Tracking cancer, tobacco tactics and citizen scientists
Kat: This is the Cancer Research UK podcast for April 2013. We’ll be finding out about a blood test that can track breast cancer, how our cancer risk is encoded in our genes, and why a tobacco company spent millions of pounds on misleading adverts. Plus we report on the computer nerds taking on cancer, and bring you this month’s heroes and zeros.
Hello and welcome, I’m Dr Kat Arney, and with me to discuss the latest news is Henry Scowcroft.
Now the first story I wanted to talk about was some research from our scientists at the Cambridge Research Institute and they've been comparing three different techniques for monitoring how breast cancers progress over time and how they respond to treatment – measuring circulating tumour cells (these are cells that have escaped from tumours and are going around in the bloodstream). They've also looked at a specific protein, what we call a biomarker, in the blood, and also circulating tumour DNA.
Henry: Explain a bit about where this DNA comes from in the blood. That sounds really interesting, where does that come from?
Kat: This is DNA that's come from cancer cells that have died as a result of treatment or as a result of natural processes and their DNA gets broken up into small fragments and disperses into the bloodstream. Now there's not a lot there, and there's also a lot of DNA in the blood from healthy cells that have dies that is floating about. But you can detect it and you can specifically detect it. So that's what the researchers have done.
They measured these three things – circulating tumour cells, the circulating protein and the circulating tumour DNA an d mapped it against CT scans from around 30 patients to see how all these three things correlated with how they were progressing and how their cancers were doing in response to chemo. Now they did find that of all three, the best match was with the circulating tumour DNA. It was the most sensitive and they could detect it in the most people, so this is really quite promising.
Henry: It really is, and this is similar to some of the work they did last year with ovarian cancer. And this seems to be a building idea – looking at the DNA from the cancer in the bloodstream.
Kat: I think it could be a really powerful way of measuring not just breast or ovarian cancer but all kinds of solid cancers.
Henry: And, of course, this is really interesting because as we learn more and more about how tumours evolve over the course of treatment, and some of the big work that came out last year in this regard, this allows hopefully in the future to be able to follow that process and adjust treatment as the tumour adapts to it and to really make progress in personalising medicine in that way.
Kat: Exactly. At the moment they've just looked at a few genes in this tumour DNA and they can see how some of these genes change over time, so that's almost mapping how the tumours are involving. Now what would be really powerful is if you could do that for the whole cancer genome, not just these selected genes. But I guess we'll have to watch this space for that. Now the next story – there was a fantastic story in the Guardian I saw. What was this about?
Henry: This was about how the Government seems to be moving towards bringing in standardised packaging for tobacco – this is the idea that tobacco packaging will be debranded so it won't be able to market the tobacco brand on the surface of the packs. We've got to stress that this is a rumour so far – it's something that was spotted by the Guardian. The Department of Health seem to be strenuously denying that this is fact as yet, but we're hopeful that this is going to be happening. And this would be a really great milestone in preventing marketing to children particularly.
Kat: Because that's what standardised packs are really all about. It's not about smokers who are already smoking?
Henry: No, absolutely not. It's about preventing the brand of a cigarette being conveyed to the next generation of smokers. Smoking is a habit that unfortunately kills half the people who take it up, so tobacco companies need to bring in the next generation of customers, if you like. We released figures just a couple of weeks ago showing that more than 200,000 children between the ages of 11 and 15 start smoking every year, so this isn't a trivial thing - this is something we really need to work on. Of course no-one's saying that standardised packs is going to be a magic wand to end smoking but it's a really important milestone.
Kat: It is incredible when you look at some of the packs now – they're so shiny, you get little purple ones, you get cigarettes with flowers on. It's amazing how they are eyecatching and clearly do appeal to children.
Henry: Absolutely, and it's something the tobacco industry is aware of. They're resisting the move to standardised packs with a £2million advertising campaign that's just been taken apart by the Advertising Standards Authority. They've ruled that the adverts that Japan Tobacco International put in the press over the last twelve months have been misleading and unsubstantiated, and really clear evidence that they're kicking against this quite hard. So we really hope that this legislation comes through.
Kat: Because, of course, it could be lifesaving. We know that smoking is the single biggest preventable cause of cancer in the world and certainly a massive cause of cancer and cause of cancer deaths in the UK. So, hopefully, bring on plain packaging, we'll see.
