Acquisition of Heightened Resistance and Susceptibility to Spontaneous Mouse Mammary Carcinomas in the Original Host

Summary Experiments were designed to answer the following question: Can mice acquire heightened reactivity of an immunological nature to their own spontaneous mammary neoplasms? Twenty-five spontaneous mammary carcinomas, arising from transplanted C3H/f/Crgl nodule outgrowth, were removed and subsequently retransplanted into their original C3H/Crgl/2 hosts. At the same time, the tumors were transplanted into series of isologous, previously tumor-free control animals. Some of the original tumor hosts and some of the isologous controls were treated with agents capable of increasing immunological responsiveness and with killed tumor cell preparations. The growth of the transplanted tumors in the original hosts and in their respective isologous controls was compared. The tumors grew in all the isologous control animals. Tumor growth was either appreciably retarded or appreciably facilitated in a majority of the original tumor-bearing animals, relative to their isologous controls. Several of the original hosts entirely failed to support growth of the neoplastic transplants, and in more than half of the remaining experiments the original animal ranked either first or last in order of resistance to the transplants. The lymph nodes draining the sites of tumor implantation showed exaggerated lymphoid hyperplasia in original animals exhibiting either resistance or enhancement. Similar experiments with spontaneous mammary carcinomas appearing in old multiparous female mice also indicated the development of heightened tumor resistance in the autochthonous host. The results of the present study strengthen the biological generality of the tumor resistance phenomena described by others working with experimentally induced neoplasms and with certain virus-initiated tumors.