The prothrombotic state in cancer.

Abstract

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.