乳腺癌微钙化形成的分子机制

Molecular mechanism of microcalcification in breast cancer

乳腺微钙化(MC)是乳腺癌重要的影像学特征。在乳腺组织中常见两种类型的MC物质,Ⅰ型MC(草酸钙)仅存在于良性病变中,而Ⅱ型MC(羟磷灰石)通常存在于恶性病变中。研究者们利用这一影像学特征制定和发明了先进的影像诊断程序和成像技术,然而MC形成的机制却了解甚少。因此,本文试图解释乳腺癌MC形成的分子机制,其重点在于部分异质性乳腺癌细胞如何获得成骨样表型并启动病理性钙化过程。同时,本文还强调了骨形成蛋白、肿瘤相关巨噬细胞以及上皮间质化过程在病理性钙化过程中的调控作用。

Breast microcalcification（MC） is an important imaging feature of breast cancer. There are two types of MC in the breast tissue; microcalcification type I（calcium oxalate） only occurs in benign lesions, whereas type II（calcium hydroxyapatite）generally in malignant lesions. Over the past few decades, researchers have formulated advanced imaging diagnostic procedures and imaging techniques based on this imaging feature, while the mechanism of its formation is still poorly understood. Hence, this paper attempts to address the molecular mechanism of microcalcification in breast cancer, with focus on how a subpopulation of heterogeneous breast tumor cells attains an osteoblast-like phenotype and activates pathophysiological microcalcification. Also, the regulatory effect of bone morphogenetic proteins, tumor-associated macrophages and epithelial-mesenchymal transition in this pathological calcification of breast has been highlighted.