The Apc^Min/+ mouse is an animal model for familial adenomatous polyposis, and aged Apc^Min/+ mice also spontaneously develop multiple tumors in their stomachs. However, gastric premalignant lesions in Apc^Min/+ mice have not been well characterized. The stomachs of Apc^Min/+ mice were compared with those of their wild type littermates at 24 weeks with hematoxylin and eosin (H&E) staining and alcian blue staining. Ki67, CD68 and CA199 expression was analyzed by immunohistochemistry. The results revealed the presence of epithelial proliferation and inflammatory infiltration in the forestomachs, glandular atrophy and intestinal metaplasia in the gastric bodies, and dysplasia in the gastric antra. The effect of mutations in the Apc gene on chronic gastritis and gastric precancerous lesions was characterized in Apc^Min/+ mice. These results suggest that Apc^Min/+ mice represent a genetic model for mechanistic studies and drug discovery in gastric precancerous lesions.