HPV, Michael Douglas, and the latest cancer headlines

Cancer Research UK
We discuss HPV, cancer and oral sex, and finding out how melanoma cells go on the move. Plus, we look at the quiet epidemic of oesophageal cancer.

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Transcript

Kat: This is the Cancer Research UK podcast for July 2013. This month we’re discussing HPV, cancer and oral sex, and finding out how melanoma cells go on the move.  Plus, we take a look at the quiet epidemic of oesophageal cancer in UK men. And we’ve got 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, News and Multimedia Manager at Cancer Research UK.  Now this month there’s been quite an exciting story in the news in the form of HPV – the human papillomavirus – hitting the headlines at the beginning of the month as actor Michael Douglas told the world (through the Guardian newspaper) that he had apparently contracted his throat cancer from oral sex, and this was also helping to “ease” his cancer.

Henry: He did go on to retract the story the next day after quite a lot of interest on the internet and commentary, and I saw you quite a lot on the television and heard you on the radio talking a lot about it, Kat.

Kat: Yes, it was a very interesting day. But certainly there were lots of headlines about “Oral sex causes cancer and a lot of interest in it. So to find out a bit more about HPV, cancer and oral sex, I spoke to Jess Harris, who’s our senior health information manager.

Jess: HPV is a really common virus. It lives on the skin and what lines some of your body cavities like your mouth or your genitals. It infects almost everybody at some point in their life, and it can be passed on through any kind of close skin-to-skin contact, whether that’s through sex or  - for some types of HPV  - through any kind of touching, really. Most HPV types don’t cause you any harm at all – in fact you don’t even know you’re got them. Some of them can cause warts, either on the skin or on the genitals, but there are a few types of HPV that can lead to cancer. And those types tend to have no symptom at all, not even warts. So most people will get an infection, never know that they had it, and their body will just clear it up automatically on its own.

Kat: But in some cases it doesn’t, and it can lead to cancer. What sort of cancers are we talking about?

Jess: The most common type of cancer that’s linked to HPV is cervical cancer. Cervical cancer’s quite common but it can also lead to other types of cancer as well, like other genital cancers – penile or anal cancers, vaginal or vulval cancers. And it can also lead to some types of mouth and throat cancer as well.

Kat: And this is where the Michael Douglas story comes in, because he did claim that his throat cancer – cancer at the back of his throat – was caused by HPV. What do we know about the link between HPV and these types of cancers?

Jess: We do know that HPV can increase the risk of developing certain types of mouth and throat cancers. What we don’t really know yet is all the information we need about how HPV infections behave in the mouth, what happens to make them turn into a cancer, how easily are they spread, and how they can be cleared. But we do know that having HPV infections in the mouth can increase the risk of these types of cancer.

Kat: If HPV infection is incredibly common, and most of us who are sexually active have it at some point, why is it that only a relatively small number of people will get cancer?

Jess: It’s such a common infection, and – and you said – very few people will actually go on to develop cancer. There’s quite a lot of reasons for that. Most people’s immune systems will be able to just kill the virus infection off, and then they’ll never need even know that they had it. In some people they’re immune system doesn’t succeed in clearing that infection, and it can set up what’s known as a persistent infection – that’s an infection that doesn’t go away. And, again, in most people that have a persistent infection, they’ won’t get cancer. But in a few people who have these persistent infections, they can go on to develop into cancer. Other things can be involved in this – for example we know that smoking increases the risk of cervical cancer. And that probably happens because it lowers your body’s ability to fight off this infection, and it can accelerate that progression into cancer. So an enormous number of people have it, but only a very few get cancer as a result.

Kat: So you mentioned cervical cancer – we have a very effective screening programme in the UK for this, and there’s been some recent news I’ve seen where currently we have HPV testing after you’ve done a cervical smear test, you’ll then test of HPV. But a new study suggests that it might be better to test everyone for HPV first, and then go on to do cervical smear tests. Does this sound plausible, does this sound like a good idea?

Jess: This is really interesting research, because it just goes to show how we can take two tests that we already have that are good tests, and just use them in a different way and get a much better outcome. So at the moment the only women who get tested for HPV are women who’ve had a slightly abnormal smear. And if you have got HPV with a slightly abnormal smear, it can mean you need some further investigation. If you haven’t, it’s almost completely likely to go away on its own.  This study shows that by flipping the order of those tests, by doing HPV testing first, we’ll pick up more women that could be at risk of cervical cancer, and so we’ll be able to prevent more cancers.  The study suggested it could save about 500 extra cancers each year, so it could prevent those extra 500 cancers just by swapping the order of the tests. And the reason this could work is that HPV testing is better at picking up those more serious precursors of cervical cancer, so those women who have those types of changes can get treated, and prevent cervical cancer from even developing in the first place. So it’s great research.

