Abstract
In extensive experiments with mice and rats performed during the past decade, especially by Lorenz and Stewart and their co-workers (2-12), a relatively high proportion of precancerous and cancerous lesions were produced in the forestomach and small intestine by incoporating hydrocarbons in the diet, and gastric adenocarcinomas were readily produced by injecting methylcholanthrene into the wall of the stomach. No tumor, however, was induced in the glandular stomach and large intestine by oral administration of the carcinogenic substances. It was stated that the glandular stomach and large intestine are refractory to tumor formation because of the constant protective action of the mucous secretion.
On the other hand, several authors have reported on the occurrence of carcinoma of the colon in rats, using such substances as 2-acetylaminofluorene (13), radioactive yttrium (14), benzidine (15) and motor lubricating oil (16).
In this laboratory, it is demonstrated that the mucosae of the glandular stomach and large intestine in rat are not completely refractory to tumor induction. However, there is a strong contrast between the case of inducing tumors in the forestomach and small intestine (Lorenz and Stewart) and the production of adenoma or adenocarcinoma in the glandular stomach and colon (the present experiment).
The investigation on the production of hyperplastic lesions of the glandular stomach in rats by oral administration of methylcholanthrene were extended by an increase in amount of carcinogen ingested. Majority of rats showed more or less definite adenomas or adenomatous lesions in the glandular stomach. Intestinal epithelial cells were observed in the gastric mucous membrane of one rat. An colonic adenocarcinoma with mucosal hyperplasia was induced in one out of 12 rats.
