Parathyroid tumors are the second most common endocrine neoplasia, and it is almost always associated with hypersecretion of the parathormone (PTH), involved in calcium homeostasis, causing primary hyperparathyroidism (PHPT). Parathyroid neoplasia has a stromal component particularly represented in atypical adenomatous and carcinomatous lesions. Recently, data about the features and the function of the parathyroid tumor microenvironment (TME) have been accumulated. Parathyroid TME includes heterogeneous cells: endothelial cells, myofibroblasts, lymphocytes and macrophages, and mesenchymal stem cells have been identified, each of them presenting a phenotype consistent with tumor-associated cells. Parathyroid tumors overexpress proangiogenic molecules including vascular endothelial growth factor (VEGF-A), fibroblast growth factor-2 (FGF-2), and angiopoietins that promote both recruitment and proliferation of endothelial cell precursors, thus resulting in a microvessel density higher than that detected in normal parathyroid glands. Moreover, parathyroid tumor endocrine cells operate multifaceted interactions with stromal cells, partly mediated by the CXCL12/CXCR4 pathway, while, at present, the immune landscape of parathyroid tumors has just begun to be investigated. Studies about TME in parathyroid adenomas provide an example of the role of TME in benign tumors, whose molecular mechanisms and functions comprehension are limited.

Parathyroid Tumor Microenvironment / C. Verdelli, V. Vaira, S. Corbetta (ADVANCES IN EXPERIMENTAL MEDICINE AND BIOLOGY). - In: Tumor Microenvironments in Organs : From the Brain to the Skin. Part A / [a cura di] A. Birbrair. - Prima edizione. - [s.l] : Springer, 2020. - ISBN 9783030362133. - pp. 37-50

Parathyroid Tumor Microenvironment

C. Verdelli
Primo
Investigation
;
V. Vaira
Penultimo
Writing – Original Draft Preparation
;
S. Corbetta
Ultimo
Writing – Review & Editing
2020

Abstract

Parathyroid tumors are the second most common endocrine neoplasia, and it is almost always associated with hypersecretion of the parathormone (PTH), involved in calcium homeostasis, causing primary hyperparathyroidism (PHPT). Parathyroid neoplasia has a stromal component particularly represented in atypical adenomatous and carcinomatous lesions. Recently, data about the features and the function of the parathyroid tumor microenvironment (TME) have been accumulated. Parathyroid TME includes heterogeneous cells: endothelial cells, myofibroblasts, lymphocytes and macrophages, and mesenchymal stem cells have been identified, each of them presenting a phenotype consistent with tumor-associated cells. Parathyroid tumors overexpress proangiogenic molecules including vascular endothelial growth factor (VEGF-A), fibroblast growth factor-2 (FGF-2), and angiopoietins that promote both recruitment and proliferation of endothelial cell precursors, thus resulting in a microvessel density higher than that detected in normal parathyroid glands. Moreover, parathyroid tumor endocrine cells operate multifaceted interactions with stromal cells, partly mediated by the CXCL12/CXCR4 pathway, while, at present, the immune landscape of parathyroid tumors has just begun to be investigated. Studies about TME in parathyroid adenomas provide an example of the role of TME in benign tumors, whose molecular mechanisms and functions comprehension are limited.
Parathyroid tumors; Primary hyperparathyroidism; PTH; Parathyroid adenomas; Parathyroid carcinomas; Tumor-associated myofibroblasts; Tumor-associated endothelial cells; Tumor-infiltrating lymphocytes; Tumor-associated macrophages; Collagen matrix; CXCR4; SDF-1/CXCL12; VEGF-A; CD34; CD31; alpha-SMA
Settore MED/13 - Endocrinologia
Settore MED/08 - Anatomia Patologica
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2434/807479
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