Kat: That was Jess Harris, our senior health information manager. And, as she told us, there’s quite a lot in this story, and it certainly did help to raise awareness of HPV and certainly oral cancers as well.

Henry:  Absolutely, and it’s always interesting when celebrities do have a big cancer story like that – we saw it with Angelina Jolie last month. It’s just interesting how this raises awareness among the public of the different aspects of cancer.

Kat: But I have to say there is no scientific evidence that oral sex can treat any form of cancer, as far as I know.

Henry: Not as far as I know either!

Kat:  Moving to more scientific matters, there were two new research papers from our scientists this month looking at how melanoma cells spread. They were both published in Nature Cell Biology.  Melanoma cells are pretty clever cells, aren’t they?

Henry:  It’s a type of cancer that does tend to spread very easily, and it’s quite different from other forms of cancer in how shape-shifty and invasive it can be. The first paper, from researchers at our London Research Institute, wasn’t really a lab study, it was more using computer modelling to try and create a virtual environment where they could study how cells moved under different conditions. The scientists now know that there are different ways that cells can spread through different types of tissues. The obvious implication for that is that if you’re going to stop cancer from spreading, you need to understand and potentially stop each of those types of spreading. For example, how they crawl and squeeze through different types of tissues. Or sometimes they sort of blob across flat surfaces and mesh-like surfaces.

Kat: There was a lovely analogy used by one of the researchers who said it’s basically like you use different shoes for different environments. You have running shoes for a jog in the park, you need strong boots for hiking in the hills. But if you just take the hiking boots away from these cells, they’ve still got their trainers, so we need to find ways to block all these types of movement. And in fact the second paper, from researchers at The Institute of Cancer Research and their colleagues in Houston in America, they’ve not started to pin down the genes that are responsible for switching between the different types of movement. That was a great paper showing that they found a number of key genes, studying fruit flies and human cells in the lab, that show how this switch happens, so those could be good targets for treatments.

Henry: This just ties in to a lot of excitement in the field of melanoma research at the moment. We’ve already had a couple of drugs come through in the last year targeting the faulty molecules inside melanoma cells, or the immune system and how it interacts with it. This is particularly exciting because this is a cancer that really hasn’t had much progress for a very long time. There’s a good few decades between now and the last really big treatment for it. So we’ll keep an eye out on how it’s progressing, and it’s definitely an exciting time for melanoma researchers.

Kat: And finally, it’s also an exciting time for naked mole rat researchers. Tell me about these little guys!

Henry: Naked mole rats are one of the weirdest creatures on the planet – certainly the weirdest mammals on the planet. They’re colonial rodents – colonial as in ants and bees and stuff. They live in underground colonies in the Sahara. They do look like a slightly saggy sausage with teeth. Anyway, the relevance for cancer is that they don’t get it. Researchers have studied them in all sorts of different environments, and they don’t get cancer. Everyone’s been wondering why. And this new research is particularly interesting because researchers studying naked mole rats were trying to grow cells from them in the lab, and they just found this gloop coming out of the cells, and they thought “what the hell is this?” They pinned it down to being a particularly sticky form of sugar called hyaluronan - that’s a bit of a mouthful. All mammals make this, and it’s a particularly sticky protein. It’s like the Polyfilla that holds our cells together in our body. The type of this sugar that the naked mole rats make is absolutely massive. It’s way, way bigger than the ones our own cells make, and the evidence from this study shows that this really stops the cells, if anything does develop a bit like a cancer in a naked mole rat, this just absolutely stops it from spreading or causing any problems at all.

Kat: It’s very interesting – it’s work from researchers in the US. I mean, at the moment it’s just a bit of science trivia – it’s certainly very interesting but it’s hard to see how it could be directly applicable to humans. And in fact, I remember about a year or so ago some of our researchers at the Cambridge Research Institute found that the same molecule in cancer cells –hyaluronan – tumours can use this to resist chemotherapy by making themselves sturdier and stronger. So there’s certainly a lot more to understand about this protein.

Henry: Absolutely. And studying basic molecules, basic systems, and studying these fundamental things can give real insight into how life works, how things go wrong, and what cancer actually is, which is of course fundamental to finding out new ways to treat it.

Kat: Thanks Henry. That’s Henry Scowcroft, our News and Multimedia manager.

Also this month, we published startling statistics revealing a quiet epidemic of oesophageal cancer – that’s cancer of the gullet, or foodpipe - in UK men. Rates of one particular type, known as adenocarcinoma, are rising faster than any other male cancer. And more than five and half thousand men are diagnosed with oesophageal cancer every year in the UK, compared to fewer than three thousand women. Yet despite this rapid rise in cases, survival remains very poor, and just over one in ten patients will live for five years or more.

To find out more about oesophageal cancer, what might lie behind this startling rise in rates, and what we’re doing to beat it, I spoke to Tim Underwood, an oesophageal cancer surgeon in Southampton – apologies for the background noise in this piece, which was recorded at our busy press conference.

