These actions may contribute to metastatic spread and tumor growth ( 2). During TCIPAplatelets protect circulating tumor cells from the deleterious effects of shear forces and also preserve the tumor cells from the immune system by creating a physical barrier around cancer cells ( 8). TCIPA has been documented to be involved in tumorigenesis in several types of cancers including breast ( 5)lung ( 6)and pancreatic ( 7). This mechanism is now called tumor cell–induced platelet aggregation (TCIPA) ( 4). Further studies demonstrated that tumor cells can induce platelet activation and aggregation.

He emphasized the association of malignancies with the creation of venous and arterial platelet–rich microthrombi in the vasculature ( 3). In 1865 Armand Trousseau first described cases of thrombophlebitis in patients with cancer.

The primary hemostatic function of platelets is well known however, increasing evidence supports the crucial role of platelets in cancer biology ( 1, 2). In this review, we present the recent discoveries of mechanisms by which cancer cells activate platelets, and discuss new platelet-targeted therapeutic strategies. On the other hand, the use of drugs that are mostly easily accessible and widely used in general practice may be an opportunity to propose an unparalleled antitumor prophylaxis. On the one hand, it may affect patients’ prognosis by enhancing known therapies in advanced-stage tumors. Targeting tumor cell-induced platelet aggregation (TCIPA) by antiplatelet drugs may open ways to develop new treatment modalities. For a better understanding, we briefly discuss the physiological role of the factors in the platelet activation process, and subsequently, we provide scientific evidence and discuss their potential role in the progression of specific cancers. These factors may be presented on the surface of tumor cells as well as in their microenvironment, and some may trigger more than just one simple receptor–ligand mechanism. Herein, we present a wider view on the induction of platelet aggregation by specific factors primarily developed by cancer, including coagulation factors, adhesion receptors, growth factors, cysteine proteases, matrix metalloproteinases, glycoproteins, soluble mediators, and selectins.

During the process, platelets protect circulating tumor cells from the deleterious effects of shear forces, shield tumor cells from the immune system, and provide growth factors, facilitating metastatic spread and tumor growth at the original site as well as at the site of metastasis. This has been documented to be involved in tumor progression in several types of cancers, such as lung, colon, breast, pancreatic, ovarian, and brain. Tumor cells have the ability to induce platelet activation and aggregation. 2Department of General and Oncological Urology, Collegium Medicum in Bydgoszcz, Nicolaus Copernicus University in Toruń, Toruń, Poland.1Department of Clinical Pathomorphology, Faculty of Medicine, Collegium Medicum in Bydgoszcz, Nicolaus Copernicus University, Toruń, Poland.Wiktoria Strasenburg 1*†, Jakub Jóźwicki 1†, Justyna Durślewicz 1, Błażej Kuffel 2, Martyna Parol Kulczyk 1, Adam Kowalewski 1, Dariusz Grzanka 1, Tomasz Drewa 2 and Jan Adamowicz 2

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