Cummings K B, Robertson R P
J Urol. 1977 Nov;118(5):720-3. doi: 10.1016/s0022-5347(17)58172-0.
The syndrome of hypercalcemia in patients with renal cell carcinoma without metastasis to bone, in association with elevated levels of immunoreactive prostaglandin E and normal parathyroid hormone levels, prompted the investigation of an etiologic relationship of increased prostaglandin in this syndrome. Ethyl acetate extracts of tissue culture effluents, primary and metastatic renal cell carcinoma, and plasma were chromatographed on silicic acid columns and assayed by double antibody immunoprecipitative methods for immunoprecipitative methods for immunoreactive prostaglandins A and E. Increased levels of immunoreactive prostaglandins A and E were found 1) to be generated in parallel with cell growth during a period of time by renal cell carcinoma in monolayer growth, 2) in extracts of primary and metastatic renal cell carcinoma tissue and 3) in the venous effluent of a kidney bearing a renal cell carcinoma. These findings support the hypothesis that renal cell carcinoma can produce prostaglandins. Furthermore, reported syndromes of patients with renal cell carcinoma associated with elevated prostaglandin levels may result from the autonomous production of prostaglandins in vivo by the tumor.
在无骨转移的肾细胞癌患者中出现高钙血症综合征，伴有免疫反应性前列腺素E水平升高及甲状旁腺激素水平正常，这促使人们对该综合征中前列腺素增加的病因关系进行研究。对组织培养液、原发性和转移性肾细胞癌以及血浆的乙酸乙酯提取物在硅酸柱上进行色谱分析，并采用双抗体免疫沉淀法检测免疫反应性前列腺素A和E。结果发现，免疫反应性前列腺素A和E水平升高：1）在单层生长的肾细胞癌一段时间内与细胞生长平行产生；2）在原发性和转移性肾细胞癌组织提取物中；3）在患有肾细胞癌的肾脏静脉流出液中。这些发现支持肾细胞癌能够产生前列腺素这一假说。此外，报告的肾细胞癌患者伴有前列腺素水平升高的综合征可能是肿瘤在体内自主产生前列腺素所致。
