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Tumor Resistance Induced by Syngeneic Bone Marrow Transplantation and Enhanced by Interleukin 2: A Model for the Graft versus Leukemia Reaction¹

Division of Oncology, Department of Medicine, Stanford University Medical School, Stanford, California 94305-5306

Lethally irradiated C3H/HeN mice reconstituted with normal syngeneic bone marrow survived significantly longer than unmanipulated control mice following challenge with a lethal dose of 38C13 lymphoma cells 2 to 3 weeks post-bone marrow transplantation (BMT). Although the magnitude of this effect was modest, it was highly reproducible. This resistance-producing effect of BMT could be enhanced by interleukin 2 administration and could be abrogated by anti-asialo-G_M1 antiserum treatment of recipients. These findings are consistent with the hypothesis that cells with a natural killer phenotype are activated by BMT and can mediate tumor resistance. These studies provide a model to explore the cellular basis, independent of donor alloreactivity, of the graft antitumor effect of BMT observed in humans.

¹ Supported in part by Grants CA49605, CA34233, and CA33399 from NIH.

² Recipient of a Young Investigator Award from the American Society of Clinical Oncology. To whom requests for reprints should be addressed, at Biological Response Modifiers Program. National Cancer Institute, Building 567, Room 205, Frederick, MD 21702-1201.

³ American Cancer Society Clinical Research Professor.

Received 1/21/92. Accepted 5/20/92.