基因突变状态与肿瘤相关性静脉血栓关系的研究进展

Advances in the relationship between gene mutation status and cancer-associated venous thrombosis

肿瘤相关性静脉血栓栓塞疾病(venous thromboembolic disease,VTE)已成为当下肿瘤患者的第二大死因,诸多学者提出多种血栓风险模型,从而筛选出血栓发生风险可能较高的患者进行药物及物理干预措施,减少肿瘤相关性VTE的发生。随着精准医学的不断发展,现有结论已不能满足医务人员探索肿瘤相关性VTE相关问题的要求。基因检测已经成为肿瘤患者的“基线”检查,检测常见的驱动基因如表皮生长因子受体(epidermal growth factor receptor,EGFR)、间变性淋巴瘤激酶(anaplastic lymphoma kinase,ALK)、v-ros UR2肉瘤病毒癌基因同源物1(v-ros UR2 sarcoma virus oncogene homolog 1,ROS1)和鼠类肉瘤病毒致癌基因(kirsten ras sarcoma,KRAS)等已成为常态且被指南推荐应用于临床,基因突变状态在影响临床预后和治疗决策方面的地位日益凸显。基因突变状态与肿瘤相关性VTE之间是否存在关联,可否根据基因状态筛选出具有较高血栓风险的癌症人群,从而为更好地实施预防管理策略提供理论基础。本文旨在对基因突变状态与肿瘤相关性VTE之间关系的研究进展及其潜在机制进行综述。

Cancer-associated venous thromboembolic disease(VTE)has become the second leading cause of death among cancer patients.Some scholars have proposed a variety of thrombosis risk models to screen out patients with a higher thrombosis risk and then offer them drug or physical intervention measures to reduce the incidence of cancer-associated VTE.However,with the continuous development of precision medicine,these conclusions can no longer meet the requirements of medical personnel to explore the problems of cancer-associated VTE.Genetic testing has become the"baseline"test in cancer patients.Common driver genes,such as the epidermal growth factor receptor(EGFR),anaplastic lymphoma kinase(ALK),v-ros UR2 virus oncogene homolog 1(ROS1),and kirsten ras sarcoma(KRAS),have become the normalcy and are recommended by the guidelines for clinical use.The status of gene mutations in clinical prognosis and treatment is increasingly prominent.This review discusses whether there is a correlation between cancer-associated VTE and gene status and whether we can screen out cancer populations with a higher risk of thrombosis according to gene status,thus providing a theoretical basis for better implementation of prevention management strategies.