Aspirin, platelet inhibition and cancer prevention

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.

Keywords: Aspirin; colorectal cancer; cyclooxygenases; platelet activation; prostaglandin E2; thromboxane A2.