Six carcinomas of the canine thyroid were studied. Five of the six tumors were functional on 131I scan and caused hyperthyroidism in two cases. The tumors were all of predominantly compact cellular histology with rare to moderate numbers of microfollicles. After surgical removal tumor slices were incubated with 32P in Krebs-Ringer-tris buffer with or without 0.1 U/ml of bovine TSH, and the specific activity of the extracted phospholipids was measured. TSH stimulated phosphatide turnover clearly in 5 cases and probably also in the 6th. Analysis of fractionated phospholipids in 2 cases showed that the response to TSH was mainly in the phosphatidic acid and phosphatidylinositol. These studies show that a malignant tumor may still retain at least one complete control system extending from TSH receptors to the final metabolic response.