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No involvement of Ki‐ ras or p53 gene mutations in colitis‐associated rat colon tumors induced by 1‐hydroxyanthraquinone and methylazoxymethanol acetate
Author(s) -
Suzui Masumi,
Yoshimi Naoki,
Ushijima Toshikazu,
Hirose Yoshinobu,
Makita Hiroki,
Wang Aijin,
Kawamori Tshihiko,
Tanaka Takuji,
Mori Hideki,
Nagao Minako
Publication year - 1995
Publication title -
molecular carcinogenesis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.254
H-Index - 97
eISSN - 1098-2744
pISSN - 0899-1987
DOI - 10.1002/mc.2940120403
Subject(s) - single strand conformation polymorphism , ulcerative colitis , biology , azoxymethane , exon , microbiology and biotechnology , cancer research , colitis , colorectal cancer , carcinogenesis , adenocarcinoma , gene , pathology , cancer , immunology , genetics , medicine , disease
1‐Hydroxyanthraquinone (1‐HA), which is present in some herbs, and methylazoxymethanol (MAM) acetate, a metabolite of azoxymethane, show synergistic carcinogenicity in rat colon, and 1‐HA induces ulcerative changes with simultaneous severe inflammation of the entire colon. In this study, mutations in Ki‐ ras (exons 1 and 2) and p53 (exons 4–7) were studied by polymerase chain reaction (PCR)–single‐strand conformation polymorphism (SSCP) analysis. Of 18 adenomas and 38 adenocarcinomas induced in male F344 rats (52 tumors induced by 1‐HA plus MAM acetate, three by 1‐HA alone, and one by MAM acetate alone), no mutations in Ki‐ ras of p53 were detected under two conditions of PCR‐SSCP analysis. Because human colon carcinomas from patients with ulcerative colitis have a very low incidence of Ki‐ ras mutation, this experimental system would be a good animal model of human colon carcinomas with ulcerative colitis and of human colon carcinomas without Ki‐ ras of p53 mutations. © 1995 Wiley‐Liss Inc.