Aspirin has been used to reduce the risk of both colon cancer and cardiovascular disease for more than 100 years, yet the mechanism by which the pain reliever has been achieving this is largely unknown. Researchers at Duke Health have identified a new mechanism of aspirin’s action and they believe they have solved the age-old riddle. The study revealed that aspirin affects the function of a gene regulatory protein directly. This protein suppresses tumors in the colon and has an influence on the function of platelets.
Deepak Voora, M.D., assistant professor in Duke’s Center for Applied Genomics & Precision Medicine and lead author, explains that known pharmacology does not predict the new behavior of aspirin identified by the research. It has however been known that COX-1, an enzyme involved in both blood clotting and inflammation, is blocked by aspirin, and this results in its blood thinning and pain reducing characteristics.
Aspirin’s blocking of COX-1 does however not fully explain how it influences cardiovascular health. It has also not been proven that COX-1 has any link to cancer at all.
The research team concentrated their study on a pattern of gene activity they call an aspirin response signature. This signature was previously developed by the same team. A network of genes that correlate with heart attack and platelet function was identified by this signature.
The approach taken with aspirin was use genomic data comprehensively to evaluate the actions of a drug. According to co-author Geoffrey Ginsburg, M.D., director of the Center for Applied Genomics & Precision Medicine, this paradigm shift could change how drugs are developed and positioned for clinical use in future. He added that they intend to use the same approach to explore the pleiotropic effects of drugs on a broader basis and believes this will assist in anticipating their side effects, as well as understanding their full range of actions clinically.
Full study has been published online in the EBioMedicine.