This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Trydal, T. Articles by Aarskog, D. Search for Related Content PubMed PubMed Citation Articles by Trydal, T. Articles by Aarskog, D.

1,25-Dihydroxyvitamin D₃ Receptor Measurement in Primary Renal Cell Carcinomas and Autologous Normal Kidney Tissue¹

Department of Pediatrics [T. T., L. A., D. A.] and Department of Surgery [A. B.], Haukeland Hospital, University of Bergen, N-5021 Bergen, Norway

Recently it was reported that 1-,25-dihydroxyvitamin D₃ [1,25-(OH)₂D₃] inhibited cell growth in a cell line derived from a metastasis from renal cell carcinoma. We have examined samples from 23 primary renal cell carcinomas for 1,25-(OH)₂D₃ receptor content, and compared it with the concentrations in autologous normal kidney tissue. Nineteen of 23 (83%) renal cell carcinomas had detectable (above 1 fmol/mg protein) 1,25-(OH)₂D₃ receptor levels, and 15 of 23 (65%) had levels above 5 fmol/mg protein. Mean value for the renal cell carcinomas was 8.2 fmol/mg protein (range, 0–28 fmol/mg protein), and the mean value for autologous normal kidney tissue was 23.1 fmol/mg protein (range, 6.6–53.7 fmol/mg protein). The 1,25-(OH)₂D₃ receptor levels in the renal cell carcinomas were significantly lower than in the autologous normal kidney tissue (P < 0.001). The 1,25-(OH)₂D₃ receptor was characterized by sucrose gradient analysis and DNA-cellulose chromatography. The features found for renal cell carcinoma were similar to the 1,25-(OH)₂D₃ receptor in normal human tissue. No correlation of 1,25-(OH)₂D₃ receptor levels to clinical parameters was found. This study shows that carcinomas originating from the kidney, the major vitamin D regulating organ, usually contain the 1,25-(OH)₂D₃ receptor. The receptor may have a cellular function in the transformed cell.

¹ This work was supported by the Norwegian Cancer Society, Norwegian Research Council for Science and the Humanities, the legacies of the Family Blix, and Astrid and Edvard Riisøen.

² Research fellow of the Norwegian Cancer Society. To whom requests for reprints should be addressed.

Received 8/ 5/87. Revised 12/29/87. Accepted 1/29/88.