Prostaglandin: Increased Production by Renal Cell Carcinoma

Publisher Website
Google Scholar
Abstract
The syndrome of hypercalcemia in patients with renal cell carcinoma without metastases 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 immunoreactive prostaglandins A and E. Increased levels of immunoreactive prostaglandins A and E were generated in parallel with cell growth during aperiod of time by renal cell carcinoma in monolayer growth, in extracts of primary and metastatic renal cell carcinoma tissue and in the venous effluent of a kidney bearing a renal cell carcinoma. These findings support the hypothesis that renal cell carcinoma can produce prostaglandins. 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.