| Literature DB >> 3685994 |
N Horiuchi1, M P Caulfield, J E Fisher, M E Goldman, R L McKee, J E Reagan, J J Levy, R F Nutt, S B Rodan, T L Schofield.
Abstract
One mechanism considered responsible for the hypercalcemia that frequently accompanies malignancy is secretion by the tumor of a circulating factor that alters calcium metabolism. The structure of a tumor-secreted peptide was recently determined and found to be partially homologous to parathyroid hormone (PTH). The amino-terminal 1-34 region of the factor was synthesized and evaluated biologically. In vivo it produced hypercalcemia, acted on bone and kidney, and stimulated 1,25-dihydroxy-vitamin D3 formation. In vitro it interacted with PTH receptors and, in some systems, was more potent than PTH. These studies support a long-standing hypothesis regarding pathogenesis of malignancy-associated hypercalcemia.Entities:
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Year: 1987 PMID: 3685994 DOI: 10.1126/science.3685994
Source DB: PubMed Journal: Science ISSN: 0036-8075 Impact factor: 47.728