Parathyroid Glands and Hyperparathyroidism: A General Overview

Hyperparathyroidism (HPT) is a clinical condition caused by the increase of parathyroid hormone (PTH) synthesis by the parathyroid glands. PTH has a central and fundamental role in the control of calcium and phosphorus homeostasis. Its action on the kidney, bone, and, indirectly, intestinal cells implies a rapid increase in extracellular calcium flow. This clinical condition may be due to an intrinsic parathyroid disorder or secondary to an imbalance of calcium metabolism in patients with systemic diseases, such as chronic renal failure. The treatment of hyperparathyroidism may be clinical, with the control of calcium, phosphorus, and PTH levels, or surgical, depending on the various forms presented. The purpose of the chapter is to discuss the types of hyperparathyroidism, their relationship with phosphorus and mainly calcium metabolism, as well as the main forms of diagnosis and treatment

Heparanase 1 Upregulation Promotes Tumor Progression and Is a Predictor of Low Survival for Oral Cancer

Background: Oral cavity cancer is still an important public health problem throughout the world. Oral squamous cell carcinomas (OSCCs) can be quite aggressive and metastatic, with a low survival rate and poor prognosis. However, this is usually related to the clinical stage and histological grade, and molecular prognostic markers for clinical practice are yet to be defined. Heparanase (HPSE1) is an endoglycosidase associated with extracellular matrix remodeling, and although involved in several malignancies, the clinical implications of HPSE1 expression in OSCCs are still unknown.Methods: We sought to investigate HPSE1 expression in a series of primary OSCCs and further explore whether its overexpression plays a relevant role in OSCC tumorigenesis. mRNA and protein expression analyses were performed in OSCC tissue samples and cell lines. A loss-of-function strategy using shRNA and a gain-of-function strategy using an ORF vector targeting HPSE1 were employed to investigate the endogenous modulation of HPSE1 and its effects on proliferation, apoptosis, adhesion, epithelial-mesenchymal transition (EMT), angiogenesis, migration, and invasion of oral cancer in vitro.Results: We demonstrated that HPSE1 is frequently upregulated in OSCC samples and cell lines and is an unfavorable prognostic indicator of disease-specific survival when combined with advanced pT stages. Moreover, abrogation of HPSE1 in OSCC cells significantly promoted apoptosis and inhibited proliferation, migration, invasion, and epithelial-mesenchymal transition by significantly decreasing the expression of N-cadherin and vimentin. Furthermore, a conditioned medium of HPSE1-downregulated cells resulted in reduced vascular endothelial growth.Conclusion: Our results confirm the overexpression of HPSE1 in OSCCs, suggest that HPSE1 expression correlates with disease progression as it is associated with several important biological processes for oral tumorigenesis, and can be managed as a prognostic marker for patients with OSCC.Peer reviewe

Somatic copy number alterations in pleomorphic adenoma and recurrent pleomorphic adenoma

Objective. As the genetic changes in recurrent pleomorphic adenoma (RPA) have not yet been investigated, the aim of this study was to assess the genomic profile of somatic copy number alteration in RPA and pleomorphic adenoma (PA) by using array comparative genomic hybridization (aCGH). Study Design. Four cases of RPA and 13 cases of PA were evaluated by using aCGH, using a 180 K platform. Data were analyzed by using Nexus Copy Number Discovery. Results. The RPA group rarely showed any copy number alteration, except for 1 case that exhibited losses in 5 p15.33 p15.1, 5 g13.1 q35.3 and 12 q12 813.11. The PA group also showed few copy number alterations, and the most frequent findings involved chromosomes 8: 8p21.3-p12 (gain), 8q12.1 (loss), 8p23.3-q24.3 (gain), and 8q12.1-q21.11 (gain). Genomic amplifications were revealed in the PA group, and the relevant affected genes were MAML2 and LIFR. Conclusions. PA and RPA exhibit few somatic copy number alterations and show a similar genomic profile on aCGH.12915964FAPESP – Fundação de Amparo à Pesquisa Do Estado De São Paulo11/23204-5; 11/23366-5; 15/07304-0; 17/00831-