Abstract
Almost 40 years have elapsed since Albright1 first suggested that the neoplastic tissue in a patient with renal-cell carcinoma and hypercalcemia might produce parathyroid hormone or a similar substance that would raise serum calcium. During this period, there has been enormous progress in our understanding of the fundamental biochemistry and physiology of para-thyroid hormone and vitamin D, and of the relation of these hormones to calcium homeostasis. In patients with elevated serum calcium and a known malignant disease, a variety of pathogenic mechanisms, both humoral and nonhumoral, have been proposed. The report by Stewart et al. in this issue of . . .

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