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Dependence of the Regression of Sarcoma 180 in Vitamin B₆- deficient Mice upon the Immunologic Competence of the Host¹

Department of Experimental Therapeutics, Roswell Park Memorial Institute, New York State Department of Health, Buffalo, New York 14203

The incidence of complete regression of Sarcoma 180 (S-180) in vitamin B₆-deficient Swiss mice was significantly reduced in animals thymectomized 1–5 days after birth but not in sham-thymectomized mice, neonatally thymectomized mice implanted s.c. with thymus autografts, mice thymectomized 9 or 30 days after birth, or neonatally splenectomized mice. The initial retardation of the growth of S-180 caused by the dietary depletion was not different in neonatally thymectomized and sham-operated mice; the delayed retardation of tumor growth was reduced in mice which had been thymectomized neonatally. Thus in nonthymectomized mice the delayed retardation of tumor growth appears to be caused by both the therapeutic treatment and the immunologic response of the host.

Comparison of the regression of S-180 and the rejection of allogenic skin grafts indicated that dietary vitamin B₆ depletion causes only minor impairment of the immunologic responses of the host at levels sufficient to impair the tumor effectively.

¹ This investigation was supported in part by a research grant (CA 04130) from the National Cancer Institute, USPHS, and by an Institutional Research Grant (I-SOI-FR-5562-03) from the USPHS.

² Present address: Department of Radiology, Stanford University Medical School, during the tenure of an Eleanor Roosevelt International Cancer Fellowship from the International Union Against Cancer.

Received 6/27/66. Accepted 10/ 3/66.