Volume 37, Issue 2 pp. 299-307
Basic Science Review

Molecular profiling in primary hyperparathyroidism

Oliwia Anna Segiet MD

Corresponding Author

Oliwia Anna Segiet MD

Department of Histology and Embryology, Zabrze, Medical University of Silesia, Katowice, Poland

Corresponding author: O. Segiet, Department of Histology and Embryology in Zabrze, 41-808 Zabrze Rokitnica, ul. Jordana 19, Poland. E-mail: [email protected]Search for more papers by this author
Mariusz Deska MD

Mariusz Deska MD

Chair and Clinical Department of General Surgery, Bytom, Medical University of Silesia, Katowice, Poland

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Marek Michalski PhD

Marek Michalski PhD

Department of Histology and Embryology, Zabrze, Medical University of Silesia, Katowice, Poland

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Jacek Gawrychowski MD, PhD

Jacek Gawrychowski MD, PhD

Chair and Clinical Department of General Surgery, Bytom, Medical University of Silesia, Katowice, Poland

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Romuald Wojnicz MD, PhD

Romuald Wojnicz MD, PhD

Department of Histology and Embryology, Zabrze, Medical University of Silesia, Katowice, Poland

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First published: 04 March 2014
Citations: 17

Abstract

Background

Primary hyperparathyroidism (HPT) is one of the most common endocrine disorders, defined by hypersecretion of parathormone. Primary HPT can be caused by adenoma, hyperplasia, and carcinoma. A great amount of mechanisms contribute to the pathogenesis of this disease, such as genetic predispositions because of the germline-inactivating mutations in the multiple endocrine neoplasia type 1 (MEN1) and HRPT2 tumor suppressor genes. Somatic mutations in these genes were found also in sporadic parathyroid neoplasias. Cell cycle regulators, growth factors, apoptosis-inducing ligands, death receptors, and other transmitter substances have also been implicated in the etiology of primary HPT. Parathyroid carcinoma is often misdiagnosed as parathyroid adenoma and long-term survival is conditioned by the extent of the primary surgical resection, therefore, of great interest is the discovery of definitive diagnostic markers for carcinoma. This article presents current state of knowledge of the molecular pathogenesis of primary HPT. © 2014 Wiley Periodicals, Inc. Head Neck, 2014 © 2014 Wiley Periodicals, Inc. Head Neck 37: 299-307, 2015

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