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Molecular Aspects of Thyroid Calcification

机译:甲状腺钙化的分子方面

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摘要

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.
机译:在甲状腺癌中,钙化主要存在于古典乳头状甲状腺癌(PTC)和髓质甲状腺癌(MTC)中,尽管在良性病变和其他甲状腺癌的其他亚型中描述。根据其直径和位置对甲状腺钙化进行分类。在超声检查中,微钙化出现为直径≤1mm的高档斑点,并且可以被命名为基质钙化,骨形成或pBS)(PBS),而钙化> 1 mm是宏观经理。他们的形成机制仍然明白。微钙通常被认为是恶性肿瘤的可靠指标,因为它们主要代表PBS。为了在甲状腺肿瘤中发生的钙化机制的理解,特别是在PTC中,我们决定使用组织病理学作为甲状腺癌中可能钙化形成细胞和分子机制的基础。我们探讨了runt相关转录因子-2(runx-2),骨胶/分泌蛋白酸性和富含半胱氨酸(SPARC),碱性磷酸酶(ALP),骨唾液蛋白(BSP)和骨桥蛋白(OPN )在形成钙化。本综述提供了对甲状腺癌钙化发展的机制的新颖洞察力。

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