Several lines of evidence are consistent with the hypothesis that activated platelets contribute to colorectal tumorigenesis and metastatization through direct cell-cell interactions and the release of different lipid and protein mediators, and microvesicles. This review examines the clinical pharmacology of low-dose aspirin as a basis for discussing the mechanisms underlying the contribution of platelets to neoplastic transformation and progression of cancer via the development of metastases.

Aspirin, platelet inhibition and cancer prevention.

Patrignani, Paola
Primo
;
Patrono, Carlo
2018

Abstract

Several lines of evidence are consistent with the hypothesis that activated platelets contribute to colorectal tumorigenesis and metastatization through direct cell-cell interactions and the release of different lipid and protein mediators, and microvesicles. This review examines the clinical pharmacology of low-dose aspirin as a basis for discussing the mechanisms underlying the contribution of platelets to neoplastic transformation and progression of cancer via the development of metastases.
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Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/11564/695049
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