Aspirin and Cancer

By Rachel Airley, EPB Board member and Senior Lecturer in Pharmacology

There is now wealth of evidence from clinical trials that aspirin can not only prevent cancer, but can also slow the growth and spread of bowel cancers already present.  While the evidence is there, doctors and pharmacists have been somewhat reticent when it comes to recommending the wholesale use of aspirin in patients at risk, or already undergoing treatment for bowel cancer, due to fears that this will lead to side effects such as gastric ulcer or bleeding.

We are now moving away from a “one size fits all” approach to medicines towards a new concept   of a patient-focused approach to medicines use and treatment.  Part of this means that where previously we concentrated on using the correct drug at the correct dose, for the correct disease, we are now adding “for the correct patient” into the mix.

An article in the New England Journal of Medicine called for a renewed use of aspirin in bowel cancers highlighting a way of targeting those patients most likely to respond to aspirin.  These patients have tumours with a mutated gene PI3KCA.  Where this form of the gene is present, the patients are more likely to respond to aspirin, which will target cell division and spread of tumour cells to other parts of the body.  By restricting aspirin use to only those patients most likely to respond, we reduce the risk of treating patients with the accompanying risk of side effects, only for it to have no beneficial effects.

The use of aspirin to prevent and treat cancers is an exquisite example of how cancer research is coming out of its box and is being inspired by research into other disease areas.  Cancer can no longer be thought of in isolation from other diseases.   Malignancy has properties of other conditions, where there is similarity with arthritis, diabetes, obesity, some skin disorders and immune conditions, due to common mechanisms in the body which control physiological processes such as cell division, inflammation and metabolism of nutrients.

As cancer is a disease of increased cell division, changes in glucose and fat metabolism which provide an energy source to support this new cell growth are needed.  In turn, the cancer becomes more aggressive, these cells developing survival mechanisms to evade the immune response, becoming tolerant to our own defences.

Amazingly, any biological process that involves growth and development of organs in the body is now highly interesting to cancer researchers – such as the way we heal when wounded, or even the development of new life itself during pregnancy.

By understanding how PI3KCA gene works in bowel and other cancers we begin to see how medicines traditionally used for treatment of other conditions, such as aspirin, inspire new ways of thinking about how we treat cancer.  Scientists have been interested in the PI3KCA gene for quite some time, as it controls production of the protein PI3K, an important component of our metabolism which controls how we use glucose to make energy and fits this to the rate at which we make new cells and regenerate tissue.  PI3K may also be activated by insulin, the hormone which diabetics lack so knowing more about PI3K will also help us make advances in the treatment of metabolic conditions such as diabetes and obesity.

Now that we have scientific proof that the anticancer effects of aspirin are connected to PI3K, new possibilities open up to exploring in greater depth how conditions affecting millions of patients are connected, and how the scientists and health professionals researching them might benefit from working together more closely.  Perhaps the big picture that aspirin is painting for us is that, rather than aspirin being a “cure all”, the future of pharmaceutical research lies in “multitasking” where a search and destroy plan aimed at just a few all-important genes might produce a cure for a multitude of diseases.