There is considerable evidence now that aspirin seems to reduce the risk of developing colorectal cancer in particular.

There are numerous epidemiological studies and now there are randomised controlled trial studies which have really shown quite formally that aspirin reduces the risk of either developing colorectal cancer or dying from colorectal cancer.

More recently, that study has been expanded to really examine other types of cancer and it looks like the effect of aspirin could also extend beyond cancer of the colon to include cancer of the GI tract and maybe even other cancer sites.

What sorts of people are likely to benefit from aspirin, any particular groups?

Certainly individuals that are at risk for developing colorectal cancer and, quite frankly, that’s most of the general population.

We really think that colorectal cancer is a very significant public health problem.

Anyone over the age of 50 really warrants colorectal cancer screening; so, really, anyone over the age of 50 potentially could benefit from the use of aspirin for this purpose.

You’re a gastroenterologist and an epidemiologist but you’re looking at molecular risk stratification. What do you mean by that and what is it going to do to benefit you in terms of GI cancers and aspirin?

Clearly there is a benefit of aspirin use but there’s also the downside.

We do obviously worry about the side effects of aspirin therapy and we know that patients who take aspirin have a higher risk of gastrointestinal bleeding.

So while we’d love to be able to recommend it for the general population, we understand that we still need to probably more directly isolate individuals that are going to derive potential benefit and also potentially have smaller amounts of risk.

So we’ve been really relying on a molecular approach where we try to understand how it is that aspirin actually prevents cancer and by understanding some of the molecular mechanisms we can use some of those molecular mechanisms to develop biomarkers to risk stratify individuals.

And in terms that cancer doctors would find relevant, what are those processes?

We know that aspirin seems to actually inhibit the production of prostaglandins.

These are proteins that are known to promote cancer and we know there are particular molecular pathways by which prostaglandins actually are formed.

So we can actually use some of these molecular markers to better characterise individuals for how important these pathways are in their bodies.

If we can identify these types of patients they may be the ones that are at greater risk of actually developing cancer and benefitting from aspirin therapy.

Clearly you want to make sure that you don’t give aspirin to people who would be at high risk of bleeding but you do want to give it to those who are at high risk of a GI cancer. Have you been able to say anything yet about that?

We haven’t really been able yet to clearly identify markers of GI bleeding but what we have been able to identify is potential markers of preferential benefit.

So we do know that there are certain individuals that tend to develop GI related cancers that also tend to develop them in a format that seems to stand to benefit more from aspirin therapy.

So it appears that there are particular biomarkers that seem to predict whether the cancers that they develop will potentially be inhibited by aspirin therapy.

We do feel that there are potential biomarkers, for example, that could be used in the future.

One is potentially a biomarker that is found in the urine; we do know that individuals that have high levels of a biomarker which suggests a high level of prostaglandins in their body tend to respond better to aspirin.

So if we could actually use that as a biomarker that may ultimately help us to determine which patients could be the ones that should be treated more aggressively with aspirin therapy.

The take home message is that aspirin is effective in the prevention of colorectal cancer but, given the potential side effects, there clearly is a need to develop methods to risk stratify individuals for therapy.

At this point in time, based on our work in developing our understanding of the mechanisms by which aspirin interrupts cancer, we have been able to potentially develop new biomarkers that can help predict who will preferentially benefit.

Down the road ultimately we hope to use these markers in the clinic and also potentially connect them to markers which predict who might actually develop side effects.

Together these markers will help us to really personalise therapy and allow us to more precisely determine who could benefit and who should be on aspirin therapy long-term.