ABSTRACT
Rodents such as rats, mice, and hamsters have a forestomach located between the esophagus and the glandular stomach. Taurocholic acid, sodium taurocholate, and sodium chloride weakly promote rat glandular stomach carcinogenesis when administered after N-methyl-N-nitro-N-nitrosoguanidine initiation. Most forestomach carcinogens cause forestomach tumors after intragastric administration or by admixture to the diet or drinking water, although inhaled epichlorohydrin and 1,3-butadiene can induce forestomach tumors. Proliferative lesions of the rodent forestomach can be classified into hyper-plasia, papillomas, papillomatosis, fibroepitheliomas, atypical hyperplasia or dysplasia, carcinomas, benign tumors of connective tissue origin, and sarcomas. When male Wistar rats underwent gastrojejunostomy to divert the duodenal contents into the resected stomach through afferent and efferent loops, carcinomas developed more frequently in the gastric mucosa around the anastomosis of the afferent loop. The glandular stomach is equivalent to the human stomach functionally and morphologically. Despite the high mortality rate from gastric cancer in some Asian countries, only a few environmental glandular stomach carcinogens have been recognized.
