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Metabolism Branch [C. A. M., M. M. C., R. M. B.] and Laboratory of Pathology [A. T. L., W. G. S-S., L. A. L.], Division of Cancer Biology, Diagnosis and Centers, National Cancer Institute, NIH, Bethesda, Maryland 20892, and Departments of Medicine and Cell Biology, Vanderbilt University Medical Center, Nashville, Tennessee 37232 [S. B.]
Murine fibrosarcoma cell lines transduced with retroviral vectors containing the murine interleukin 6 (IL-6) gene constitutively secreted IL-6. When injected s.c. into normal mice these IL-6-secreting tumors exhibited reduced tumorigenicity. This reduced tumorigenicity was not seen in nude or irradiated mice, implicating a T-cell-dependent, radiosensitive host response activated by the cytokine. Subcutaneous IL-6-secreting tumor did not retard the growth of distant deposits of wild-type tumor in the same host. However, animals rejecting IL-6-secreting tumors exhibited resistance to later challenge with wild-type tumor. When injected i.v. in an experimental metastasis model the IL-6-secreting tumors failed to or were extremely inefficient in giving rise to pulmonary nodules; this was observed in both normal and immunoincompetent mice, implicating a second, nonimmune mechanism affecting the growth of the tumor modified to secrete IL-6.
1 To whom requests for reprints should be addressed, at NIH, National Cancer Institute, Metabolism Branch, Building 10, Room 4N115, Bethesda, MD 20892.
2 M. M. C. is a Howard Hughes Medical Institute NIH Research Scholar.
3 S. B. is a Lucille P. Markey Biomedical Scholar and his work is supported in part by the Lucille P. Markey Charitable Trust.
Received 4/27/92. Accepted 8/24/92.
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