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Special Issue "Molecular Biology of Parathyroid Tumors"

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Endocrinology and Metabolism".

Deadline for manuscript submissions: closed (31 December 2020).

Special Issue Editor

Prof. Dr. Sabrina Corbetta
E-Mail Website
Guest Editor
Endocrinology and Diabetology Service, Department of Biomedical, Surgical and Dental Sciences, University of Milan, IRCCS Istituto Ortopedico Galeazzi, Milan, Italy
Interests: primary hyperparathyroidism; Calcium-sensing receptor; parathyroid tumors; microRNAs; MEN1; osteoporosis
Special Issues and Collections in MDPI journals

Special Issue Information

Dear colleagues,

Parathyroid tumors are the second most common endocrine neoplasia. They are mainly benign lesions associated with parathormone (PTH) inappropriate secretion, determining the metabolic disorder known as primary hyperparathyroidism (PHPT). Parathyroid tumors are characterized by calcium-sensing receptor (CASR)-mediated reduced sensitivity to extracellular calcium. Genetic and epigenetic alterations resulting in aberrant expression of protein-coding and non-coding genes have been identified in parathyroid tumors. Besides inactivating mutations of the oncosuppressors MEN1 and HRPT2/CDC73, epigenetic changes have been reported. Impaired DNA methylation involving single genes, the deregulated expression of microRNAs, and long noncoding RNAs have started to be to be investigated. However, many aspects of the molecular biology of the parathyroid tumors need to be explored, such as the molecular pathways related to the genetic and epigenetic aberrations, and their effects on parathyroid cell proliferation and/or sensitivity to extracellular calcium, in order to provide targets for new therapeutic approaches, which are lacking.

The Special Issue aims to widely explore the molecular and biological features of parathyroid tumorigenesis, focusing on genetic and epigenetic aspects, parathyroid cell proliferation and biology, tumor microenvironment, CASR-mediated sensitivity to extracellular calcium, deregulation of the PTH release, and the differences between the benign and malignant behavior of the parathyroid cells, considering original articles and review papers.

Prof. Dr. Sabrina Corbetta
Guest Editor

Manuscript Submission Information

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Keywords

  • Parathyroi adenomas
  • Parathyroid cancers
  • MEN1
  • CDC73
  • Calcium sensing receptor (CASR)
  • microRNAs
  • methylation
  • LncRNAs
  • Epigenetics
  • PTH
  • Parathyroid cell proliferation

Published Papers (1 paper)

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Review

Review
Parathyroid Cell Proliferation in Secondary Hyperparathyroidism of Chronic Kidney Disease
Int. J. Mol. Sci. 2020, 21(12), 4332; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21124332 - 18 Jun 2020
Cited by 3 | Viewed by 2022
Abstract
Secondary hyperparathyroidism (SHP) is a common complication of chronic kidney disease (CKD) that correlates with morbidity and mortality in uremic patients. It is characterized by high serum parathyroid hormone (PTH) levels and impaired bone and mineral metabolism. The main mechanisms underlying SHP are [...] Read more.
Secondary hyperparathyroidism (SHP) is a common complication of chronic kidney disease (CKD) that correlates with morbidity and mortality in uremic patients. It is characterized by high serum parathyroid hormone (PTH) levels and impaired bone and mineral metabolism. The main mechanisms underlying SHP are increased PTH biosynthesis and secretion as well as increased glandular mass. The mechanisms leading to parathyroid cell proliferation in SHP are not fully understood. Reduced expressions of the receptors for calcium and vitamin D contribute to the disinhibition of parathyroid cell proliferation. Activation of transforming growth factor-α-epidermal growth factor receptor (TGF-α-EGFR), nuclear factor kappa B (NF-kB), and cyclooxygenase 2- prostaglandin E2 (Cox2-PGE2) signaling all correlate with parathyroid cell proliferation, underlining their roles in the development of SHP. In addition, the mammalian target of rapamycin (mTOR) pathway is activated in parathyroid glands of experimental SHP rats. Inhibition of mTOR by rapamycin prevents and corrects the increased parathyroid cell proliferation of SHP. Mice with parathyroid-specific deletion of all miRNAs have a muted increase in serum PTH and fail to increase parathyroid cell proliferation when challenged by CKD, suggesting that miRNA is also necessary for the development of SHP. This review summarizes the current knowledge on the mechanisms of parathyroid cell proliferation in SHP. Full article
(This article belongs to the Special Issue Molecular Biology of Parathyroid Tumors)
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