Aspirin, obesity, NICE and focusing on pancreatic cancer

Cancer Research UK
We look at aspirin for cancer prevention, obesity and cancer risk, why NICE turned down new breast and prostate cancer drugs, and focus on how to make progress in pancreatic cancer.


Kat: This is the Cancer Research UK podcast for September2014. This month we look at aspirin for cancer prevention, obesity and cancer risk, why NICE turned down new drugs, and focus on making progress in pancreatic cancer. Plus our heroes and zeros.

Hello and welcome, I’m Kat Arney. Found in bathroom cupboards everywhere, aspirin has gained attention in recent years for its potential for preventing cancer. But there’s still a lot that isn’t known about how best to use the drug – such as what dose is best, who might benefits, and what are the risks. 

Now a new review of the evidence, led by our researcher Professor Jack Cuzick at Queen Mary University of London, suggests that taking aspirin every day can reduce the chance of developing or dying from bowel and stomach cancers, and if everyone aged 50 and above in the UK took a daily low dose of the drug for 10 years, over 100,000 deaths could be prevented over two decades. 

But it’s very important to note that aspirin can cause internal bleeding and isn’t right for everyone –while the data show that if 1,000 people aged 60 took the drug for 10 years there might be 16 fewer deaths from cancer and one less heart attack death, there would be two extra deaths from bleeding.

Our reporter Alan Worsely spoke to our Head of Health Information, Dr Julie Sharp, to find out more about the study and whether we should all be popping those little white pills.

Julie: So this was a group of international researchers led by scientists at Queen Mary University and they were reviewing all the available evidence on aspirin and its role in preventing cancer. And they found it could be really successful in preventing cases of bowel, oesophageal and stomach cancers, and also reducing the risk of dying from those cancers as well.

Alan: Well that sounds really good, should I be taking aspirin myself?

Julie: Well the study was looking at people who start taking aspirin in their 50s or early 60s, and take it for at least five years, and benefits were still being shown in people who took it for longer, even up to ten years. 

Alan: So we know there are benefits, but we also know there is a risk. Could you tell us about the downsides of taking aspirin every day?

Julie: Well if you look at the analysis, it shows that if 1000 people in their 60s were to take aspirin for ten years, that you’d have 17 lives saved from cancer and heart disease, but at the same time you’d have two to three people dying from strokes, bleeding or stomach ulcers. It’s still not clear exactly what the right dose should be, how long people should be taking aspirin for, and at the moment we don’t have a good way of predicting who would be at risk of the side-effects. So we really need to understand who’s at risk, and also how long should people take it for, to avoid some of those risks in later life. 

The potential of aspirin is really exciting, but before we tell people to sort of rush out and start taking it right away, it’s really important that we get answers to some of those questions around who’s at risk of the side-effects. If people are considering taking aspirin, because obviously it’s a widely available and cheap drug, we’d advise you to go and talk to your GP first, and he can just advise you a little bit more.

Kat: Dr Julie Sharp there. Obesity hit the headlines this month when scientists at the London School of Hygiene and Tropical Medicine published the results of a major study linking higher body mass index (or BMI) to increased risk of various types of cancer. To find the links, the team looked back at anonymised GP records from more than 5 million people in the UK, starting as far back as the 1980s. I asked lead researcher Krishnan Bhaskaran to explain what he and his team found, and started by asking him how he could be sure that it was definitely BMI having an effect on cancer risk.

Krishnan: We have to take into account other the things that might be common causes of having high BMI and later on, getting cancer.  So, this is where we do our statistical modelling and tried to use other information we have from the record to discount the effects of other common causes like for example, socio-economic status, smoking habits, drinking.  These things could all affect both cancer risk and BMI.  So, they could lead to spurious association.  So, we tried to collate all the information, on those factors and include them in our modelling so that we really had what we thought was – the real effect of body mass index.

Kat:  So, what do you find from the data?

Krishnan: We confirmed that as we thought there were important relationships between body mass index and cancer risk.  And what was quite striking, because this was a broad study and I think the first time, a single dataset where we’ve looked across so many cancers - we looked at 22 of the commonest cancers.  It was striking – the variation in effect actually.  So for the major of cancers, there was an association and for 10 cancers, there was a very clear positive correlation.  So, the higher people’s body mass index was the greater their cancer risk seem to be – and for a few cancers though, it’s very little effect.  For some, there was even apparently lower rates of cancer among those with the higher body mass index.  But I was the minority and those are the slightly more surprising results, but again, they are consistent with what has been shown before.

Kat: Which cancers are we talking about here that are most strongly linked to obesity?