Henry: And finally, the last story we saw was a huge international study involving over a thousand scientists in a hundred research groups that was led by some of our researchers at the University of Cambridge and the Institute of Cancer Research. It's multiple papers that have been published in the journal Nature Genetics looking at these things called SNPs. These are single 'letters' of DNA that are different between different people and they're linked to their risk of cancer, and particularly they were looking at breast, prostate and ovarian cancer.
Henry: Let's be clear, these aren't actual mutations – these aren't faulty genes are they?
Kat: It's a bit difficult because SNPs are just letters that are different. They could be in a gene that's important and cause the gene to be faulty in some way. But they could also be in a control region that tells you when to switch a gene on or off, or how much of that gene product to make. Or they could be doing nothing at all, but they could just be near something that's important. So basically they're just a markers. The researchers looked at 100,000 people with breast, ovarian or prostate cancer and 100,000 people without these cancers and found a whole bunch of new SNPs – more than 80 new SNPs – that were linked to these cancers and linked to an increased risk of these cancers. And that's double the number we've previously known about. In fact I was talking to one of the researchers involved and he said they'd run a sweepstake out of all the scientists [involved] across Europe as to how many they were going to find.
Henry: So what use is this knowledge? It's all very well mapping this stuff out and saying 'we've found 80 new SNPs, that's great!' What happens next? How does this help patients?
Kat: Well this is the multi-million dollar question, isn't it? To find out a little bit more, we spoke to Professor Doug Easton, who was one of the main authors on the study.
Prof Easton: Now that we've identified all these markers, the next question is how we can put this information together to define individual risk, and then potentially this could be used to identify people at higher risk. And that could be used, for example, to modify the screening programmes or to put people into trials for some sort of chemoprevention. And then in the longer term the aim is to use the information about what these markers actually do in order to develop therapies based on the particular genes and pathways that are involved.
Kat: So it does look like the main benefits are going to be in risk, and understanding an individual person's risk of cancer, and maybe whether they should have screening from an earlier age.
Henry: one of the things that came out of the breast screening review last year was that if we can target screening better to the women who need it more, and give it less to the women who don't need it so much we can reduce the harms associated with screening as well as detecting as many or potentially more cancers.
Kat: Absolutely, and we also know that for women with, say, a mutation in a gene called BRCA1 which greatly increases their risk of cancer, some of them will have a very high risk of cancer, some of them will have a lower risk of breast cancer. And they think that maybe it's the combination of these SNPs you have as well will dial up or dial down your risk. And in prostate cancer as well where we don't have good screening at the moment, we can do a lot more in understanding how a man's individual genetic makeup is affecting his risk.
Henry: A lot of the stuff we've seen in the news recently has been about whole genome sequencing – sequencing the entire genetic data within a patient's cancer and in their normal DNA and comparing that, looking for the differences and the mutations. How does looking for these little markers compare to that technology, which seems to be so powerful and so exciting?
Kat: Well at the moment I think it's going to be running in parallel and be complementary. It's also important to point out that these kind of SNP studies are way cheaper – I think it's a factor of about a hundred cheaper to do than whole genome sequencing at the moment. Talking to the researchers involved, I think that over the years whole genome sequencing will become much, much cheaper, you'll be able to look at all the genes and it will supercede it. But certainly for now, these kinds of studies are giving us a lot of useful information that will help to guide screening and understanding people's risk in the future. So that's the news for this month, thanks very much, Henry.
Last month, Cancer Research UK hosted what’s known as a GameJam at Google’s London campus, bringing together world-leading scientists alongside gurus from top technology companies and computer programmers, gamers and designers to develop a mobile phone game to accelerate cures for cancer.
Our researchers are generating huge amounts of data about the genetic faults in cancers. Analysing and interpreting this data is the key to finding new ways to diagnose and treat patients in a more targeted way. While advances in technology mean our scientists can process data faster than ever to identify new patterns and faults in tumours, much of it still needs to be analysed by people rather than machines. So by bringing together the collective power of hundreds of thousands of people with a simple game that is actually analysing real cancer data, we can plough through this information much more quickly, and save lives faster.
Once finished, the game – provisionally titled GeneRun - will be available to download for free from summer 2013. This means that anyone with a smart phone and a few minutes to spare will be able to play a fun game and simultaneously be helping our researchers to analyse vital scientific data.
