Aim: reveal the degree of expression of Ki-67 antigen in gastric carcinoma and in non-malignant gastric mucosa with Helicobacter pylori-induced inflammatory modifications. Material and Methods: Immunohistochemical study performed on 24 patient’s postoperative tissue samples (tumor and non-neoplastic gastric mucosa): 10–diffusely infiltrating undifferentiated carcinomas, 14-intestinal type moderately differentiated adenocarcinoma. Preoperatively H.pylori IgG antibodies were determined. Results: Ki-67 expression in gastric mucosa varied depending on the severity of changes produced by infection H.pylori, usually the type of chronic gastritis, the severity being assessed according to the histological criteria of Sydney system. In gastric mucosa with insignificant degree of inflammation, Ki-67 was expressed in foveolar epithelium and in epithelium of the gland’s isthmus, while in atrophic gastritis with rare glands–only in foveolaristhmic epithelial cells. In gastritis with a severe degree of inflammation Ki-67 positive cells were frequently detected in intramucosal lymphoid follicles. Immunopositivity in intestinal type adenocarcinomas was much higher than in nonmalignant mucosa. The highest immunopositivity was found in areas of less differentiated carcinoma structures. In diffuse-infiltrative carcinomas the percentage of Ki-67 positive neoplastic cells was much lower than in intestinal type adenocarcinomas. Conclusions: H.pylori infection in gastric mucosa creates conditions for local proliferation and promotion of intestinal type gastric cancer by a higher rate of proliferation of epithelial cells in adenocarcinomas of intestinal type than in the diffuse-infiltrative type, and by a higher rate of lymphoid cell proliferation in peritumoral mucosa with inflammatory infiltration than in the stroma of carcinomas.