Horiuchi N, Caulfield M P, Fisher J E, Goldman M E, McKee R L, Reagan J E, Levy J J, Nutt R F, Rodan S B, Schofield T L
Regional Bone Center, Helen Hayes Hospital (New York State Department of Health), West Haverstraw 10993.
Science. 1987 Dec 11;238(4833):1566-8. doi: 10.1126/science.3685994.
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.
一种被认为是恶性肿瘤常伴发高钙血症的机制是肿瘤分泌一种改变钙代谢的循环因子。最近确定了一种肿瘤分泌肽的结构，发现它与甲状旁腺激素（PTH）部分同源。合成了该因子的氨基末端1-34区域并进行了生物学评估。在体内，它会导致高钙血症，作用于骨骼和肾脏，并刺激1,25-二羟基维生素D3的形成。在体外，它与PTH受体相互作用，并且在某些系统中比PTH更有效。这些研究支持了一个关于恶性肿瘤相关性高钙血症发病机制的长期假设。
