Hyperplastic polyposis and diffuse carcinoma of the stomach. A study of a family

The authors previously described a large pedigree with familial gastric polyposis and a high incidence of gastric cancer and demonstrated the autosomal dominant pattern of inheritance. The current study described the histologic and immunohistologic features of the lesions in an attempt to clarify the mechanisms underlying gastric carcinogenesis in this family.

The authors studied the histopathologic and histochemical features of several gastric specimens of nine members of this family and searched for the expression of carcinoembryonic antigen (CEA), p21 protein (ras oncogene), p53 protein (p53 suppressor gene), and simple mucin-type carbohydrate antigens (Tn, sialosyl-Tn, and T antigen before and after neuraminidase) and for the presence of Helicobacter pylori.

The two carcinomas available for histologic revision were of the diffuse type. One of them apparently originated from a hyperplastic polyp. Hyperplastic polyps were diagnosed in five of seven patients without carcinoma. The remaining two patients had marked foveolar hyperplasia. Chronic atrophic gastritis with complete intestinal metaplasia (IM) was seen in three patients. p53 protein was not expressed in any of the cases. CEA and ras p21 oncoprotein were found in six and eight cases, respectively (mainly in hyperplastic foveolar epithelium). Tn, sialosyl-Tn, and T antigen were expressed in every case. H. pylori colonization was detected in all but the two patients with carcinoma.

The authors concluded that foveolar hyperplasia/hyperplastic polyps play a key role in the development of diffuse carcinoma in this inherited polyposis, confined to the stomach, with hyperplastic phenotype. The genetic and environmental mechanisms underlying this particular situation remain to be clarified.