Scientists from the NEJM journal have suggested that this medicine may inhibit platelet activation. Why more research is needed Aspirin is a popular anti-inflammatory and painkiller that relieves pain and helps lower temperature. But now its potential to reduce the risk of developing certain types of tumours is being investigated. Scientists at the MRC Clinical Trials Unit at University College London (UCL) in the United Kingdom have discovered the mechanism by which aspirin may prevent cancer, an issue that has been debated for decades.
The study was published in The New England Journal of Medicine. It showed that the drug works by inhibiting platelet activation, which could change current prevention and treatment strategies, especially in people at hereditary risk. Professor Ruth Langley, lead author of the study, said: “We are very excited about this new collaboration. In addition to focusing on the mechanism of action, we have gathered data from worldwide clinical trials with patients taking aspirin after a cancer diagnosis.”
The initiative, called SPARC, brings together experts in aspirin pharmacology, molecular genetics, and clinical trials to answer the question of how aspirin can prevent cancer. The SPARC group’s findings show that low-dose aspirin (75-100 milligrams per day) inhibits platelet activation, which is a key function in preventing the growth of new tumours and limiting the spread of cancer.
Professor Sir John Bern, from Newcastle University, pointed out: ‘The recent results from the long-term CAPP-3 trial, which show that low-dose aspirin, 100 milligrams per day, is as effective as higher doses in preventing hereditary cancers in Lynch syndrome, confirm our hypothesis that the effect of aspirin on platelets is key to understanding how it prevents cancer.’ Patients with Lynch syndrome should talk to their doctors about the possibility of taking low-dose aspirin, Bern advised.
Studies also show that when activated, platelets not only promote blood clotting, but also can contribute to tumour growth by increasing inflammation and preventing immune action on disseminated cancer cells. In animal models, platelet activation has been found to contribute to inflammation and facilitate the formation of new tumours, while aspirin blocks this process. These findings are especially important for those living with hereditary risk.
Tracy Smith, representative of Lynch Syndrome UK, said: ‘For families living with a hereditary risk of cancer, this research offers real hope.’ Smith added that “understanding how aspirin inhibits platelet activation brings us closer to understanding who can benefit most from it and how to use it safely. Every advance gives patients more confidence, more opportunities and more time, and that is invaluable.” The Add-Aspirin study, conducted by Langley’s team, examines whether aspirin can reduce the likelihood of recurrence of certain types of cancer. Early results showed that participants had high levels of platelet activation for several months after cancer treatment, which led to the creation of SPARC.
In addition, recent data from the ALASSCA study in Sweden indicate the possibility of identifying patients who are more likely to benefit from aspirin after surgery, depending on the genetic characteristics of their tumours.
Data from the ALASSCA study suggest that the genetic characteristics of tumours influence the response to aspirin after surgery. Langley cautioned: ‘There is still much work to be done to fully understand the link between platelet activation and cancer prevention. Aspirin increases the risk of bleeding, and people should not take it regularly without the supervision of a healthcare professional.’
The patients’ perspective was one of the key aspects of the project. Charlotte Avery, public relations advisor, said the research brings ‘peace of mind knowing that new prevention possibilities are being studied. SPARC research may help identify a simple and widely accessible approach to cancer prevention.’