Absence of p53 Mutations in Rat Colon Tumors Induced by 2‐Amino‐6‐methyldipyrido[1,2‐a:3′, 2′‐d]imidazole, 2‐Amino‐3‐methylimidazo[4,5‐f]quinoline, or 2‐Amino‐1‐methyl‐6‐phenylimidazo[4,5‐b]pyridine

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.