IMR Press / FBL / Volume 5 / Issue 3 / DOI: 10.2741/mallya

Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on imrpress.com as a courtesy and upon agreement with Frontiers in Bioscience.

Open Access Article
Cyclin D1 in parathyroid disease
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1 Center for Molecular Medicine, University of Connecticut Health Center, Farmington, CT 06030-3101, USA
Academic Editor:Richard Pestell
Front. Biosci. (Landmark Ed) 2000, 5(3), 367–371; https://doi.org/10.2741/mallya
Published: 1 March 2000
(This article belongs to the Special Issue Cell cycle dysregulation in disease)
Abstract

Primary hyperparathyroidism (HPT), most commonly due to parathyroid adenoma, is a disorder characterized by excessive secretion of PTH. So far, abnormalities in two genes, cyclin D1 and MEN1, have been implicated in the development of parathyroid adenomas. Cyclin D1, now an established Oncogene involved in numerous human cancers, was first identified and recognized as an Oncogene in the study of parathyroid tumors. A subset of parathyroid adenomas contains a clonal rearrangement that places the PTH gene's regulatory sequences in proximity to the cyclin D1 Oncogene causing its overexpression, and 20-40% of parathyroid adenomas overexpress the cyclin D1 protein. Transgenic animal models have further confirmed the role of cyclin D1 as a driver of abnormal parathyroid cell proliferation. Future studies on the mechanism of cyclin D1's oncogenicity and its interactions with other parathyroid growth regulators will further our understanding of parathyroid cell biology and may prove useful clinically.

Keywords
Parathyroid
Adenoma
Cyclins
Neoplasms
Cancer
Tumor
Growth
Proliferation
Review
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