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Cycling with the parathyroid.

Parathyroid (PT) cells divide infrequently, but they retain the latent ability to proliferate to form large, hyperfunctioning glands. Primary hyperparathyroidism (HPTH), which affects all PT glands, may be due to inactivating mutations in tumor suppressor genes such as the menin gene (MEN1), or activating mutations of the RET proto-oncoprotein, the product of the MEN2a gene (1). Mutations in MEN1 are also found in some isolated PT adenomas, while other PT adenomas carry a chromosomal translocation, in which the parathyroid hormone gene (PTH) promoter drives a translocated sequence encoding cyclin D1. Indeed, this cyclin, which is now known to be important for the entry of proliferating cells into G1 of the cell cycle, was discovered by Arnold’s laboratory through their genetic analysis of PT adenomas. As described in this issue of the JCI, this same group has now generated transgenic mice in which expression of cyclin D1 is targeted to the PT, resulting in HPTH (2).