Abstract
When old females of a Swiss strain of mice developed mammary tumors they were placed on a B12-deficient ration. After removal of the stomach and intestines, the mice were ground for assay by the chrysomonad method. When non-tumorous mice were kept on the deficient ration, their vitamin B12 content decreased for 2.5 weeks, after which it remained fairly constant at approximately 9 milligamma/ g, regardless of the age of the mice when put on the deficient ration. Tumorous mice treated in the same way contained twice as much B12 as the controls. 12 normal Swiss mice were fed on the deficient ration from the first week of pregnancy until close to parturition and had the same B12 content as non-pregnant controls, thus giving no indication of synthesis of B12 by the embryos. Separate assays of a spontaneous tumor and the carcass from which it came gave a higher B12 content in the carcass than in the tumor. In order to test the assumption that destruction of B12 occurred when the cancer was ground for assay, the cancer from a mouse maintained on the deficient ration was excised. Half the cancer was minced with scissors in water, ground with sand, and, after incubation for 1 hour at 37[degree]C, the suspension was autoclaved. The supernatant contained 2.5 milligamma of B12/g of fresh tissue. The other half of the cancer was mixed with 20 milligamma of B12/g of fresh tissue before mincing, then handled in the same way, but it contained 13 milligamma instead of 22.5 milligamma/g. Differences were found among individual cancers in their B12-destroying capacity, and evidence was obtained that the cancer tissue destroyed some of the B12 in the carcass when both were ground together before the analysis. If the cancer was discarded before grinding, there were still differences in B12 content among mice, indicating a quantitative difference in the ability to synthesize B12- 3 mice bearing established transplants of cancer strain W137 were fed the deficient ration for one week, after which the tumors were discarded. The B12 content of the carcasses was higher than that of the controls indicating that the transplant had synthesized B12, although the possibility of storage of traces of B12 in the diet by the transplant could not be overlooked. The transplanted tumor strain W113 did not give evidence for synthesis of B12, but did destroy the vitamin, since non-tumorous controls had over three times as much B12 as mice implanted with strain W113. Division of a strain W113 cancer into two parts and treatment as described above indicated 74% destruction of added vitamin. Three out of 4 transplanted strains tested gave evidence for synthesis of B12 in Swiss mice and all 4 gave evidence for destruction of B12 in vitro.