The effect of pretransplant total-body irradiation on the survival time of BALB/c mice bearing line 1 alveolar cell carcinomas, and on the growth and metastasis (spontaneous and artificial) of these tumors, has been studied. Totalbody, but not localized thoracic, exposure of BALB/c mice to 500 R inhibits the growth of subsequently transplanted tumors, accelerates the rate at which spontaneous metastases develop, and significantly shortens survival time relative to unirradiated tumor-bearing mice. The slowing of the tumor growth rate and the acceleration of metastasis can also be induced by hydrocortisone acetate, and both can be reversed in irradiated mice by the transplantation of syngeneic spleen cells. Spleen cells from mice immunized against the tumor (with irradiation-killed tumor cells) are more efficient than similar cells from untreated mice, both in terms of their ability to return the depressed tumor growth rate to normal and in terms of the prevention of irradiation-induced increases in the development of artificial metastases following the i.v. injection of tumor cells. That metastatic spread, itself, could slow the tumor growth rate was demonstrated by comparing s.c. growth of the tumor in mice that did or did not also receive i.v. injection of tumor cells, i.e., artificial metastases. The tumor growth at the s.c. injection site was depressed in mice that received the artificial metastases in addition to the s.c. implant, but the artificial metastases produced as many lung tumor colonies in this group as they did in mice without the s.c.-growing tumor. Metastases, therefore, can inhibit s.c. tumor growth without themselves being affected. A mechanism based on local versus systemic control is proposed.


Research supported by the U. S. Atomic Energy Commission under contract with Union Carbide.

This content is only available via PDF.