Departamento Clínico de Hematología, División Onco-Hematologia, UMAE, Hospital de Especialidades, Centro Médico Nacional de Occidente, Instituto Mexicano del Seguro Social, Guadalajara, Jalisco, México; Extensión, Consulting and Research Division, Universidad de Monterrey, San Pedro Garza García, Nuevo León, México; Unidad de Investigación Biomédica 02, UMAE, Hospital de Especialidades, Centro Médico Nacional de Occidente, Instituto Mexicano del Seguro Social, Guadalajara, Jalisco, Mexico.
Departamento Clínico de Hematología, División Onco-Hematologia, UMAE, Hospital de Especialidades, Centro Médico Nacional de Occidente, Instituto Mexicano del Seguro Social, Guadalajara, Jalisco, México.
Adv Clin Chem. 2021;105:213-242. doi: 10.1016/bs.acc.2021.03.001. Epub 2021 Apr 19.
Neoplasms result from changes in the mechanisms of growth, differentiation, and cellular death. Cancers are of high clinical relevance due to their prevalence and associated morbidity and mortality. The clinical and biological diversity of cancer depends mainly on cellular origin and degree of differentiation. These changes result from alterations in molecular expression that generate a complex clinical, biochemical, and morphologic phenotype. Although cancer is associated with a hypercoagulable state, few cancers result in a thrombotic event. Many factors influence thrombotic incidence, such as advanced disease, central catheter placement, chemotherapy, neoplasia, and surgery. The pro-coagulant state is associated with anomalies in the vascular wall, blood flow, blood constituents (tissue factor, thrombin), coagulation state, and cell growth factors. Tumor cells perpetuate this phenomenon by releasing tissue factor, inflammatory cytokines, and growth factors. These changes favor cellular activation that gives rise to actions involving coagulation, inflammation, thrombosis, tumor growth, angiogenesis, and tumor metastases. These, in turn, are closely linked to treatment response, tumor aggressiveness, and host survival. Activation of the coagulation cascade is related to these phenomena through molecules that interact in these processes. As such, it is necessary to identify these mediators to facilitate treatment and improve outcomes.
肿瘤是由于生长、分化和细胞死亡机制的改变而产生的。癌症由于其普遍性以及相关的发病率和死亡率而具有重要的临床意义。癌症的临床和生物学多样性主要取决于细胞起源和分化程度。这些变化是由于分子表达的改变导致复杂的临床、生化和形态表型而产生的。尽管癌症与高凝状态有关，但很少有癌症导致血栓形成事件。许多因素影响血栓形成的发生率，例如晚期疾病、中央导管放置、化疗、肿瘤和手术。促凝状态与血管壁、血流、血液成分（组织因子、凝血酶）、凝血状态和细胞生长因子的异常有关。肿瘤细胞通过释放组织因子、炎症细胞因子和生长因子来延续这种现象。这些变化有利于细胞激活，导致涉及凝血、炎症、血栓形成、肿瘤生长、血管生成和肿瘤转移的作用。反过来，这些又与治疗反应、肿瘤侵袭性和宿主生存密切相关。凝血级联的激活与这些现象通过相互作用的分子有关。因此，有必要识别这些介质以促进治疗并改善结果。