We spoke to Amy Carton, Citizen Science lead at Cancer Research UK, and some of the so-called hackers involved in the GameJam to find out why this new project is so special.
Amy: Well the most fantastic thing about our GameJam was that for the first time on record, as far as we know, Amazon Web Services, Google and Facebook collaborated for one common theme, and the theme this time was to collaborate to beat cancer. These guys were instrumental in helping us to shape the GameJam, and alongside them we had hackers from our previous Hackathon held in May. We also had some new hackers that came to us via the Channel 4 Games Commissioner, and an EventBrite call-out. We had a fantastic blend of hackers, and we also had students from Imperial and City University.
During the GameJam we had fantastic support from six scientists from Carlos Caldas' lab, and they generously provided us with some data for the hackers to use and incorporate into their game. And what we're going to be doing going forward is looking at all of the games that we've created – we had nine teams formed and twelve game ideas came out of that. We're going to be working with the scientists to understand which ones are most likely to produce the most robust scientific results, and alongside that we'll be making sure that whatever game we produce is future-proofed and will be able to incorporate gene data from any institution.
Chris: I'm Chris Childs from City University, London, and I run the Games Msc at City. I've been running a workshop here about how to brainstorm a game idea. The tricky thing we've got here is that we have some data that isn't a game, and we have some games that don't necessarily use the data. So we have to have some way of making a game out of the data to make everyone interested in playing it, without breaking the data itself. We've had some fantastic ideas so far – we've had guys doing Frogger games and collecting data in buckets and flying spaceships through asteroids full of data. I think it's going to be a really interesting thing – there's lots of great ideas come out of it and I hope at the end of this we have the game that will help find cures for cancer, so I'm really excited about it.
Oscar: I'm Oscar Rueda, a scientist in Professor Caldas' laboratory in Cambridge. We are trying to discover which genes are driving breast cancer. We have recently profiled 2,000 breast cancer samples and we have discovered that breast cancer is ten different diseases. We are trying now to find out which are the genes that are driving the disease. In order to do that we have to look at thousands of plots showing slight changes in copy number of the genes. It's a task that machine-learning algorithms can do, but they don't work really well. The human eye can be more accurate in defining these copy-number changes. So now we expect that if we can get help from everybody, trying to look at all these plots, we can try to find out where all these changes in copy-number are occurring, it could help us enormously in our research.
Amy: We've already had success in this area with CellSlider.net, and what that does is looks at our breast cancer tumour data. And that's something we collaborated with the Citizen Science Alliance and we held a Hackathon in May in order to inspire the look and feel of CellSlider as it is today. So far we launched in October, and within the first three months we've produced a data set that would have typically taken 18 months to do. So we know we're onto something really good.
This time round, however, when we're looking at our gene data, we want to wrap that up in a far more engaging way. We want to capture people's micro-moments – a couple of minutes when you're waiting for the bus or the train – that's the time that we want you to come and play our game. And play the game because you actually like the game, and as a happy coincidence, you are genuinely contributing to bringing forward the day when cancers are cured.
That was Amy Carton, Oscar Rueda and Chris Childs.
While you’re waiting for this new game, you can get on with helping our researchers analyse real cancer data through our first Citizen Science project, CellSlider, at cellslider.net.
And finally, we have two heroes to celebrate this month. The first is footballer Bobby Moore, who gives his name to our Bobby Moore Fund for bowel cancer research. Stark new statistics show that bowel cancer rates among men have risen by nearly 30% over the past 35 years, with the biggest increase in men in their 60s. April is bowel cancer awareness month, and also the launch of our new Make Bobby Proud campaign. Visit our website – cruk.org – to find out more about the campaign, as well as facts about bowel cancer and symptoms to look out for, and information about our research and progress.
Our second hero is a woman called Jane Redman, who’s one of our regional press officers. In an incredibly moving and honest post on our Science Update blog, she shares her experience of being a mum to Amy, who was diagnosed with a brain tumour when she was just nine years old. Her story is well worth a read, and can be found at bit.ly/JaneRedman
And our zero of the month is the Daily Mail, for running a story that failed to tell the difference between ladies and mice. The headline claimed that “Surgically removing pot bellies could help to cut the risk of bowel cancer in obese women”, but the research was only done on mice, and doesn’t prove that the same idea will work in actual human women yet.
That’s all for this month, 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 firstname.lastname@example.org, 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.