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Histopathologic Study of the Mode of Inhibition of Cellular Proliferation: Effect of 4-Dimethylaminostilbene on the Growth of Walker Rat Carcinoma 256^*

(From the Department of Pathology, The University of Chicago, Chicago 37, Illinois)

The inhibitory effects of 4-dimethylaminostilbene hydrochloride on celluar proliferation have been studied in the Walker rat carcinoma 256, jejunal crypts of intact male, and vaginal basal epithelium of the ovariectomized rat. The findings of Haddow and his group have been confirmed (6, 11), that this compound is a powerful inhibitor of tumors and its inhibitory effect is dependent in part on the nutritional state of the host. It has been shown that a spectacular change in the histologic appearance of the tumors occurs under the influence of this drug, and that this histologic change of tumor giant cell formation, overgrowth of fibroblasts, and heavy reticulum formation is greatest in those tumors whose hosts have had the poorest nutritional state and lost the most weight. In addition it has been found that in tumors treated with aminostilbene there is an increase in incidence of abnormal mitotic figures of the type which are postulated to give rise to post mitotic cells. It is suggested that these post mitotic cells may not be available for further tumor growth. The more specific effect of inhibition of mitosis of tumor cells by this drug has been described. This inhibition of mitosis has been found whether the host was on either a high or low protein diet. The jejunal crypt mitotic rate was not affected by the drug in these animals. This compound was also found to inhibit the vaginal epithelium of the ovariectomized rat which had been given stilbestrol. The inhibition of mitosis of the stilbestrol stimulated vaginal epithelium of the rat is not due to marked weight loss of the treated animals.

On the basis of this study 4-dimethylamino-stilbene hydrochloride appears to inhibit tumor growth by: production of abnormal mitotic figures giving rise to post mitotic cells, inhibition of tumor cell mitosis, and by interfering with normal protein synthesis in the tumor bearing rat.