癌症相关的血栓形成的血小板活化机制:专注于骨髓增殖性肿瘤

• ¹血液学和血液恶性肿瘤,贝斯以色列女执事医疗中心,美国哈佛医学院
• ²波士顿大学医学院医学系,,美国
• ³惠特克心血管研究所、美国波士顿大学医学院的
• ⁴生物化学、美国波士顿大学医学院的

无核红细胞,血小板血栓和止血中扮演关键性的角色。血小板也在效应细胞恶性肿瘤的微环境和已知癌症。因此,这些细胞提供中央止血系统之间的联系,炎症和癌症恶化。血小板的激活癌症被假定为肿瘤转移和发展当地的入侵。同样,cancer-activated血小板可以增加的风险发展动脉和静脉血栓形成;癌症的发病率的主要因素。血小板颗粒分泌肿瘤内环境或等离子体提供了一个丰富的潜在生物标记物预测血栓形成的风险或肿瘤恶化。在骨髓增殖性肿瘤(或然数),特点是骨髓前体细胞克隆扩张和不正常的功能和红细胞数量、白细胞和血小板,患者罹患血栓性和出血性并发症。推动这种机制很可能多因子的但仍知之甚少。几个鼠标模型发展到接近或然数表型的突变,开车在JAK2 (JAK2V617F)或在calreticulin (CALR)或骨髓白血病病毒致癌基因受体(MPL),研究了血栓性表型。 Variability and discrepancies were identified within different disease models of MPN, emphasizing the complexity of increased risk of clotting and bleeding in these pathologies. Here, we review recent literature on the role of platelets in cancer-associated arterial and venous thrombosis and use MPN as case study to illustrate recent advances in experimental models of thrombosis in a malignant phenotype. We address major mechanisms of tumor-platelet communication leading to thrombosis and focus on the role of altered platelets in promoting thrombosis in MPN experimental models and patients with MPN. Recent identification of platelet-derived biomarkers of MPN-associated thrombosis is also reviewed, with potential therapeutic implications.