Krishnan: In terms of what are the impacts on the population, one has to also think about how common these cancers are.  So, it’s a slightly different answer if you're saying, which of these cancers are worst affected as a population level.  But specific cancer type, they already had the most striking positive relationship with body mass index with cancer of the uterus in women.  That’s womb cancer, which is actually the fourth most common cancer in women.  For cancer of the uterus, we found that increasing the body mass index by 5 units which is for an average height woman would be adding about two stones of weight actually increased the risk of uterus cancer by over 60% so really quite a large effect.  

Breast cancer has a smaller relative effect or association with body mass index.  But I think the actual number of cases of breast cancer that we’ve estimated that would be attributable to excess weight is larger for womb cancer because it’s the function of these two things at how largely the effect is and how common the cancer is.

Kat: How many cases of cancer are we talking about?

Krishnan: That’s something we try to estimate in this study.  So, by using both the National Cancer Statistics and also the effects that we estimated for body mass index, we estimated for the ten cancers that were really clearly positively associated with body mass index, over 12,000 could be attributable to having excess weight.

Kat: Is that every year in the UK?

Krishnan: That’s every year, yeah.  So, that's if you like, if we could somehow magically remove all excess weight from the population, we would expect from these results to prevent about 12,000 cancer cases.  So, it’s really quite a large population impact.

Kat: So, with this study, you kind of feel that this is the strong evidence that we could go out there and say we really know this now.

Krishnan: Yes, I think so.  I think this really sort of seals it.  So, we already knew there were these important effects, but now, we’ve already put some more meat on it and worked out exactly what the impacts are.  And it really just adds ever more to a case of some ambitious policies to deal with obesity in the population which we know are affecting cardiovascular risk, we know they're affecting diabetes risk, and now, we really know the extent to which they're affecting cancer risk as well.

Kat: Krishnan Bhaskaran from the London School of Hygiene and Tropical Medicine. NICE, the National Institute for Health and Care Excellence, found itself the target of nasty news reports when it turned down two cancer drugs on grounds of price – Kadcyla for breast cancer and abiraterone, also known as Zytiga, for prostate cancer. We’re deeply disappointed that NICE and the drug manufacturers couldn’t come to an agreement on price, and are concerned about the wider issues of drug availability and pricing which may prevent patients getting access to treatments that could help. To find out more about the decisions, Sarah Wells spoke to our Senior Policy Manager Emlyn Samuel.

Emlyn: So NICE, which is the body that makes the decisions on which drugs should be available on the NHS routinely, rejected two cancer drugs in the last month. One of them, called Kadcyla, was a breast cancer drug, and another was a prostate cancer drug. The decisions around them were quite different. The first one, on breast cancer, Kadcyla was deemed too expensive for the NHS to afford. I think it was around £90,000 per patient. And that goes way beyond the threshold of affordability that the NHS and NICE looks at drugs for.

With abiraterone, it was a bit more complicated. Abiraterone is currently used on the NHS, to treat prostate cancer at the end of life. This decision was about using that drug before men with prostate cancer even have chemotherapy. And because it was for that use, it was then deemed too expensive for routine use on the NHS. Again, both drugs are seen as effective drugs but too expensive for the NHS to pay for.

Sarah: So what do these decisions mean for patients?

Emlyn: Well I think that we should be clear that while these drugs have been rejected by NICE, in England we have a thing called the Cancer Drugs Fund. Which means even though they have been rejected by NICE, patients can still access them. And that’s a really important point to make, so patients out there with these diseases are still able to get these drugs. In Scotland, Wales and Northern Ireland, they have to go through a different process, called an individual funding request system. But they should be able to access drugs through that mechanism as well.

Sarah: So these decisions about drug availability are obviously really difficult to make, so what can you say about the larger policy framework in which that happens?

Emlyn: You’re right, they are very difficult and actually, NICE does a very good job, generally, and does a very hard job, I think. But these two latest decisions are the last in a fairly long line of rejections from NICE on cancer drugs which is really concerning. But I think what these two decisions in particular highlight, just shows that the way that drugs are assessed by NICE at the moment doesn’t really work for cancer.

We have a very fragmented policy framework in England at the moment where we have drugs being rejected by NICE, but the Cancer Drugs Fund, which also provides those drugs, and then other mechanisms to make sure patients can access drugs. What we need is a long term solution. We need to make sure that we have a robust system of appraising cancer drugs in place so that everyone can be confident that the right decisions have been made and that patients can get the best evidence based treatments possible. And that’s what we’d like government to do.

Sarah: So what do people really need to take away about what happened here with the NICE decisions?

