Molecular mechanisms of thrombotic complications in glial tumors

A. V. Savelyeva, Y. Zhilenkova, M. A. Simakova, O. V. Sirotkina
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引用次数: 0

Abstract

Cancer patients are at increased risk of venous thromboembolic complications (VTE), which are the second leading cause of death in these patients. Moreover, the maximum incidence of VTE occurs in tumors of the central nervous system [1]. Research is being conducted to identify laboratory biomarkers of increased risk of VTE, but to date data on their role are ambiguous. Patients with a mutation in the isocitrate dehydrogenase (IDH) gene are at lower risk of VTE, and the IDH mutation is associated with suppression of the production of tissue factor (TF) and podoplanin, the most studied molecules responsible for the occurrence of thromboembolic complications [2]. The main specific markers of VTE are based on immunohistochemical methods, which are possible only with histological examination of the tumor material. Therefore, it is important to find noninvasive biomarkers that could be used to assess the risk of venous thromboembolic complications. In this review, we will focus on highlighting the accumulated knowledge on this theme.
胶质瘤血栓并发症的分子机制
癌症患者罹患静脉血栓栓塞并发症(VTE)的风险增加,这是导致这些患者死亡的第二大原因。此外,中枢神经系统肿瘤的 VTE 发生率最高[1]。目前正在进行研究,以确定增加 VTE 风险的实验室生物标志物,但迄今为止有关其作用的数据尚不明确。异柠檬酸脱氢酶(IDH)基因突变的患者罹患 VTE 的风险较低,IDH 突变与抑制组织因子(TF)和荚膜蛋白的产生有关,而组织因子和荚膜蛋白是研究最多的导致血栓栓塞并发症发生的分子[2]。VTE 的主要特异性标志物是基于免疫组化方法,只有通过对肿瘤材料进行组织学检查才能获得。因此,寻找可用于评估静脉血栓栓塞并发症风险的无创生物标志物非常重要。在本综述中,我们将重点介绍在这一主题方面积累的知识。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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