In patients with cancer, hypercalcemia is a common complication and appears to result from multiple causes, some of which are humoral.1 One group of possible mediators that has recently attracted attention is the E series of prostaglandins (PGE1 and PGE2). These 20-carbon fatty acids are potent stimulators of bone resorption in vitro.2 , 3 The possibility that prostaglandins might play an etiologic role in vivo in the hypercalcemias of neoplasia was suggested by a series of experiments in two animal model systems. In these systems, hypercalcemia is observed in mice bearing the HSDM1 fibrosarcoma4 and in rabbits carrying . . .
No takes yet. Share an insight, caveat, or question.
Armen H. Tashjian (1975) studied this question.
Synapse has enriched 4 closely related papers on similar clinical questions. Consider them for comparative context: