Tobacco packs, work-related cancers and overweight Britons
This month, a survey reveals ignorance of cancers caused by smoking, 8,000 people a year are dying from work-related cancers, cancer threat fails to motivate weight loss, testosterone on trial for young male cancer survivors, and - with the Olympics looming - we meet one of our prize-winning researchers who has truly gone the distance.
Welcome to the Cancer Research UK podcast. I’m Dr Kat Arney
A survey of more than 4000 people commissioned by Cancer Research UK revealed that four out of five people do not know there is a link between smoking and nearly eight different types of cancer.
At least two thirds of those surveyed knew smoking caused cancers of the lung, mouth and throat, but less than one in five knew tobacco is also linked to leukaemia and cancers of the liver, pancreas, bowel, kidney, bladder, cervix, and ovary.
The results coincide with the five year anniversary of all pubs, bars and public spaces in England going smoke free. The UK government is now consulting on whether to remove glitzy tobacco packaging - a proposal that Cancer Research UK is backing with our new campaign, ‘The Answer is Plain’.
Jean King, Cancer Research UK’s director of tobacco control, tells us why the survey findings are so worrying and how you can help our campaign.
“Well, it is shocking how many parts of the body are affected by tobacco. It’s a very heavy addiction – once you start it’s not easy to quit. So we really want to stop young people from starting to smoke in the first place. One of the key ways to do that is to make packaging less attractive.
We know that young people are attracted to these glamorous packs and so we want to have plain packaging with just the health warnings on. And we would like people to tell the government that that’s what they support too, and they can do that by signing our campaign at www.theanswerisplain.org”
Around 8,000 deaths from cancer each year in Britain are linked to occupations – especially those where asbestos, diesel engine fumes or shift work are involved – according to a new study published in the British Journal of Cancer this month. This is equivalent to one in twenty cancer deaths.
Just under half of these deaths were among male construction workers. These people are most likely to come into contact with asbestos as well as other important carcinogens such as silica and diesel exhaust fumes.
The findings come hot on the heels of the International Agency for Research on Cancer upgrading diesel exhaust fumes to a ‘definite carcinogen’ – putting them in the same category as chemicals such as asbestos.
Hazel Nunn, Cancer Research UK’s head of health information, talks us through the findings.
“This new research shows that around 8,000 cancer deaths each year are linked to occupation. Obviously that’s quite a high number – it’s not in the same ball park as smoking which is over 40,000 deaths – but it is up there in the top six causes of cancer death each year.
Now, what we do know is that over the next few years the number of deaths linked to asbestos, which is one of the key drivers of this figure, are likely to start falling. That’s because we’ve got better health and safety today than we had in recent decades, meaning that fewer people are exposed to asbestos in the workplace. But in terms of the other occupation-related risk factors that are particularly prevalent in terms of diesel fumes and shift work, there’s still more work to be done.
We’re awaiting the results of a report from the Health and Safety Executive on shift work which should clarify a little more about the evidence, and should also give us some more information about steps that might need to be taken. And in the case of diesel fumes, we look to the Government to see what needs to be put in place in terms of protecting workers further from the effects of diesel fumes.”
Nearly two-thirds of overweight Britons say they are struggling to find the drive to lose weight despite the vast majority knowing it increases their risk of cancer – according to a new Cancer Research UK report published earlier this month.
This is the first time a survey has shown that even when heavier people know excess body weight is linked to cancer, they still feel that a lack of willpower is a barrier.
After smoking, being overweight or obese is one of the most important avoidable cancer risks. Scientists think that in the UK, overweight and obesity could be leading to 19,000 cases of cancer a year.
Dr Emily Power, Cancer Research UK’s senior health evaluation officer, explains why shedding those extra pounds is so important.
“After smoking, excess weight is one of the biggest causes of cancer. A recent study has found that around 17,000 cases of cancer each year can be attributed to being overweight or obese, so it is a big problem in the UK and it is contributing to several different types of cancer.
We know it’s very difficult for people to keep a healthy weight, and especially difficult for people who are already overweight or obese to lose that excess weight. We have got some simple and easy-to-follow Ten Top Tips on our website. These have been shown in randomised controlled trials to significantly reduce weight over time, so they are going be effective for most people that try them. So we recommend having a look at those.”
Earlier this month, Cancer Research UK launched a trial to see if male cancer survivors might benefit from testosterone therapy. Levels of testosterone – the male sex hormone - can be below average in men who have been treated for cancer at a young age, causing side effects such as weight gain, less energy and lower sex drive.
The trial is aiming to recruit 270 male cancer survivors aged 25 to 50 from around the UK to see if a skin gel containing testosterone might help alleviate some of these symptoms.
James Ashton, an aerospace engineering student at Sheffield University, was invited to be a patient advisor for the trial after first being diagnosed with testicular cancer ten years ago. We asked James to explain the difference the treatment had made to his life, and what the trial might mean for other young men like him.
“Basically, having the testosterone has been a bit of a life-saver. In my experience, I was diagnosed as having borderline testosterone levels while I was in my first year at university. I couldn’t keep up and I failed my first year of university. I was having trouble being able to concentrate after lunch, even keeping my eyes open, absolutely feeling burnt out all the time and I just lost my evenings.
Since I’ve started the testosterone replacement, it gives you much more of a good approximation of my previous life, previous to being diagnosed with low testosterone levels, when I was a fitter, younger man. I was able to compete more, able to sustain more of a pressured life. Basically I’ve got my evenings back, and I’m living a more normal life now.
A trial like this hopefully could prove that there are ways to help young male cancer survivors who are suffering from these kinds of symptoms.”
This month thousands of the world’s top athletes will flock to London for the start of the greatest athletics competition in the world. With Olympic fever setting in, we were inspired to meet up with one of our Nobel Prize-winning researchers - the equivalent of an Olympic gold medal in scientific terms.
Sir Tim Hunt joined Cancer Research UK in 1990, where he was Head of the Cell Cycle Control Laboratory at our London Research Institute Clare Hall Laboratories until his retirement last year. His lab focused on understanding how cells copy themselves – a process that is at the heart of cancer, as well as being central to all life on Earth.
His work has paved the way for important new approaches for treating cancer, with drugs that block key proteins involved in the cell cycle currently being tested in clinical trials.
Our reporter Ailsa Stevens went to find out more about this Nobel Prize-winning research. She started by asking him to explain how cells divide.
Tim Hunt: The answer is they go through a series of processes, or events, which they have to complete in order to make two of them. Basically they have to double everything, and they do it in a particular way. Then when you can’t see them dividing, they’re busy duplicating their DNA and other components. So the cell cycle is a series of processes that have to be completed in order to make one cell give rise to two cells.
Ailsa: How exactly can the cell cycle go wrong in cancer?
Tim: Many cells in your body don’t actually divide, they just stay the same. But some cells have to reproduce themselves because they need to be repaired and replaced all the time, like the cells in your gut – they suffer so much damage they have to continually be replaced - or the cells in your blood which are dying all the time, and need to be replaced.
And normally that rate of replacement exactly matches the rate at which they’re lost, so that your gut doesn’t get any bigger or any smaller, it stays exactly the same throughout your lifetime. Cancer cells, however, disobey those rules and they start dividing a little bit faster than they die, so the lump gets bigger and bigger and bigger with time. It’s a simple as that.
Ailsa: Can you think back to the year you won your Nobel Prize – what was going on in your life at that time?
Tim: Actually at the time of the Nobel Prize I was at a bit of a loss, really. I didn’t quite know where I was going because we’d solved the first problem – we knew what was going on. And when you’ve solved a problem you don’t know where you’re going. And suddenly out of the blue comes this call from Stockholm saying “You’ve won the Nobel Prize!”
I was a bit surprised to be honest, because I wasn’t expecting it in the least. But it was a very nice surprise, of course. The actual celebrations in Stockholm were absolutely amazing – I hadn’t really appreciated it. It turns out that one of the best things about winning the Nobel Prize is finding out what it’s like to win a Nobel Prize!
Ailsa: And what is it like?
Tim: The first reaction is embarrassment actually. I remember running into my colleague Paul Nurse, who was my boss at the time, about two or three weeks after the prize had been announced, and he said “Oh Tim, I’ve had a most dreadful weekend – I felt so inadequate!” And I knew exactly what he meant – the thing is so big that it’s really too much for anyone to bear. After a while you get used to it, but at first it’s very emotional and difficult.”
Ailsa: What were the key findings that led to you being awarded the Nobel Prize? Were there any Eureka moments that stick in your mind?
Tim: My discovery really was a Eureka moment, and very untypical in my research experience. I simply discovered that a protein went away. It disappeared – poof! – just like that. It’s hard to say you won a prize for discovering something vanishes – it’s a bit negative really, I suppose. But that was it.
The importance of it is that it turned out to be absolutely true, this protein is an important component of the enzyme that catalyses cell division. It’s actually the protein that joins together with Paul Nurse’s famous protein called Cdc2. But without cyclin, which is my protein, Cdc2 can’t operate at all. It’s an essential component of the enzyme.
And then it turns out that you have to get rid of it, you have to destroy it in order for the cell cycle – as the name implies, like a cycle wheel it goes round and round – the wheel gets jammed. You have to reset the clock, so to speak, every time the cycle runs. And this resetting turns out to involve protein destruction.
This seemed so impossible to understand at the time that nobody had even thought of it as a theoretical possibility. I just did a very simple experiment using sea urchin eggs, funnily enough, which just showed this protein disappearing. I could see it really clearly, and the only possibility was that it was disappearing, so from that moment on I was the only person in the world who knew how the cell cycle worked. Then gradually it spread and the idea caught on.
Ailsa: A lot of your work has involved studying model organisms like sea urchins. How does that approach help us to learn about cancer in humans?
Tim: You know, we would never have discovered cyclin if we hadn’t been using sea urchin or clam eggs. Later I switched to using frog eggs, because sea urchin eggs are only available in late June and early July, which is not very satisfactory really, whereas you can have frog eggs all year round. But if I had worked on human cells, even just using cells as a model, we’d never have seen it because they’re very minor components in that situation. But in the unfertilised sea urchin egg, these things stood out like a sore thumb.
And I think one of the great rules of fundamental science is study something that’s really easy to study, because it’s incredibly difficult to study these things, and much easier when there’s an awful lot of them and they really stand out. It was interesting because at the time, in fact, the director of the Cancer Research UK institute where Paul and I worked was criticised for hiring somebody who worked on yeast – people said “come on, we understand cancers pretty well, you just cut them out, why work on yeast? Yeast don’t get cancer!”
Then when Paul discovered that yeast cell division depended on Cdc2, and human cells had Cdc2 in them, the critics were immediately silenced because they realised we didn’t know the first thing about cell division, which is the most fundamental thing of cancer! So understanding how cell division is controlled and how it’s executed is absolutely fundamental. We would never have discovered this, I don’t think, if we’d only worked on human cells. It would have been incredibly difficult, so using model organisms is a short cut to finding out what’s really going on.
Ailsa: So the basic processes are common to all organisms?
Tim: At the time it wasn’t so obvious how much humans had in common with yeast and plants and flies and sea urchins and frogs and things like that. To some extent, that came out of this work and it’s very, very helpful. In many ways, studies in flies and worms have made major contributions to understanding the processes that go wrong in cancer in human cancerous cells, so I think it’s really important to do that.
You don’t want to do the experiments on cancer patients, basically, unless you’re getting very close to a treatment. But you’d never get anywhere near close to a treatment without doing these basic experiments first, because you’ve got to fiddle around – even be playful, explore wild ideas. Because often when we don’t really understand things, the truth is far stranger than one would have thought.
Ailsa: It seems despite your retirement last year you’re still very active in the scientific community. Do you think there’ll ever come a time when you feel you want to hang up your labcoat, or will you just keep going?
Tim: I have hung up my labcoat but I’m still pretty busy!
Ailsa: Because you were with Cancer Research UK throughout most of your career...
Tim: I was with CR-UK for the last twenty years or so. Before that I was a researcher in Cambridge, but it was very good to join Cancer Research UK and I enjoyed my time here.
Ailsa: Where do you see cell cycle research going in the future?
Tim: Well there are an awful lot of things that we still don’t really understand very well. I went to a seminar today actually by a young man who’s working on the control of growth in flies. We don’t really understand how growth and cell division are co-ordinated and what controls cell growth – this is a very important and very complicated subject. So there’s still an awful lot to be discovered. Whether that will lead to wonderful new cures for cancer, who’s to say? But if we don’t know we’ll never find out, will we?
That was Ailsa Stevens talking to Sir Tim Hunt. We’ll be back next month with all the latest news, but in the meantime you can keep up to date by following us on Facebook – that’s facebook.com/cancerresearchuk