Aspirin is known to lower the risk for some cancers and a new study from UC San Francisco offers a possible explanation - aspirin slows the accumulation of DNA mutations in abnormal cells.
The new study was based on patients with a pre-cancerous condition called Barrett's esophagus who were tracked for 6 to 19 years. Some patients started out taking daily aspirin for several years, and then stopped, while others started taking aspirin for the first time during observation. The goal was to track the rate of mutations in tissues sampled at different times.
The researchers found that biopsies taken while patients were on aspirin had accumulated new mutations about 10 times more slowly than biopsies obtained during years when patients were not taking aspirin.
"This is the first study to measure genome-wide mutation rates of a pre-malignant tissue within patients for more than a decade, and the first to evaluate how aspirin affects those rates," researcher Carlo Maley said.
Cancers are known to accumulate mutations over time much more rapidly than normal tissue, and different mutations arise in different groups of cells within the same tumor. The acquisition of key mutations ultimately allows tumor cells to grow out of control.
"Aspirin and other non-steroidal anti-inflammatory drugs, which are commonly available and cost-effective medications, may exert cancer-preventing effects by lowering mutation rates," suggests Maley. "Rather than aiming to kill the most tumor cells, it may be better to try to halt or slow growth and mutation."
He adds that more studies are needed to further explore the link between non-steroidal anti-inflammatory drugs, mutation rates and the development of invasive cancer.
He now plans to test a hypothesis that may explain the results - that aspirin's lowering of mutation rates is due to the drug's effect of reducing inflammation. Inflammation, a response of the immune system, in recent years has been recognized as a hallmark of cancer. Maley said that less inflammation may result in less production within pre-cancerous tissue of oxidants known to damage DNA, and may dampen growth-stimulating signaling.
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Source: University of California - San Francisco