Platelets, NETs and cancer. Issue 164 (April 2018)

• Record Type: Journal Article
• Authors: Cedervall, Jessica; Hamidi, Anahita; Olsson, Anna-Karin
• Is Part Of: Thrombosis research. Issue 164(2018)Supplement 1
• Page Start: S148
• Page End: S152
• Publication Date: 2018-04
• Subjects: NETs neutrophil extracellular traps -- VTE venous thromboembolism -- PE pulmonary embolism -- DIC disseminated intravascular coagulation -- DVT deep vein thrombosis -- TF tissue factor -- MP microparticle -- CP cancer procoagulant -- MMP matrix metalloproteinase -- VEGF vascular endothelial growth factor -- MPO myeloperoxidase -- NE neutrophil elastase -- LPS lipopolysaccharides -- TLR Toll like receptor -- poly (I:C) polyinosinic:polycytidylic -- TRALI transfusion-related acute lung injury -- ADP adenosine diphosphate -- vWF von Willebrand Factor -- HMGB1 high-mobility group box 1 -- RAGE Receptor for Advanced Glycation End products -- PSGL-1 P-selectin glycoprotein ligand-1 -- ED-A extra domain-A; Cancer -- Thrombosis -- Platelets -- Neutrophil extracellular traps -- NETs -- Thrombosis; Thrombosis -- Periodicals; 616.135
• DOI: 10.1016/j.thromres.2018.01.049
• Languages: English
• ISSNs: 0049-3848

Abstract

Abstract: In addition to the central role of platelets in hemostasis, they contribute to pathological conditions such as inflammation and tumor progression. Aberrant expression and/or exposure of pro-coagulant factors in the tumor microenvironment induce platelet activation and subsequent release of growth factors from platelet granules. Cancer patients are commonly affected by thrombotic events, as a result of tumor-induced platelet activation. A novel player potentially contributing to cancer-associated thrombosis is the formation of neutrophil extracellular traps (NETs). NETs are composed of externalized DNA of nuclear or mitochondrial origin, bound to histones and granular proteases such as neutrophil elastase (NE) and myeloperoxidase (MPO). These extracellular traps help neutrophils to catch and kill pathogens such as bacteria, virus and fungi. It is now clear that NETs form also under conditions of sterile inflammation such as cancer and autoimmunity and can promote thrombosis. Recent data show that platelets play a key role in determining when and where NETs should form. This review will highlight our current insight in the role of platelets as regulators of NET formation, both during infection and sterile inflammation.