The adoptive transfer of tumor-specific transplantation immunity was accomplished in a syngeneic rat tumor-host system. Rats which received intravenous injections of spleen cells from Fisher 344/N rats immunized by amputation of growing isografts of a benz(a)pyrene-induced fibrosarcoma (BP-1R) manifested a significant decrease in the incidence of development of tumor isografts. The intravenous administration of normal spleen cells to syngeneic rats was not effective. In other experiments, Fisher 344/N rats were immunized in a similar manner, and RNA was extracted from their spleens. Normal F-344/N spleen cells were incubated with this “immune” RNA, and injected intravenously into F-344/N rats which were then challenged with viable BP-1R cells. A marked decrease in tumor growth rate resulted. The intravenous administration of spleen cells incubated with RNA extracted from the spleens of unimmunized rats was ineffective. In the same tumor-host system, RNA, extracted from the nodes and spleens of guinea pigs immunized with the BP-1R sarcoma, was mixed with sodium dextran sulfate, a potent inhibitor of ribonuclease, and administered to normal F-344/N rats which were then challenged with BP-1R cells. A significant reduction in the incidence of tumor development was noted. Dextran sulfate alone had no effect on the incidence of tumor isograft development, and RNA extracted from the lymph nodes and spleens of unimmunized guinea pigs and mixed with dextran sulfate was also ineffective. The systemic administration of “immune” RNA, or the administration of autologous lymphocytes pre-incubated in “immune” RNA to human cancer patients may be an effective method of suppressing or eliminating small foci of persistent or metastatic cancer, and could be an important immunotherapeutic adjuvant to established modalities of cancer therapy.