Molecular profiling in primary hyperparathyroidism
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 authorMariusz Deska MD
Chair and Clinical Department of General Surgery, Bytom, Medical University of Silesia, Katowice, Poland
Search for more papers by this authorMarek Michalski PhD
Department of Histology and Embryology, Zabrze, Medical University of Silesia, Katowice, Poland
Search for more papers by this authorJacek Gawrychowski MD, PhD
Chair and Clinical Department of General Surgery, Bytom, Medical University of Silesia, Katowice, Poland
Search for more papers by this authorRomuald Wojnicz MD, PhD
Department of Histology and Embryology, Zabrze, Medical University of Silesia, Katowice, Poland
Search for more papers by this authorCorresponding 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 authorMariusz Deska MD
Chair and Clinical Department of General Surgery, Bytom, Medical University of Silesia, Katowice, Poland
Search for more papers by this authorMarek Michalski PhD
Department of Histology and Embryology, Zabrze, Medical University of Silesia, Katowice, Poland
Search for more papers by this authorJacek Gawrychowski MD, PhD
Chair and Clinical Department of General Surgery, Bytom, Medical University of Silesia, Katowice, Poland
Search for more papers by this authorRomuald Wojnicz MD, PhD
Department of Histology and Embryology, Zabrze, Medical University of Silesia, Katowice, Poland
Search for more papers by this authorAbstract
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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