Inhibition of Spontaneous Mammary Carcinoma of Mice by Treatment with Interferon and Poly I:C 1

Abstract

A variety of virus-induced neoplasias have been reported to be retarded by prophylactic or therapeutic treatment with inducers of interferon or passively administered interferon (1-5). Recently, Gresser and colleagues (6) have shown that spontaneously occurring leukemia in AKR mice responds to repeated doses of mouse brain interferon. Treatment with material obtained from “normal” mouse brain did not retard the leukemia. These studies (1-6) indicate a potent antitumor activity of endogenous and exogenous interferon and prompted this preliminary study to determine the influence of similar therapy upon the development of a solid tumor in mice. The system employed RIII mice, a strain in which approximately 90% of the females spontaneously develop mammary adenocarcinomas. The development of the mammary tumors is governed by the presence of the mammary tumor virus (MTV) as well as other factors (7, 8). It is not yet clear whether the tumor-inhibiting activity of interferon resides in its virus inhibitory activity, or if interferon may inhibit transformed cells directly by some presently unknown mechanism. In this study mice were observed for the appearance of MTV in milk and for the rate and incidence of mammary tumor development.

Materials and Methods. Mice. RIII mice were distributed into four groups of 15 each. One group was not treated and served as a control. One group was treated with 100 μg of poly I:C in 0.5 ml of phosphate buffered saline (PBS). “Normal” mouse serum or 0.5 ml of serum containing 1000-2500 units of interferon was administered to the other two groups. Interferon was assayed by 50% plaque inhibition method described by Wagner (9). Treatments of 1 injection/week began when mice were 6 weeks (38-44 days) of age and continued for 35-42 weeks.