Abstract
Investigations of the clonal growth of gastric carcinomas clearly suggest that individual cancers are derived from single cells with multi-potential activities and that cellular differentiation of gastric cancer cells occurs secondarily. By mucin histochemistry, gastric cancer cells of each histological group could be clearly classified into a gastric type and an intestinal type. The present results suggest the independent induction of intestinal metaplasia and gastric cancers and the occurrence of change of phenotypic expression of tumor cells from the gastric type to the intestinal type during growth of tumors. The Pepsinogen altered pyloric gland (PAPG) detected immunohistochemically may be considered to be a preneoplastic change. Rare mutations of p53 and ras genes in rat and mouse stomach cancers were found and p53 knockout mice (-/-) are more susceptible than (+/-) or (+/+) mice to N-methyl-N-nitrosourea stomach carcinogenesis.
