New Implication in the Platelet–Cancer Interplay

Dear Colleagues,

Ever since Trousseau’s prophetic observation in 1865 that clotting disorders are associated with metastatic cancer—later shown to be linked to elevated platelet counts (thrombocytosis)—there has been growing appreciation of the significant role platelets may play in cancer biology. Furthermore, regular consumption of aspirin, a potent antiplatelet agent via irreversible COX-1 inhibition, has been associated with a significant reduction in the incidence and metastatic spread of several cancers in numerous clinical trials, with the strongest evidence seen in patients with colorectal cancer.

Building on this foundation, our laboratory has demonstrated in preclinical cancer models that aspirin and phosphatidylcholine (PC)-associated aspirin inhibit the growth of colonic, ovarian, breast, and pancreatic cancers in both in vivo and in vitro systems. This effect is linked to their ability to suppress platelet activity, as indicated by the inhibition of thromboxane generation. We also demonstrated that co-culture of cancer cells with platelets results in activation of both cell types, an effect that can be prevented by adding aspirin to the culture medium in a dose–response manner.

Taken together, these observations support the conclusion that platelet activation plays an important role in the metastatic spread of numerous cancers—an effect that can be irreversibly blocked by the daily consumption of low-dose aspirin.

Dr. Lenard M. Lichtenberger
Guest Editor

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