The rising incidence and persistent thrombosis in multiple cancers including those that are immunosuppressive highlight the need for understanding the tumor coagulome system and its role beyond hemostatic complications. Immunotherapy has shown significant benefits in solid organ tumors but has been disappointing in the treatment of hypercoagulable cancers, such as glioblastoma and pancreatic ductal adenocarcinomas. Thus, targeting thrombosis to prevent immunosuppression seems a clinically viable approach in cancer treatment. Hypercoagulable tumors often develop fibrin clots within the tumor microenvironment (TME) that dictates the biophysical characteristics of the tumor tissue. The application of systems biology and single-cell approaches highlight the potential role of coagulome or thrombocytosis in shaping the tumor immune microenvironment (TIME). In-depth knowledge of the tumor coagulome would provide unprecedented opportunities to better predict the hemostatic complications, explore how thrombotic stroma modulates tumor immunity, reexamine the significance of clinical biomarkers, and enable steering the stromal versus systemic immune response for boosting the effectiveness of immune checkpoint inhibitors in cancer treatment. We focus on the role of coagulation factors in priming a suppressive TIME and the huge potential of existing anticoagulant drugs in the clinical settings of cancer immunotherapy.

多种癌症（包括免疫抑制癌症）的发病率上升和持续血栓形成突出表明需要了解肿瘤凝固组系统及其在止血并发症之外的作用。免疫疗法在实体器官肿瘤中显示出显着的益处，但在治疗高凝癌症（例如胶质母细胞瘤和胰腺导管腺癌）方面却令人失望。因此，针对血栓形成来预防免疫抑制似乎是临床上可行的癌症治疗方法。高凝肿瘤通常在肿瘤微环境（TME）内形成纤维蛋白凝块，这决定了肿瘤组织的生物物理特征。系统生物学和单细胞方法的应用突出了凝固组或血小板增多症在塑造肿瘤免疫微环境（TIME）中的潜在作用。对肿瘤凝固组的深入了解将为更好地预测止血并发症提供前所未有的机会，探索血栓基质如何调节肿瘤免疫，重新审视临床生物标志物的重要性，并能够控制基质与全身免疫反应以提高免疫检查点的有效性癌症治疗中的抑制剂。我们重点关注凝血因子在启动抑制性 TIME 中的作用以及现有抗凝药物在癌症免疫治疗临床环境中的巨大潜力。