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Impacts of Cancer on Platelet Production Activation and Education and Mechanisms of Cancer-Associated Thrombosis

机译:癌症对血小板产生活化和教育的影响以及与癌症相关的血栓形成的机制

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摘要

Platelets are small anucleate cells that are traditionally described as the major effectors of hemostasis and thrombosis. However, increasing evidence indicates that platelets play several roles in the progression of malignancies and in cancer-associated thrombosis. A notable cross-communication exists between platelets and cancer cells. On one hand, cancer can “educate” platelets, influencing their RNA profiles, the numbers of circulating platelets and their activation states. On the other hand, tumor-educated platelets contain a plethora of active biomolecules, including platelet-specific and circulating ingested biomolecules, that are released upon platelet activation and participate in the progression of malignancy. The numerous mechanisms by which the primary tumor induces the production, activation and aggregation of platelets (also known as tumor cell induced platelet aggregation, or TCIPA) are directly related to the pro-thrombotic state of cancer patients. Moreover, the activation of platelets is critical for tumor growth and successful metastatic outbreak. The development or use of existing drugs targeting the activation of platelets, adhesive proteins responsible for cancer cell-platelet interactions and platelet agonists should be used to reduce cancer-associated thrombosis and tumor progression.
机译:血小板是小的无核小细胞,传统上被描述为止血和血栓形成的主要效应物。然而,越来越多的证据表明血小板在恶性肿瘤的进展以及与癌症相关的血栓形成中起着多种作用。血小板与癌细胞之间存在明显的交叉交流。一方面,癌症可以“教育”血小板,从而影响其RNA谱图,循环中的血小板数量及其激活状态。另一方面,受肿瘤影响的血小板含有过多的活性生物分子,包括血小板特异性和循环摄入的生物分子,它们在血小板活化后释放并参与恶性进展。原发性肿瘤诱导血小板生成,活化和聚集的多种机制(也称为肿瘤细胞诱导的血小板聚集或TCIPA)与癌症患者的血栓形成前状态直接相关。此外,血小板的活化对于肿瘤生长和成功的转移性暴发至关重要。应使用针对血小板活化,负责癌细胞-血小板相互作用的粘附蛋白和血小板激动剂的现有药物的开发或使用,以减少与癌症相关的血栓形成和肿瘤进展。

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