By: Raymond DuBois, M.D., Ph.D.
We have known for the past two decades that aspirin and non-steroidal anti-inflammatory drug (NSAID) use reduces the risk of colorectal and other cancers. Today the Lancet published new reports indicating that low dose daily aspirin reduces the risk of distant metastasis of several cancers (Lancet Early Online Publication.)
The data came from 51 trials that included over 77,000 patients.
This protective effect appears to occur within 3-5 years of beginning aspirin use. It was previously thought that this protective effect would take up to 10 years to have an impact. These trials were originally designed to compare aspirin with no treatment for the prevention of heart disease.
In carefully looking at the data it became apparent that regular aspirin use reduced the risk of colorectal cancer as well as esophageal, gastric, biliary and breast cancer. People using 75-300 mg per day were found to have a significant reduction in the total number of cancer cases. Aspirin also reduced the risk of cancer death by 15% within 5 years and people using aspirin for longer duration had a 37% reduction in risk.
Interestingly, low dose aspirin appeared to reduce the spread of colorectal cancer to other parts of the body by about 40-50%. This finding is important since it indicates that there might be a role for aspirin use in patients who have cancer or who or at high risk for cancer recurrence. It is important to point out that taking aspirin does have a downside because it increases the risk of bleeding and peptic ulcer disease.
The key question now is how do these anti-inflammatory drugs reduce cancer risk and metastatic spread?
Aspirin is known to inhibit platelet function by its ability to inhibit the cyclooxygenase enzymes. This blocks the production of pro-inflammatory prostaglandins (like PGE2) that are known to promote the hallmarks of cancer. Recently, PGE2 was also shown to regulate epigenetic changes, like methylation of tumor suppressor and DNA repair genes known to play a key role in the development of cancer (Nat Med, 2012; 18, 224-226).
Other mechanisms are likely in play as well and a full understanding of the molecular mechanisms responsible for this protective effect could lead to major breakthroughs in the field of chemoprevention of cancer.