Molecular Aspects of Thyroid Calcification

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.

Nomogram prediction for the involution of the ablation zone after radiofrequency ablation treatment in patients with low-risk papillary thyroid carcinoma

“…According to Weiskopf et al [32], an age-related decline in immune functions could affect the capacity of the immune system to respond to pathogens and repair damaged tissue. Macrocalcification is defined as calcifications >1 mm with posterior acoustic shadows [33]. Our results showed that the larger the calcification, the less likely is the complete ablation zone disappearance in the first year.…”

Jejunal Dieulafoy lesion with intraintestinal calcification on computerized tomography

“…[ 6 , 7 ] Meanwhile, calcification may be an external manifestation of some diseases, such as papillary thyroid carcinoma and necrotic adipose tissue and so on. [ 8 , 9 ] In addition, calcification occurred in gastric adenocarcinoma, and the cause is related to the parathyroid hormone secreted by adenocarcinoma. [ 10 , 11 ] However, up to now, there are few reports about calcification associated with GI bleeding.…”

Meninges Outside the Meninges: Ectopic Meningiomas and Meningothlelial Proliferations

“…The pathogenesis of psammoma bodies is still controversial with theories involving vascular thrombosis of papillae, followed by calcification and endothelial necrosis. More recently, osteopontin (OPN), a calcium-binding glycophosphotein has been implicated in the formation of psammoma bodies being expressed in CD68 positive macrophages along with other factors that include alkaline phosphatase, osteocalcin, metalloproteinases, bone sialoprotein, and others [56]. OPN expression has been shown to be increased in meningiomas compared to normal meninges, correlates with histological grade, and is a predictor of recurrence in WHO grade I tumors [57,58].…”