作者: Fátima Carneiro , Leonor David , Raquel Seruca , Sérgio Castedo , Janh M. Nesland
DOI: 10.1002/1097-0142(19930715)72:2<323::AID-CNCR2820720204>3.0.CO;2-G
关键词: Atrophic gastritis 、 Helicobacter pylori 、 Hyperplastic Polyp 、 Epithelioma 、 Foveolar cell 、 Medicine 、 Intestinal metaplasia 、 Carcinoma 、 Pathology 、 Carcinoembryonic antigen
摘要: Background. The authors previously described a large pedigree with familial gastric polyposis and high incidence of cancer demonstrated the autosomal dominant pattern inheritance. current study histologic immunohistologic features lesions in an attempt to clarify mechanisms underlying carcinogenesis this family. Methods. studied histopathologic histochemical several specimens nine members family searched for expression carcinoembryonic antigen (CEA), p21 protein (ras oncogene), p53 (p53 suppressor gene), simple mucin-type carbohydrate antigens (Tn, sialosyl-Tn, T before after neuraminidase) presence Helicobacter pylori. Results. two carcinomas available revision were diffuse type. One them apparently originated from hyperplastic polyp. Hyperplastic polyps diagnosed five seven patients without carcinoma. remaining had marked foveolar hyperplasia. Chronic atrophic gastritis complete intestinal metaplasia (IM) was seen three patients. not expressed any cases. CEA ras oncoprotein found six eight cases, respectively (mainly epithelium). Tn, every case. H. pylori colonization detected all but carcinoma. Conclusions. concluded that hyperplasia/hyperplastic play key role development carcinoma inherited polyposis, confined stomach, phenotype. genetic environmental particular situation remain be clarified.