The anti-inflammatory and anti-platelet properties of aspirin have made it the subject of intensive investigation for over a century. More recently, aspirin use has been correlated with reduced long-term risk of some cancers, particularly colorectal cancer. The reasons remain unknown, as does the degree to which the effect comes from direct inhibition of cancer cells and how much is due to inhibition of platelet activation and function.
A study recently completed by a team of OHSU researchers and published in the American Journal of Physiology—Cell Physiology suggests the benefit of aspirin may be due to its effect on platelets rather than acting directly on tumor cells.
In a series of experiments with cultured cells, a team led by Owen McCarty, Ph.D., chair of the Department of Biomedical Engineering in the School of Medicine, showed that inhibition of platelets with low doses of aspirin cuts the signaling link between platelets and some cancer cells, which in turn knocks back cancer growth.
It is not yet known whether the cascade of effects observed in cell cultures works the same way in people. The new findings are not sufficient to justify taking aspirin solely to help prevent cancer. Aspirin has an effect mediated by platelets that may work in concert with aspirin’s anti-inflammatory properties to oppose malignant cell growth, and low doses of aspirin might eventually prove a safe and effective way to prevent cancer in patients at risk.
The research was supported by grants from the Altarum Institute, the National Institutes of Health, and the American Heart Association.
Read the OHSU release.