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甲状腺钙化的分子方面。

Molecular Aspects of Thyroid Calcification.

机构信息

Cellular and Molecular Oncobiology Program, Research Coordination, National Institute of Cancer, Rua André Cavalcante nº 37, Rio de Janeiro 20231-050, Brazil.

Natural Science Department, Health and Humanities Institute, Fluminense Federal University, Rua Recife, Rio das Ostras 28895-532, Brazil.

出版信息

Int J Mol Sci. 2020 Oct 19;21(20):7718. doi: 10.3390/ijms21207718.

DOI:10.3390/ijms21207718
PMID:33086487
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7589718/
Abstract

In thyroid cancer, calcification is mainly present in classical papillary thyroid carcinoma (PTC) and in medullary thyroid carcinoma (MTC), despite being described in benign lesions and in other subtypes of thyroid carcinomas. Thyroid calcifications are classified according to their diameter and location. At ultrasonography, microcalcifications appear as hyperechoic spots ≤ 1 mm in diameter and can be named as stromal calcification, bone formation, or psammoma bodies (PBs), whereas calcifications > 1 mm are macrocalcifications. The mechanism of their formation is still poorly understood. Microcalcifications are generally accepted as a reliable indicator of malignancy as they mostly represent PBs. In order to progress in terms of the understanding of the mechanisms behind calcification occurring in thyroid tumors in general, and in PTC in particular, we decided to use histopathology as the basis of the possible cellular and molecular mechanisms of calcification formation in thyroid cancer. We explored the involvement of molecules such as runt-related transcription factor-2 (Runx-2), osteonectin/secreted protein acidic and rich in cysteine (SPARC), alkaline phosphatase (ALP), bone sialoprotein (BSP), and osteopontin (OPN) in the formation of calcification. The present review offers a novel insight into the mechanisms underlying the development of calcification in thyroid cancer.

摘要

在甲状腺癌中,钙化主要存在于经典型甲状腺乳头状癌(PTC)和甲状腺髓样癌(MTC)中,尽管在良性病变和其他类型的甲状腺癌中也有描述。甲状腺钙化根据其直径和位置进行分类。在超声检查中,微钙化表现为直径≤1mm 的高回声点,可命名为间质钙化、骨形成或砂粒体(PBs),而直径>1mm 的钙化则为粗钙化。其形成机制仍知之甚少。微钙化通常被认为是恶性肿瘤的可靠指标,因为它们主要代表 PB。为了深入了解甲状腺肿瘤,特别是 PTC 中钙化发生的机制,我们决定以组织病理学为基础,探讨可能的细胞和分子钙化形成机制。我们探讨了 runt 相关转录因子-2(Runx-2)、骨粘连蛋白/分泌性富含天冬氨酸和半胱氨酸的酸性蛋白(SPARC)、碱性磷酸酶(ALP)、骨唾液蛋白(BSP)和骨桥蛋白(OPN)等分子在钙化形成中的作用。本综述为甲状腺癌中钙化发展的机制提供了新的见解。

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Nodular Thyroid Disease in the Era of Precision Medicine.精准医学时代的结节性甲状腺疾病
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10
OPNa Overexpression Is Associated with Matrix Calcification in Thyroid Cancer Cell Lines.OPNa 过表达与甲状腺癌细胞系中的基质钙化有关。
Int J Mol Sci. 2018 Sep 30;19(10):2990. doi: 10.3390/ijms19102990.