Aspirin may fight cancer by slowing DNA damage

Aspirin can lower risk for some cancers by slowing DNA damage, scientists, including one of Indian-origin, have found.
The study led by a University of California, San Francisco scientist found that aspirin slows the accumulation of DNA mutations in abnormal cells in at least one pre-cancerous condition.
"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," said Carlo Maley, a member of the UCSF Helen Diller Family Comprehensive Cancer Center.
In the study, published in the journal PLOS Genetics, Maley working with gastroenterologist Brian Reid, of the Fred Hutchinson Cancer Research Center, analysed biopsy samples from 13 patients with a pre-cancerous condition called Barrett's esophagus who were tracked for six 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 an aspirin regimen had on average accumulated new mutations about 10 times more slowly than biopsies obtained during years when patients were not taking aspirin.

Maley now plans to test a hypothesis that may explain 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 recognised 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 signalling.

For the duration of 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, with the exception of one patient.
While mutations accumulated at a steady rate, the vast majority of mutations arose before the abnormal tissue was first detected in the clinic, the researchers concluded.
These findings are consistent with the fact that although Barrett's esophagus is a significant risk factor for esophageal cancer, the vast majority of cases do not progress to cancer, Maley said.
In the one patient who later went on to develop cancer, a population of cellular 'clones' with a great number of mutations emerged shortly before he started taking aspirin.

Rather than aiming to kill tumour cells, it may be better to try to halt or slow growth and mutation, Maley said.
Additional authors include Amitabh Srivastava and Robert Odze from Harvard University.