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Enhancement by Somatostatin of Experimental Gastric Carcinogenesis Induced by N-Methyl-N'-nitro-N-nitrosoguanidine in Wistar Rats

Departments of Gastrointestinal Oncology [M. T., H. I., M. B.] and Pathology [H. T.], The Center for Adult Diseases, Osaka, 3-3, Nakamichi I-chome, Higashinari-ku, Osaka 537, Japan

The effects of somatostatin on the incidence, number, and histological type of gastric cancers induced by N-methyl-N'-nitro-N-nitrosoguanidine were investigated in Wistar rats. Rats received alternate-day s.c. injections of 100 or 200 µg/kg body weight of somatostatin in depot form after 25 weeks of p.o. treatment with the carcinogen. Prolonged administration of somatostatin at both dosages significantly increased the incidence and number of gastric cancers of the glandular stomach in Week 52. Furthermore, somatostatin at 200 µg/kg caused a significant increase in the incidence of gastric cancers penetrating the muscle layer or deeper layers. However, somatostatin at both dosages did not influence their histological appearance. Histologically, somatostatin at both dosages significantly elevated the labeling index of gastric cancers but not of the antral mucosa and significantly reduced the gastrin levels. These findings indicate that somatostatin enhances gastric carcinogenesis after N-methyl-N'-nitro-N-nitrosoguanidine treatment and that this effect may be related to its effect in increasing proliferation of gastric cancers and decreasing serum gastrin level.

¹ To whom requests for reprints should be addressed.

Received 3/31/89. Revised 6/19/89. Accepted 7/ 6/89.