Schneider P B, Leav I
Endocrinology. 1977 Feb;100(2):346-50. doi: 10.1210/endo-100-2-346.
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.
对6例犬甲状腺癌进行了研究。6个肿瘤中有5个在131I扫描时具有功能，2例导致甲状腺功能亢进。肿瘤均主要为致密细胞组织学，微滤泡数量稀少至中等。手术切除后，将肿瘤切片在含有或不含有0.1 U/ml牛促甲状腺激素（TSH）的 Krebs-Ringer-三羟甲基氨基甲烷缓冲液中与32P一起孵育，并测量提取的磷脂的比活性。TSH在5例中明显刺激了磷脂周转，第6例可能也有刺激。对2例分级磷脂的分析表明，对TSH的反应主要在磷脂酸和磷脂酰肌醇中。这些研究表明，恶性肿瘤可能仍然保留至少一个完整的控制系统，从TSH受体延伸到最终的代谢反应。
