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 aminoterminal 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-dihydroxyvitamin 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.
Original language | English (US) |
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Pages (from-to) | 1566-1568 |
Number of pages | 3 |
Journal | Science |
Volume | 238 |
Issue number | 4833 |
DOIs | |
State | Published - 1987 |
Externally published | Yes |
ASJC Scopus subject areas
- General