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Semin Thromb Hemost 2014; 40(03): 296-305
DOI: 10.1055/s-0034-1370767
Thieme Medical Publishers 333 Seventh Avenue, New York, NY 10001, USA.

Platelet–Cancer Interactions

Hadi A. Goubran
1   Saskatoon Cancer Centre and Division of Oncology, Department of Medicine, College of Medicine, University of Saskatchewan, Saskatoon, Canada
,
Julie Stakiw
1   Saskatoon Cancer Centre and Division of Oncology, Department of Medicine, College of Medicine, University of Saskatchewan, Saskatoon, Canada
,
Mirjana Radosevic
2   Human Protein Process Sciences, Research and Development Department, Lille, France
,
Thierry Burnouf
3   Institute of Biomedical Materials and Tissue Engineering, College of Oral Medicine, Taipei Medical University, Taipei, Taiwan
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Publikationsdatum:
03. März 2014 (online)

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Abstract

Platelets play a crucial role in the pathophysiological processes of hemostasis and thrombosis. Increasing evidence indicates that they fulfill much broader roles in balancing health and disease. The presence of tumor cells affects platelets both numerically, through a wide variety of mediators and cytokines, or functionally through tumor cell–induced platelet activation, the first step toward cancer-induced thrombosis. This induction results from signaling events through the different platelet receptors, or may be cytokine-mediated. Reciprocally, upon activation, the platelets will release a myriad of growth factors from their dense and α-granules and peroxisomes; these will directly impact tumor growth, tethering, and spread. A similar cross-talk is initiated between tumor microvesicles stimulating the platelets and platelet microparticles, promoting both thrombosis and tumor growth. A vicious loop of activation thereafter takes place. Platelets directly and indirectly promote tumor growth, and enable a molecular mimicry coating the malignant growth and allowing metastasizing cells to escape T-cell–mediated immunity and natural killer cell surveillance. Breaking this vicious activation loop with nonspecific platelet inhibitors, such as aspirin, or by targeting specific sites on the activation cascade may offer a mean to reduce both the risks of development and progression of cancer and the risk of thrombosis.

Keywords

cancer - platelets - TCIPA - metastasis - antiplatelets - microparticles