Emlyn: Bottom line I think patients should understand that these drugs are available on the NHS. But in the wider sense, the system for accessing cancer drugs is currently not working well for cancer, and we really need a long term solution to make it a robust system to make sure patients can get the best treatments possible.

Kat: That was Emlyn Samuel talking to Sarah Wells. Pancreatic cancer is one of the most challenging types of cancer to treat – currently around four in every 100 patients survive for five years, and survival rates have changed little over recent decades. 

It’s a situation that urgently needs to change, and one that we’re particularly focusing on as part of our new research strategy. Someone who’s trying hard to alter the outlook for patients with the disease is pancreatic cancer expert Professor Andrew Biankin, Regius Professor of Surgery at Glasgow University and group leader at our Beatson Institute in the city. 

Last year we tempted him away from the sunny weather of Sydney, Australia, to pursue his pioneering work in Scotland’s cooler climes.  I met up with him to find out how he’s working to change the picture for pancreatic cancer patients in the future, and how he first got involved in research into the disease.

Andrew: To a certain degree it was a matter of circumstance. At that time I was finishing my surgical training and I was doing a secondment or a term as part of a team looking after patients with pancreatic cancer. And of all the cancers that I treated, it looked as if we had the most room for improvement. There was opportunity there because nothing really worked. We operated on patients and still 80% of them died and we didn’t understand why. And there was also not as much activity in pancreatic cancer research as there should have been – in fact there was nothing going on in Australia before I started. 

So I saw that as an opportunity, and I wandered across the road to the research institute to meet the then-director of the cancer research programme at the Garvan Institute, who became my mentor – a guy called Rob Sutherland, who sadly recently passed away from pancreatic cancer actually. I said “I’m a surgeon but I’m really interested in research – what can I do?” And he said “What sort of research do you want to do?”, and I said “Pancreatic cancer” and he said “We’ve got a problem.” “What do you mean?” and he said “You don’t know anything about research, and I don’t know anything about pancreatic cancer. But here’s a desk, start writing a few grants, if you get some money you can stay.” So I got some money and I stayed there ever since. 

Kat: In the intervening years it’s been a journey that’s taken you to America and back to Australia and now, most recently, to Glasgow to spearhead our pancreatic cancer research there. Obviously, apart from the fine Scottish weather, what was it that drew you to Glasgow?

Andrew: I was drawn to the UK in broad terms because it seemed to have the best information systems, the best patient system, healthcare systems and the best research attitude with regard to a stratified or personalised approach to healthcare in the world. We looked at different places and felt that the UK was well positioned to advance stratified medicine, or precision medicine, personalised medicine – whatever you want to call it. 

Particularly Scotland because of the ability to track patients. We can do a lot of our genomic work, a lot of the high-tech work, but where we struggle is patient information, information about how that patient was treated, what their treatment course was. And that’s very important and there’s not enough investment in that in many of the projects that have been done in the past, and that’s why we chose to move to the UK.  Glasgow in particular because they were developing a track in pancreatic cancer research, particularly at the Cancer Research UK Beatson Institute. And really the opportunity there was substantial.

Kat: You mentioned that your work is in genomics. Tell me a bit about that, and what do we mean by genomics when it comes to pancreatic cancer. What are you trying to do?

Andrew: We think about genomics as about understanding the structure of DNA, how that represents disease in a broad sense, and that’s what we call cohort genomics – we look at disease in a broad group.

Kat: What’s gone in the DNA of patients that’s giving them this cancer?

Andrew: That’s right. What’s gone wrong in the blueprint. How a cancer develops, we think, is that you have 23 chromosomes and you have things called genes which encode the proteins that make your body function. But what happens when the cell starts to grow out of control is that some of those proteins are broken or they’re deranged, so they send the cell different messages. So the cell starts to grow out of control. So we think cancer is a disease of the genes. Some of the genes can be inherited, but on the whole 90%, something just happens during the process. We know there are some risk factors like tobacco and sun exposure that can cause breakages in the DNA and cause these genomic abnormalities. But on the whole we don’t understand those processes well enough.  

Then the next step is really what happens in a cohort of patients, in a group of patients – understanding what the commonalities and the differences are between those patients by the blueprint or the roadmap of their individual genomes that they have in their cancer. And then we think we could start to relate that to important things like treatment, the pattern of disease etc. And we start to call that translational genomics.

Kat: So this is moving away from the one-size-fits-all, everyone in the same bucket gets the same treatment?

