U. 770 INSERM, Hôpital de Bicêtre, France.
Thromb Res. 2010 Apr;125 Suppl 2:S84-8. doi: 10.1016/S0049-3848(10)70021-9.
Thrombotic complications have been documented in patients with cancer, and associated with tumor progression. Cancer patients have an increased level of circulating submicrometric (0.1-1 microm) membrane fragments termed microvesicles (MV) or microparticles. Variations in MV levels and phenotypes make them relevant pathogenic markers of thrombotic disorders and vascular damage. MV are released from the plasma membrane of activated or apoptotic cells, and are considered efficient effectors of the hemostatic or thrombotic responses. They are mostly characterized by the presence of procoagulant phospholipids at their surface and eventually that of tissue factor depending on the cells they originate from. These procoagulant entities allow them to initiate and propagate thrombotic reactions within the blood vessels. MV are also recognized as proximal or remote mediators of cell-to-cell communication. The mechanisms through which MV interact with target cells remain unclear although a number of studies suggest involvement of MV-cell fusion and/or ligand-receptor interactions. It has however to be emphasized that MV do not necessarily elicit deleterious responses. This review focuses on the role of MV in cancer-associated thrombosis.
血栓并发症已在癌症患者中得到证实，并与肿瘤进展相关。癌症患者的循环亚微米（0.1-1 微米）膜片段水平升高，这些片段被称为微囊泡（MV）或微颗粒。MV 水平和表型的变化使它们成为血栓形成障碍和血管损伤的相关致病标志物。MV 从激活或凋亡细胞的质膜释放出来，被认为是止血或血栓反应的有效效应物。它们主要的特征是表面存在促凝磷脂，并且最终根据它们起源的细胞，存在组织因子。这些促凝实体允许它们在血管内启动和传播血栓反应。MV 也被认为是细胞间通讯的近端或远程介质。MV 与靶细胞相互作用的机制尚不清楚，尽管许多研究表明 MV-细胞融合和/或配体-受体相互作用的参与。然而，必须强调的是，MV 不一定会引起有害反应。这篇综述重点介绍了 MV 在癌症相关血栓形成中的作用。
