Significance
Parathyroid adenomas, the main cause of primary hyperparathyroidism (PHPT), are thought to result from clonal expansion of tumor cells and to be insensitive to normal calcium feedback due to the loss of the calcium-sensing receptor (CASR). Utilizing flow cytometric analysis to isolate and individually study oxyphil cells, chief cells, and lymphocytes from resected parathyroid tumors and glands, we now report previously unrecognized heterogeneity in these tissues with respect to calcium responsiveness, CASR expression, and clonal origin of parathyroid tumors. Such heterogeneity of parathyroid adenomas likely reflects the complex etiopathogenesis and clinical heterogeneity of PHPT.