Induction of tumor dormancy in BALB/C mice against nonimmunogenic b cell leukemia

Relapse following successful initial induction of remission cannot be avoided in a large number of patients, despite availability of potent anticancer drugs and cumulative experience with multiple chemotherapy protocols. Unfortunately, elimination of the last tumor cells using conventional or even high doses of chemoradiotherapy is far from being realistic. Therefore, alternative therapeutic modalities are desperately needed in order to improve the cure rate of a large variety of chemoradiosensitive malignancies, which are based on more sophisticated approaches to block or eliminate residual tumor cells escaping chemoradiotherapy. Continuous presence of tumor cells in apparently cured animals, the so-called tumor dormant state, represents a unique model in experimental animals for exploring potentially useful mechanisms for increasing host resistance against relapse by residual tumor cells by several possible mechanisms, depending on the unique properties of the tumor and tumor-host relationship. We would like to describe our experimental approaches using a murine model of human B cell leukamiaylymphoma (BCLl), described by Slavin and Strober 1 for investigating the feasibility of induction of tumor dormancy by amplification of host antitumor effector mechanisms as well as induction of tumor dormancy in conjunction with allogeneic bone marrow transplantation. Tumor dormancy by syngeneic host cells can represent a model for induction of tumor dormancy in conjunction with autologous BMT (ABMT), whereas induction of tumor dormancy in conjunction with allogeneic BMT represents a model for amplification of graft vs leukemia (GVL) effects independently of allogeneic interactions between immunocompetent donor lymphocytes and normal host alloantigens, which leads to development of graft vs host disease (GVHD).