| [ Summary ] |
Epidemiological cohort studies have suggested that duodenal reflux plays a role in remnant stomach carcinogenesis after surgery. However, the exact mechanism of carcinogenesis has not been fully elucidated. Recently, several animal models have been reported, in which remnant stomach cancers were shown to arise due to duodenal reflux without carcinogenic treatment. In these models, adenocarcinomas were seen in more than 70% of the animals, and peculiar histologic changes in stomal gastritis, resembling human gastritis cystica profunda were seen. This was thought to predispose the development of remnant stomach cancer. Sequential morphological changes in the stoma were analyzed, and it was found that pyloric-foveolar metaplasia first occurred at the bottom of glands around the stoma, followed by genesis of intestinal type goblet cells. This cell lineage, referred to as GRCL (Gut Regenerative Cell Lineage), seemed to lead to remnant stomach carcinogenesis. We proposed a concept for GRCL carcinogenesis. As a causative factor, a type of nitrosocompound was postulated, because remnant stomach carcinogenesis was inhibited by administration of thioproline, a nitrte scavenger. |