Minute gastric carcinoma of differentiated type with special reference to the significance of intestinal metaplasia, proliferative zone, and p53 protein during tumor development

BACKGROUND, The differentiated type of minute gastric carcinoma (MGC), measuring less than 5 mm in greatest dimension, has been considered to represent the incipient phase of gastric carcinoma. To determine the clinicopathologic features of MGCs, the authors examined tissues from MGCs with a view to clarifying their histopathologic diversity. The immunohistochemistry of these tissues was determined using monoclonal antibody against p53 and Ki-67, and their mucin-histochemical types were determined with reference to the presence of intestinal metaplasia (IM) within their surrounding mucosa. METHODS. One hundred three specimens were obtained from 93 patients with MGCs. Each lesion was evaluated both macroscopically and histologically, and the degree of IM was assessed. All sections were examined mucin-histochemically with Con A, GOS, and HID-AB, and stained with commercially available monoclonal antibodies, PAb 1801 and Ki-67. Additional nonminute carcinomas present within the same stomachs were used as controls. RESULTS. Macroscopically, most lesions were depressed. IM was noted in the surrounding mucosa of 85 MGCs (82.5%). Immunohistochemically, 25 MGCs (24.2%) showed p53 overexpression, although the rate of p53 overexpression was increased to 34.6% in other nonminute carcinomas from the same stomachs. Twenty-four MGCs were associated with a proliferative zone, demonstrated by Ki-67 positive cells. Statistically significant differences in the rate of p53 overexpression were observed between MGCs with a proliferative zone and those without. Mucin phenotypes of MGCs tended to imitate their own surrounding mucosa. CONCLUSIONS. The MGCs, which represent the incipient phase of early gastric carcinoma, have various histologic, immunohistochemical, and mucin-histochemical features. It would seem that p53 expression is more closely related to the progression of MGCs than to their carcinogenesis. (C) 1999 American Cancer Society.