Aspirin slows DNA damage that leads to cancer

Aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs) reduce mortality from several types of cancer by approximately 20%, and although the reasons for this are not fully understood, new research provides a clue: Investigators have discovered that the rate of accumulation of genetic abnormalities in cells decreased with the initiation of NSAID therapy in a small study of persons with Barrett's esophagus, a precancerous condition.

This knowledge was attained from a prospective observational crossover study of 13 patients with Barrett's esophagus. All participants underwent endoscopic follow-up for a mean 11.8 years (range 6.4 to 19 years), and all either began or discontinued NSAID use exactly once during follow-up. Carlo Maley, PhD, of the Helen Diller Family Comprehensive Cancer Center at the University of California–San Francisco (UCSF), and colleagues tracked the rate of mutation in tissue samples obtained from the patients at  various times.

The researchers noted the decreased accumulation rate of genetic abnormalities after the start of NSAID use. According to a UCSF statement summarizing the findings, biopsies obtained while patients were on aspirin had accumulated new mutations about 10 times more slowly, on average, than did biopsies obtained during periods of no aspirin use.

In addition, the researchers were surprised to observe that the number of abnormalities in the Barrett's tissues did not increase much over time. Throughout the study, the rate of accumulation of mutations measured in the biopsied tissue between time points was slow, even when patients were not taking aspirin. An exception was seen in one patient who progressed to esophageal cancer. Massive genomic abnormalities affecting 19% of the genome were observed in the tissue of this patient.

The study team concluded in PLOS Genetics (2013;9[6]:e1003553) that these findings suggest NSAIDs may prevent cancer by reducing the accumulation of genomic abnormalities over time, and that detection of stable versus unstable genomes may be used in the clinic to help manage treatment options in Barrett's esophagus.
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