To analyze the early stages of argyrophil cell carcinoid growth, complete serial sections were cut from the glandular portion of the stomachs of 22 Mastomys and submitted to Sevier-Munger's reaction. The 154 grossly invisible foci of argyrophil cell microproliferation thus detected were classified into three stages of microproliferations (I, II, and III), and the last stage was definitely a microcarcinoid. There was a gradual transition in cell proliferation among these three stages; the first stage (microproliferation I), in which the cells were morphologically indistinguishable from those of hyperplastic proliferation by general morphologic criteria, was where the initial change of argyrophil cell carcinoid formation was detectable by a light microscope. Whereas multiple occurrences of microcarcinoids accounted for the multiplicity of well-developed tumors in the stomachs of Mastomys, a well-developed carcinoid in this species was formed by the confluence of several microcarcinoids.

We surgically prepared a hypergastrinemia model in rats and studied the effects of hypergastrinemia on chemically induced carcinogenesis in the esophagus. Operations were performed on 5-week-old male Donryu rats as follows: (1) truncal vagotomy plus pyloroplasty (group V), (2) segmental gastrectomy plus pyloroplasty (group G), (3) antrectomy (group A), and (4) no operation (group C) as a control. From the age of 6 weeks, the animals were given 0.003% N-methyl- N-amylnitrosamine (MAN) solution as drinking water for 8 weeks. After 20 weeks of MAN administration, the animals were bled and killed. The average serum gastrin levels in groups V and G were significantly higher than those groups C or A. There were significant differences between C and V in the incidence of carcinoma, and between V and A in the incidence of carcinoma including severe dysplasia. The incidence of histologically identified lesions per animal was determined, and significant differences were observed between C and both V and G in the incidence of carcinoma including severe dysplasia. Furthermore, we also detected gastrin receptors in the esophageal lesions produced by the oral administration of MAN to rats. The results of the present study suggest that endogenous hypergastrinemia has a positive influence on chemically induced carcinogenesis in the rat esophagus.

No abstract

This study investigated the histological distribution of argyrophilic cells in experimental hepatic neoplasms, the number of these cells, and the proportion of neoplasms with such cells. Seventy 6–week–old male Donryu rats were given a 0.06% 3′–methyl–4–dimethyl–aminoazobenzene (3′–MeDAB) diet for 10 weeks, followed by an ordinary diet for an additional 10 weeks. Of the 70 rats, 50 were used for this investigation; 29 had hepatic tumors, 18 had cholangiofibrosis, and the other three had oval cell proliferation only. Hepatic tissues were stained with Grimelius and Fontana–Masson stains as well as routine hematoxylin–eosin stain. Argyrophilic cells were found in the hepatic neoplasms of 8 rats without argentaffin cells, while cholangiofibrosis was associated with argentaffin cells in almost all cases. Of the 8 rats with argyrophilic cells, three had an abundant population of these cells. The argyrophilic cells were found in areas of the neoplasms with a glandular, trabecular, tubular, or poorly differentiated pattern. Electron microscopy revealed that the neoplastic cells with a positive argyro–phil reaction contained small round electron–dense endocrine granules. In addition, in the areas of cholangiofibrosis, two different types of gut endocrine cells were present (G and EC cells). These results suggest that 3′–MeDAB might induce hepatic carcinoid under certain conditions, though we have yet to confirm the development of a pure hepatic carcinoid due to this substance.

No abstract