While they are known to lower risk for some cancers, until now researchers have had little idea exactly why aspirin and other non-steroidal anti-inflammatory drugs (NSAIDS) appear to stave off the accumulation of disease-causing mutations.
Writing in PLOS Genetics, a team led by investigators at the University of California, San Francisco (UCSF) Helen Diller Family Comprehensive Cancer Center shows that aspirin slows the accumulation of mutations in abnormal cells in cases of the precancerous condition Barrett’s esophagus. In an observational crossover study involving 13 patients with Barrett’s esophagus who were tracked for six to 19 years—some of whom started out taking daily aspirin for several years, and then stopped, others who started taking aspirin for the first time during the study—the researchers charted the rate of mutations in tissues sampled over time.
“This is the first study to measure genome-wide mutation rates of a premalignant tissue within patients for more than a decade, and the first to evaluate how aspirin affects those rates,” UCSF’s Carlo Maley, Ph.D., said in a statement. “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,” Dr. Maley added.
One hypothesis is that aspirin lowers mutation rates due to its inflammation-reducing properties. Inflammation, which has long been implicated in cancer, could result in reduced production of oxidants known to damage DNA within precancerous tissue, the researchers proposed. They now plan to investigate whether that is indeed the case.
Dr. Maley et al., noted that additional research is needed to fully understand the observed links between NSAID use, mutation rates, and development of cancer. To that end, the researchers said they would continue their studies on Barrett’s esophagus and esophageal cancer, and intend to extend their work to lung cancers.
“NSAIDs modulate clonal evolution in Barrett’s esophagus” was published in PLOS Genetics June 13.