Selective Effects of Adriamycin on Murine Host Defense Systems

The clinical value of cancer chemotherapy is limited by the fact that the , anticancer agents available to date are not sufficiently selective in their antitumor action. Because of this, it may not be possible to overcome even relatively moderate degrees of tumor resistance and still avoid unacceptable toxicity. As discussed elsewhere (Mihich 1978), current approaches in cancer chemotherapy are aimed at reducing these limitations through the development of new selective treatments. Measurable differences in antigenicity have been found in tumor cells in animals (see Mihich 1978) and in man (Reinherz & Schlossman 1981, Ritzet al. 1981). Although in humans the differences seem to be primarily quantitative in nature, their existence has led to the hope that responses of the host to tumorassociated antigens might be exploited in designing more selective treatments of neoplastic disease. Difficulties that may have to be overcome in order to exploit tumor immunity therapeuticaily include those related to the fact that anticancer drugs may suppress host defenses through the very antiproliferative action which is at the basis of their antitumor effects (Mihich 1971, 1975). Furthermore, augmented tumor growth may be a consequence of modifications of immunoregulation possibly caused by tumor, drug or immunomanipulations. Thus, an understanding of the interactions between chemotherapeutic treatments and host