One-hundred twelve hyperplastic polyps were analyzed. The aim was to study their malignant transformation. Among them, four hyperplastic polyps harbored adenocarcinoma; two were from our own institution (1.8%). The majority were pedunculated and located in the antrum with an average of 14.5 mm in diameter. The four polyps bore well-differentiated adenocarcinoma. Dysplasia and intestinal metaplasia were detected in two and three polyps, respectively. The cancer and dysplastic foci shared the same type of neutral and acid mucosubstances. p53 oncoprotein was positive in three cancer foci and in the dysplastic areas, and nucleolar organizer region counts were higher in the cancer foci. In conclusion, hyperplastic polyps have malignant potential. Such possibility increases in polyps larger than 14.5 mm. In our cases, the carcinoma foci may have arisen from dysplastic areas. Once the neoplastic changes occur, the cancer cells proliferate and behave as other adenocarcinomas of the stomach.

Six cases of type A gastritis associated with multiple carcinoids and/or endocrine cell micronests (ECM) in the atrophic fuindic mucosa were examined light microscopically, immunohistochemically, and ultrastructurally. The ECM and carcinoids were mainly composed of enterochromaffin-like (ECL) cells. The cells were hyperplastic only in the atrophic fundic glands and pseudopyloric glands, but not in the intestinal metaplastic gland. It is suggested that the development of both the ECM and the carcinoids is highly related to the atrophic change of the fundic mucosa and a trophic action of subsequently raised serum gastrin in type A gastritis and that the both lesions arise from the pseudopyloric glands or atrophic fundic glands. In addition, the definition of neoplastic ECM (microcarcinoid) of the stomach was made with comparative study on both the cases with ECM and multiple carcinoids and the cases with ECM alone.

A 75-year-old man was diagnosed as having a sessile tumor measuring 1.4 x 1.0 cm in size in the duodenal bulb after upper gastroduodenal series. The biopsy specimens revealed a proliferation of the adenomatous glands showing an acinar structure with papillary infolding; type III mucus, which is characteristic of Brunner's glands. Antral glands and mucus neck cells of the fundic glands were also observed in the adenomatous glands by concanavalin A staining. Thus, it was clear that the tumor had originated from the Brunner's glands. Three years and four months later, the sessile tumor had developed into a fungating ulcerated tumor via a polypoid form. The biopsy specimens revealed a papillary adenocarcinoma with foci of undifferentiated carcinoma. Retrospectively, the adenomatous glands in the biopsy taken from the sessile tumor should have been regarded as low grade carcinoma. Therefore, we propose that when a polyp or tumor shows an increase in size or change in macroscopic appearance, surgery should be considered.