Proliferative and antigenic modifications in human epithelial cells in chronic atrophic gastritis.

ABSTRACT

For the study of both proliferative and antigenic changes in epithelial cells in a disease predisposing to gastric cancer, endoscopic biopsy specimens were analyzed following removal from individuals with chronic atrophic gastritis (CAG); comparisons were made with specimens from normal gastric mucosa. All subjects were from Nariño, Colombia, the population of which has a high age-adjusted incidence of gastric cancer (150/100,000 population) occurring mainly in gastric antrum. After pulse incubation of biopsy specimens with tritiated thymidine ([3H]dThd), microautoradiographic distributions of [3H]dThd-labeled cells in the epithelial lining of gastric pits were correlated with expression of serologically defined gamma-fetal antigen (FA) as a second marker. Measurements were done both in gastric corpus and in antrum for entire gastric pits and over multiple gastric pit compartments. Total numbers of cells per gastric pit column did not differ between the normal and the CAG specimens either in corpus or in antrum; however, both in corpus and in antrum mean numbers of [3H]dThd-labeled cells per gastric pit column and labeling index were almost twice as large for the CAG population (P less than .006). Labeling index differences also were significant over most gastric pit compartments (P less than .02). In antrum gamma-FA-positive lesions had an expanded proliferative compartment with labeling indices significantly greater than those of antigen-negative lesions (P less than .02). This correlation did not extend to biopsy specimens obtained from corpus of stomach where the frequency of carcinoma is low. Findings indicate a hyperproliferative state in CAG compared to the proliferative state in normal gastric mucosa and, in gastric antrum, a further correlation with expression of gamma-FA in hyperproliferating cells. The two markers can be used to aid definition of the gastric mucosa in a disease associated with the development of gastric cancer and in prophylactic dietary intervention programs.