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- W2170821394 endingPage "1255" @default.
- W2170821394 startingPage "1247" @default.
- W2170821394 abstract "Platelets are highly reactive components of the circulatory system, which exert not only haemostatic activity but also contribute to the modulation of various pathological conditions including inflammation, atherosclerosis and cancer metastasis through the release of cytokines, chemokines and the presentation of several adhesion molecules. During cancer metastasis, the formation of platelet–tumor cell aggregates in the circulation facilitates immune evasion and the microvascular arrest of tumor cells at distant sites. Several adhesion molecules, such as integrins and glycoproteins, were shown to be involved in this process. Recent findings indicate that P-selectin is another main mediator of platelet–tumor cell interactions. Other effects of activated platelets on cancer progression are associated with a release of platelet-derived factors stimulating tumor growth and angiogenesis. Any interference in platelet–tumor cell interactions resulted in attenuation of cancer metastasis. The well recognized, albeit not fully characterized function of platelets during cancer progression defines platelets as potential targets for cancer therapy. Specifically, the rapid expression of P-selectin on the cell surface of activated platelets and its strong association with metastasis provide a rationale for P-selectin inhibition as an antimetastatic treatment." @default.
- W2170821394 created "2016-06-24" @default.
- W2170821394 creator A5047132606 @default.
- W2170821394 date "2008-08-01" @default.
- W2170821394 modified "2023-10-17" @default.
- W2170821394 title "The role of platelet activation in tumor metastasis" @default.
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- W2170821394 doi "https://doi.org/10.1586/14737140.8.8.1247" @default.
- W2170821394 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/18699763" @default.
- W2170821394 hasPublicationYear "2008" @default.
- W2170821394 type Work @default.