Colon
tumors were induced in F344 rats by three heterocyclic
amines (HCAs), 2-amino-6-methyl-dipyrido[1,2-a:3',2'-d]
imidazole (Glu-P-1), 2-amino-3-methylimidazo[4,5-f]
quinoline (IQ) or 2-amino-1-methyl-6-phenylimidazo[4,5-
b]pyridine (
PhIP), and examined for p53 mutations. Seven
carcinomas induced by
Glu-P-1, and nine
carcinomas and two
adenomas induced by IQ were examined by
cDNA-polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP) analysis from
codon 103 to 391 of p53, which encompasses the conserved regions II to IV. Nine
carcinomas induced by
PhIP were examined by genomic PCR-SSCP analysis of exons 5 to 7 (from
codon 124 to 304), which encompasses the 3' half of the conserved region II and all the conserved regions III-V. No band shifts were found in any of these
tumors under at least two conditions of SSCP analysis. Our previous study had shown a Ki-ras mutation in only one Glu-P-1-induced
adenocarcinoma among the same 27 colon
tumors, and no other mutation of ras family genes had been found. HCA-induced rat colon
tumors appear to represent a group of human colon
tumors in which neither Ki-ras nor p53 is involved.