Tim: So the oesophagus is the foodpipe, or gullet, that connects the mouth to the stomach. And cancer of the oesophagus tends to occur at the bottom of this pipe, and it’s a cancer that spreads quickly and tends to present late in the course of the disease.

Kat: So people are diagnosed when it’s already started spreading through the body?

Tim: Unfortunately, about two thirds of patients at the time of presentation will already have disease that’s started to spread, and we can’t think about treating them with a cure in mind.

Kat: And what’s the kind of scale of the problem? Is it increasing in the UK?

Tim: Rates of oesophageal cancer - particularly adenocarcinoma – have doubled over the last thirty years. Rates are three times the level in men than they are in women, and it’s one of the most rapidly increasing cancers in men in the United Kingdom.

Kat: And what do we know about what’s causing this rise? Is there something that’s particularly changing?

Tim: We know that oesophageal cancer is related to reflux – heartburn – and obesity. And we think those are two of the key drivers. But more research is needed to understand in detail the causes of this dramatic increase.

Kat: And what would you advise someone who’s maybe listening to this and thinking “ooh, I’ve had heartburn for quite a long time.” What should they do?

Tim: Long-term heartburn is not normal – that’s the first thing to understand. They probably haven’t got anything seriously wrong with them, but they need to go and see their GP and ask the GP “do I need to be investigated for the symptoms I’ve got?”

Kat:  And I understand that there’s a new kind of test that’s being trialled to look at these early signs that could become oesophageal cancer. Tell me more about that.

Tim: Traditionally, patients will have been refereed to hospital and they’ll have had to swallow a flexible camera, which is a relatively invasive investigation. But Cancer Research UK are sponsoring some new trials looking at something called the Cytosponge, which is a small capsule on a string that’s swallowed by the patient in the GP’s surgery. The capsule dissolved and then a sponge is pulled back up the oesophagus which is then sent to the laboratory to be analysed. It’s a quick, efficient, cost-effective, diagnostic tool for the precursor lesions, the beginnings of oesophageal cancer.

Kat: So if that works out, it could really help to save more lives by diagnosing the cancer earlier?

Tim: Yes, most definitely. It would be efficient, cheap, and save lives.

Kat: And one of the other challenges is that we don’t really understand a lot about oesophageal cancer, about what drives it, about the genes and molecules involved. How are researchers trying to understand that more?

Tim: Perhaps the most important project that’s going on at the moment worldwide for oesophageal cancer is something called the International Cancer Genome Consortium study, which is being run through Cambridge and is CRUK funded. This is looking at mapping the DNA in fine detail of 500 oesophageal tumours. We will understand the genetic landscape of this disease, to be able to tailor treatments to the individual.

Kat: And finally, you’ve talked about when you operate on someone it’s a bit like going through a marathon – you’re going through your own marathon effort for oesophageal cancer. Tell me about this.

Tim: Not just me – six of us from the team at Southampton are taking on the New York marathon in November because – as you’ve said – I say to my patients that having the operation is like doing a marathon without any training. We can do the training and we know afterwards we’ll recover. Our patients’ futures are not that certain, so we think that in solidarity with them we’ll take on something that challenges us.

Kat: And you’re trying to raise an awful lot of money to support Cancer Research UK’s research, How much money are you hoping to raise and how can people support your fundraising?

Tim: A hundred thousand pounds, which is an awful lot of money – I haven’t got that in my pocket at the moment! So I need people to contribute if they can, as little or as much as possible. They can access through two sites on the internet – thecancermarathon.org or our Justgiving site – www.justgiving.com/thecancermarathon

Kat: That was Tim Underwood, from Southampton General Hospital. You can find out more about Tim’s marathon efforts, and watch some great videos featuring Tim and his team, and the patients they’re treating, at thecancermarathon.org

And finally, it’s time for our heroes and zeros.  As we heard earlier, Tim Underwood and his colleagues are running the New York Marathon later this year to raise money for our research. So our heroes this month are all our supporters who’ve strapped their trainers on and braved the Great British weather to raise money for our life-saving work – whether it’s the many thousands of women and girls running Race For Life, our dedicated Relay for Lifers walking through the night, or anyone else taking part in a sporting event. We’re so grateful to each and every one of you.

And our zero of the month, yet again, is the tobacco industry. But this time, it’s their role in smuggling that’s under the spotlight. A new report from the National Audit Office shows that although tobacco smuggling has dropped by more than half since 2001, HM Revenue and Customs are still missing their targets when it comes to stopping illicit tobacco.  But the report also reveals that the tobacco companies themselves are playing a part in helping the smugglers, for example by sending unnecessarily large amounts of tobacco to very small countries like Andorra, which then get smuggled back into the UK. There’s more information about this and their other dodgy dealings on our Science Update blog, which is worth a read.

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 podcast@cancer.org.uk, 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.