Citation
Y. Hirayama et al., Rare mutations of p53, Ki-ras, and beta-catenin genes and absence of K-samand c-erbB-2 amplification in N-methyl-N '-nitro-N-nitrosoguanidine-induced rat stomach cancers, MOL CARCINO, 25(1), 1999, pp. 42-47
Citations number
35
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Onconogenesis & Cancer Research
Journal title
MOLECULAR CARCINOGENESIS
ISSN journal
0899-1987 → ACNP
Volume
25
Issue
1
Year of publication
1999
Pages
42 - 47
Database
ISI
SICI code
0899-1987(199905)25:1<42:RMOPKA>2.0.ZU;2-3
Abstract
Rat stomach cancers induced by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) have been widely used as a model for human stomach cancers of the different iated type. However, there has been little information regarding their mole cular basis. In this study, we examined the genetic alterations reported in human stomach cancers in 10 rat stomach cancers that had been induced in m ale ACl/N rats by administering MNNG in the drinking water. One of the 10 c ancers had a mutation of the p53 gene at the second position of codon 171 ( Val --> Glu). However, none of the 10 cancers had mutations in codons 12, 1 3, or 61 of Ki-ras or in the N-terminal phosphorylation sites of the beta-c atenin gene. southern blot analysis showed no amplification of K-sam or c-e rbB-2 in the seven cancers examined. Finally, we searched for microsatellit e alterations in 12 loci in nine cancers, but no alterations were observed. As these genetic alterations are observed in only a minor fraction of huma n stomach cancers, further analysis of genetic and epigenetic alterations i n MNNG-induced rat stomach cancers is needed to disclose the major mechanis ms of stomach carcinogenesis. (C) 1999 Wiley-Liss, Inc.