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Review
. 2018 Nov 14;10(11):441.
doi: 10.3390/cancers10110441.

Impacts of Cancer on Platelet Production, Activation and Education and Mechanisms of Cancer-Associated Thrombosis

Léa Plantureux  1 , Diane Mège  2   3 , Lydie Crescence  4 , Françoise Dignat-George  5 , Christophe Dubois  6 , Laurence Panicot-Dubois  7
Affiliations
Review

Impacts of Cancer on Platelet Production, Activation and Education and Mechanisms of Cancer-Associated Thrombosis

Léa Plantureux et al. Cancers (Basel). .

Abstract

Platelets are small anucleate cells that are traditionally described as the major effectors of hemostasis and thrombosis. However, increasing evidence indicates that platelets play several roles in the progression of malignancies and in cancer-associated thrombosis. A notable cross-communication exists between platelets and cancer cells. On one hand, cancer can "educate" platelets, influencing their RNA profiles, the numbers of circulating platelets and their activation states. On the other hand, tumor-educated platelets contain a plethora of active biomolecules, including platelet-specific and circulating ingested biomolecules, that are released upon platelet activation and participate in the progression of malignancy. The numerous mechanisms by which the primary tumor induces the production, activation and aggregation of platelets (also known as tumor cell induced platelet aggregation, or TCIPA) are directly related to the pro-thrombotic state of cancer patients. Moreover, the activation of platelets is critical for tumor growth and successful metastatic outbreak. The development or use of existing drugs targeting the activation of platelets, adhesive proteins responsible for cancer cell-platelet interactions and platelet agonists should be used to reduce cancer-associated thrombosis and tumor progression.

Keywords: cancer cells; cancer-associated thrombosis; platelets; tumor cell induced platelet aggregation (TCIPA); tumor educated platelets (TEP).

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Mechanisms of cancer-associated thrombocytosis. This figure summarizes all the mechanisms involved in the production of platelets mediated by the primary tumor. BMEC: Bone Marrow Endothelial Cells. This figure was obtained using Servier medical art. http://smart.servier.com/. GM-CSF: Granulocyte-Macrophage Colony-Stimulating Factor; G-CSF: Granulocyte Colony-Stimulating Factor; M-CSF: Macrophage Colony-Stimulating Factor; Il-6: Interleukin-6; LIF: Leukemia Inhibitory Factor; FLK-2: Fetal Liver Kinase-2; Kit-ligand (Steel factor); TPO: thrombopoietin.
Figure 2
Figure 2
Impacts of cancer on platelet production, activation and education and mechanisms of cancer-associated thrombosis. This figure summarizes all the mechanisms involved in the production, the activation and the education of platelets mediated by the primary tumor and the mechanisms of cancer-associated thrombosis. TC: Tumor Cell. This figure was obtained using Servier medical art. http://smart.servier.com/.
See this image and copyright information in PMC

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