In our preliminary attempt at experimental carcinogenesis on the basis of gastric ulcer, we succeeded in producing a chronic penetrating ulcer associated with gelatinous adenocarcinoma in rats. The present study was performed to elucidate the correlation between the induced ulcer and its epithelial proliferation which appeared in that experiment. The method of the present experiment was essentially the same as that of the previous study. Rats were divided into four groups according to the type of pellet inserted into the pouch of the stomach. Namely, (1) group B with beeswax pellet, (2) group BH with pellet of beeswax and histamine phosphate, (3) group BC with pellet of beeswax and 4-nitroquinoline-1-oxide (carcinogen) and (4) group BHC with beeswax pellet containing both histamine phosphate and 4-nitroquinoline-l-oxide. Animals were sacrificed on 5, 7, 14, 30, 61) and 120 days following insertion of pellet and the mode of ulcer development and process of epithelial proliferation in four groups were compared. Necrosis and resultant ulceration of the gastric wall were found at the site of pellet application in all animals of the four groups 14 days after the operation. Most of the once formed ulcers healed with scar tissue in groups B and BH, whereas those in groups BC and BHC where carcinogen was used underwent a change into chronic penetrating ulcers. In such chronic ulcers, epithelial proliferation deep into the scar tissue beneath the ulcer was noted, being especially marked in groups BC and BHC with carcinogenic pellet. A few cases revealed cellular atypism in such deeply penetrating epithelia. It was concluded from these facts that in our experimental procedure to produce ulcer-carcinoma in rats, an acute ulcer occurred first which took the chronic process and gradually was followed by epithelial proliferation of various grade originating at the margin and extending deep into the floor of the ulcer.
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