Inbred A × C strain male and female rats were fed 0.025 percent N-2-fluorenyldiacetamide in the diet. Progesterone or diethylstilbestrol was administered to both intact and castrated animals to evaluate their role in carcinogenesis and cirrhosis of the liver. In intact male animals given carcinogen, cirrhosis was usually present. Areas of hyperplasia developed in the parenchyma and grew to become nodules which later developed into carcinomas. In male rats receiving diethylstilbestrol, cirrhosis was prevented and the incidence of tumors was markedly reduced. These results resembled those in castrated males. In female rats, with or without diethylstilbestrol, cirrhosis was absent and the parenchymal lesions failed to progress beyond areas or nodules of hyperplasia. In all groups receiving diethylstilbestrol the hyperplastic lesions were much larger and the cells in the areas of hyperplasia in female rats were often atypical. The two male rats receiving diethylstilbestrol and the castrated males that developed tumors had fewer and smaller tumors per liver than the male rats. All the tumors in the diethylstilbestrol-treated and castrated animals were well-differentiated carcinomas. By contrast, progesterone increased the incidence of hepatocellular carcinoma in intact male, castrated male, and castrated female rats but did not affect the incidence in intact females. Also the tumors tended to be less differentiated carcinomas. The incidence of cirrhosis was also increased by progesterone in castrated animals of both sexes.
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Reuber et al. (1962) studied this question.