Andrew: Yes – it’s really the basis of personalised medicine, precision medicine or stratified medicine, and it’s important in cancer because we believe that cancer is a disease of the genes, therefore understanding which genes are broken is important and that will help us distinguish different subtypes of cancer. Also the pharmaceutical industry is making drugs that particularly target these types of genetic abnormalities, so it makes sense that rather than just randomly picking a group of cancers, we look for that particular target that the drug is made for, and then try and target that particular cancer. The idea, the supportive concept is really described as the right treatment for the right patient at the right time. 

That’s where we need to go – we need to ask that question, is this approach going to work in pancreatic cancer, because nothing else is working. And we see that pancreatic cancer may be an opportunity where we can really start to explore this in depth, because currently it’s one size fits all, and that treatment doesn’t do a lot for most of the patients. It might help a small fraction but it usually doesn’t work. So we’re giving treatment that doesn’t work to most of our patients, and then on top of that it also can be very quite toxic. So not only are we giving them any benefit, we’re doing harm. And working out what the right treatment for that patient is ahead of time is something we really need to explore.

Kat: Obviously one of the main ways we improve for patients is through clinical trials. What’s the current state of clinical trials in pancreatic cancer, and how would you like to see that change?

Andrew: The UK in particular – that’s one of the other reasons we came here, it’s particularly good at running clinical trials. The more we break down and understand these subtypes, the smaller and smaller they’re going to get. And so doing a clinical trial in a cancer that might only occur in 60 patients a year in the UK can be rather difficult, so we need to find better ways of doing that, to deal with this small number of patients, because we really don’t have enough patients to be able to test all the potential combinations. 20 or 30 years ago you might have six drugs, you might mix and match them a little bit, and you can do a clinical trial and see the difference. Now we have 800 or 1000 drugs that are out there – if you combine a thousand clinical trials of each one then you look at the combinations, I think it’s a thousand times a thousand – it’s been a while…

Kat: There’s a lot of maths there, there’s a lot of numbers.

Andrew: And then basically if you did that calculation it would probably take us a thousand or more years to test all of those and then if you did triple combinations it would take a billion years to test them. So we really need to find a different way of doing this. And really starting to delve deeper into how we interpret responses and what they mean, and really understand what’s happening to the tumour or to the cancer when we treat it and understanding what makes it resistant or what makes it sensitive, so then we can start to think more about how we rationally design these treatments.

Kat: It sounds to me like we need to work a lot smarter – how would you like to see a smart approach going forward over the next say five to 10 years?

Andrew: I think what Cancer Research UK has done with the Matrix Study in lung cancer is a really great step forward and I think we’d like to see the same thing in pancreatic cancer. It’s a complex and it’s a multi-factorial thing to get right. I think approaching it in the way that Cancer Research UK is doing and really engaging the community that’s out there, the clinical community, the research community and working with them together and saying “How do we do this? What’s the next step? How do we develop this? And how do we build that capacity with a timeline of 10 years, not a timeline of three years?” 

We can do certain things that you probably can’t do when you’re studying other cancer types or treating other cancer types. We really don’t have a lot of therapies, and the downside is that these people are dying. They’re dying of their cancer and so we want to do the best we can for them. So we need to think about how we can re-engineer some of our systems to be able to improve things for them, give them more options not just the standard of care. These patients don’t need standard – they need better than the standard, so how do we work that out? How do we make things happen? How do we build a system that gives patients and researchers and clinicians the opportunity to do the best they can.

Kat: That was Professor Andrew Biankin. Now it’s time for our heroes and zeros. Our heroes this month are all of our researchers and supporters who’ve helped to push the death rates down for the four main cancer killers – new figures from our stats team show that death rates for breast, bowel, lung and prostate cancers have dropped by almost a third over the past 20 years. There’s a still a long way to go – survival from lung cancer overall remains poor, and it’s something we’re focusing on in our new research strategy. But these new figures give us cause for hope that we can beat cancer, and if we all work together we will beat it sooner.

And finally, our zero this month is tobacco manufacturer Philip Morris International, who has
 threatened to sue the government for billions over its plan to ban branding on cigarette packs. The move could delay implementation of legislation to introduce standardised packaging for tobacco, which the government has vowed to implement before the election, following the finding by an independent study that the move would “very likely to have a positive impact on public health”. 

About 200,000 children aged between 11 and 15 start to smoke in Britain every year, and standardised, unbranded cigarette packs would give them one less reason to take up the habit, which kills half of all long-term smokers.

That’s all for this month. My thanks to Alan Worsley, Sarah Wells and Greg Jones for production, and we’ll see you again next month for a look at all the latest cancer news.

We’d also like to answer your questions in our podcast, so please email them to, post on our Facebook page, or tweet us – that’s @CR_UK. And if you’re listening to this on Soundcloud, please leave us a comment with your feedback. Thanks very much and bye for now.