A review of experimental adenocarcinoma in the intact and post-operative rat glandular stomach with particular reference to mucin histochemistry.

The majority of experimental studies on the development of gastric adenocarcinoma have been performed in the rat. There is evidence for two pathways of carcinogenesis in the intact stomach following carcinogen administration. The first has a sequence of hyperplasia, dysplasia, carcinoma with a benign proliferating phase associated with damage and repair mechanisms. The second sequence progresses through increasing grades of dysplasia in an undisturbed mucosa leading to carcinoma formation. Early experiments concerning the effects of gastric surgery on carcinogen induced adenocarcinoma may have simply altered the effectiveness of the carcinogen. Recently it has been shown that surgery alone can induce adenocarcinomas and the number of tumours is related to the degree of duodenogastric reflux. The component of that reflux which seems to be responsible is pancreaticoduodenal secretions and not bile. Intestinal metaplasia is not an important intermediate stage in carcinogenesis in the rat.