Daily aspirin use – known to reduce the risk of colon cancer – could also make the disease harder to treat if it does occur, a modelling study found.
If confirmed statistically and in the lab, would mean that aspirin's ability to ward off colon cancer may come at an unacceptably high cost, the researchers cautioned.
A growing body of research has shown that daily micro-doses of aspirin taken for at least five years can slash the risk of cancer later in life. Rates of prostate, throat and non-small-cell lung cancer all drop off significantly, with the incidence of colon cancer cut by up to half.
Other studies, meanwhile, have tested the impact of aspirin directly on cancer cells in the laboratory, showing that the common painkiller can slow the rate of cell division and boost cell death. But scientists do not yet understand the mechanism at work, or know whether aspirin might have as-yet-undiscovered effects on cancer spread.
To find out more, researchers led by Dominik Wodarz of the University of California at Irvine – who conducted these earlier experiments – investigated whether the drug may cause dangerous cancer mutations. Indeed, aspirin did boost the cancer's ability to produce aggressive, mutant cells that are drug-resistant, they found. The results could challenge the protocol for aspirin use in cancer prevention.
It is now critical to ensure that aspirin delays "the onset of colo-rectal cancer by a sufficient amount of time to avoid the negative effects of this trade-off," the study authors said. People who take the drug, especially in middle age, should be regularly screened for cancer, they added.
Roughly half of adults in the US take small doses – 80 to 325 milligrammes – of aspirin to ward off cardiovascular disease. In Britain the figure is about 40%.
The general public has not yet recognised the potential benefits for cancer prevention, notes Peter Rothwell, a professor at the Centre for Prevention of Stroke and Dementia at the University of Oxford in the report. "It takes a while, and more replication studies, to convince people that the benefits are real," he said.
Rothwell published a study earlier this year showing an increased risk of internal bleeding in people over 75 who take aspirin regularly. "You might want to take it in your 50s and 60s, but then stop," he said. "The benefits you get from cancer prevention carries on for another 10 years or so."
Aspirin is known to reduce the risk of colorectal cancer (CRC) incidence, but the underlying mechanisms are not fully understood. In a previous study, we quantified the in vitro growth kinetics of different CRC tumour cell lines treated with varying doses of aspirin, measuring the rate of cell division and cell death. Here, we use these measured parameters to calculate the chances of successful clonal expansion and to determine the evolutionary potential of the tumour cell lines in the presence and absence of aspirin. The calculations indicate that aspirin increases the probability that a single tumour cell fails to clonally expand. Further, calculations suggest that aspirin increases the evolutionary potential of an expanding tumour cell colony. An aspirin-treated tumour cell population is predicted to result in the accumulation of more mutations (and is thus more virulent and more difficult to treat) than a cell population of the same size that grew without aspirin. This indicates a potential trade-off between delaying the onset of cancer and increasing its evolutionary potential through chemoprevention. Further work needs to investigate to what extent these findings apply to in vivo settings, and to what degree they contribute to the epidemiologically documented aspirin-mediated protection.
Dominik Wodarz, Ajay Goel, C Richard Boland, Natalia L Komarova
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[link url="http://rsif.royalsocietypublishing.org/content/14/134/20170374"]Journal of the Royal Society Interface abstract[/link]