Abstract
Hypoglycemia and hypoinsulinemia accompanied the i.m. growth of mammary aplastic carcinoma in CBA mice. In hosts rendered diabetic by means of alloxan, the tumor decreased blood glucose levels to almost the level seen in non-diabetic mice. Tumors maintained in diabetic mice grew faster after each subsequent transplantation into diabetic mice, and we noted increased incorporation of 3H-thymidine into DNA of these tumor cells. The observed proliferation enhancement of mammary aplastic carcinoma maintained in diabetic mice is caused by de novo insulin and glucagon synthesis, apparently by the tumor cells themselves.