Aspirin cuts down the rate at which cell DNA is damaged, explaining its anti-cancer effect, new research has revealed.
It been known for some time, from observational studies and in particular a recent trial of bowel cancer patients looking at relapse rates, that aspirin and other NSAIDs (non-steroidal anti-inflammatory drugs) exert a strong anti-cancer effect in various organs including the lungs, oesophagus and intestines.
But how this class of agent achieves this effect wasn't known. Scientists had speculated that inflammation can trigger cells to divide and, in the process, pick up cancer-causing damage to their DNA, but there was no direct evidence that this was happening.
Now, University of California, San Francisco scientist Carlo Maley and his colleagues have used a group of patients undergoing monitoring for an oesophageal condition - some of whom started using NSAIDs during the study while others stopped using the agents - to track the rate at which the patient's cells acquired potentially cancer-causing DNA changes.
Thirteen patients, all with a condition called Barrett's oesophagus - which is a risk factor for oesophageal cancer and requires regular monitoring, were studied over a 6-19 year period.
Over 160 biopsies collected from the patients were examined to look for the rate at which DNA in their oesophageal cells was developing abnormalities.
When the patients were not taking NSAIDs, the team found, their cells picked up changes or mutations at the rate of about 7.8 new abnormalities per year. On aspirin or a related NSAID, however, the rate was ten times smaller - just 0.6 abnormalities per year - in 11 of the 13 patients.
This suggests, the team say in their PLoS Genetics paper, that "the pathway where NSAIDs exert their protective effect involves the reduction in the number of somatic germline [DNA] abnormalities..."