Professor Roger Kirby Director of the Prostate Centre, and Visiting Professor of Urology at St George's Hospital, London
Professor Malcolm Mason Cancer Research Wales Professor of Clinical Oncology
Vivienne Parry: Are you sitting comfortably? Shall we begin again? I am delighted to welcome back, for a repeat performance, by popular demand, the dynamic duo Professor Roger Kirby and Professor Malcolm Mason. I did ask them which one was Batman and which one was Robin. And Malcolm Mason said he didn't have the legs for tights. So which of you is going to speak first? Robin is going to speak first then Professor Roger Kirby. What we're going to do is hear both presentations first and then there will be time for questions afterwards. So Roger Kirby, uber-prostate man.
Professor Roger Kirby: Thank you very much, our dynamic chairperson, and lovely to see so many people here today. Almost twice as many as last year. Fantastic to be back. I'm going to tell you, I hope, a few new things.
(video clip of James Bond film)
I like that video clip. It sort of, to me, symbolises the journey through prostate cancer, which is a risky journey but hopefully with the help of some new treatments ends up with a happy ending, like our video clip.
Well let's think about some of the risk factors for prostate cancer. We were talking about them before coffee. The first three, of course, you can't really change, but the last three: diet, obesity and the amount of sunlight you are exposed to, you certainly can change. And I think that's where a lot of new work needs to be done - to look at ways of preventing prostate cancer. New ways of using chemo prevention using supplements such as selenium and vitamin E, but we need much more evidence about which of these are going to be effective.
I think there are reasons to be cheerful in prostate cancer, this charity, The Prostate Cancer Charity, is one of the organisations driving things forward. I just listed there some of the reasons to be cheerful, although there is a tremendous amount more to be done, I‘m just going to mention some of these things. Of course, in a short talk you can't mention everything.
What we are beginning to understand, as we heard in the previous lecture, is the underlying genetic mechanisms that cause prostate cancer. And as we tease those out as we have in other cancers, particularly colon cancer, where it's very well understood, and steps leading to the end cancer, and in breast cancer, where again we are far more advanced in our knowledge compared with prostate cancer. Understanding what causes those multiple hits that result in the end in people in their 50s, 60s, 70s or even 80s getting prostate cancer - that's where the real advances are going to come.
This is a little video clip that illustrates one of the areas that is quite promising in terms of basic research. This is a prostate cancer metastasis which is secreting a signal to the local blood vessels. A metastasis (tumour secondary) can't grow without a new blood supply. It's a bit scary to think of that happening in the skeleton, or the lymph nodes in the body. Maybe there are ways in which we can interfere with that process of angiogenesis, by using anti-angiogenesis inhibitors that do look quite promising.
One of the things that we are interested in right now is the hazardous waste. There are one or two of them around here, but most of you gentlemen are looking quite slim and quite trim. But I think what we are beginning to understand is that quite a few of the cardiac risk factors are also prostate risk factors. And if we address the issue of over-eating, too much saturated fat in the diet, we could perhaps make a bigger impact on prostate cancer than some of the more expensive new medications that may be on the horizon.
So risk factors for prostate cancer, the cardiac factor, the metabolic syndrome that links diabetes, hyper-lipidaemia and obesity, is a ripe area for research but a lot more needs to be done.
Well, we mentioned PSA. Some people call it the “promoter for stress and anxiety”. Norman said he'd never had his PSA done, and may just regret that one of these days. So we'll see, but it's very, very controversial. I think what's emerging in terms of PSA measurement now is that one measurement is inaccurate - but a sequential measurement of PSA actually gives you a lot of information. There's some new data at the American Urologic Society earlier this year where sequential PSA, looking for changes in the PSA or PSA velocity or PSA slope, actually gives you a tremendous amount of information. This is a patient who had a radical prostatectomy, and you see his PSA rising. Now a one-off PSA is not going to tell you that much - measure it sequentially you get a lot more information.
What about other tests? This is one that we are using now in quite a lot of patients - a UPM 3 test or a PCA 3G. It's still experimental, it's still controversial, but we find it quite helpful in terms of assessing patients who have rising PSAs but negative biopsy, or people who don't want to have to undergo a prostate biopsy. Because instead of having to put needles into the prostate which men always feel unhappy about, you can just massage the prostate. They are not ecstatic about that either actually, but which would you choose? You'd go for the massage wouldn't you, rather than the needle? And then you can measure the cells in the urine collected from the post prostatic massage. And this is an expensive machine.
It costs a load of money to do these tests, and a lot more research data needs to be put together. A study published earlier this year 443 patients, without going through all the figures, it looks like this is more accurate than PSA as a test maybe, I‘m not saying definitely. The negative predicted value that's telling you who doesn't have prostate cancer comes out at 87% and the positive predicted value that's telling you whether they do have prostate cancer, ¾ of the men with prostate cancer turned out positive, of course that's not 100% accurate but it actually rates higher, with an overall accuracy rate of 81% which is higher than PSA.
So it's promising. I don't think it's the answer, but it's just the beginning of a new wave of new tests and new markers for prostate cancer that we will see evolving.
Well, another problem that the clinicians have with men with prostate cancer is how advanced is the disease? Is it suitable for, well, is it localised or has it already spread? We spend a lot of time and energy looking at that and unfortunately none of our tests are absolutely accurate. But MRI spectroscopy - which you can see the tumour there in the prostate, the greenish prostate and the pink tumour, occupying at least half the gland there - MRI spectroscopy looks quite promising as a new marker, a new way of diagnosing.
(man on video screen talking)
“…And I give myself an annual medical, as I'm getting over the age for 45. I'm 52 and my PSA had this odd ratio test, so I went to my urologist and he said if you really want to find out what's going on you need to have a biopsy, which I did, and I didn't enjoy the result because 3 out of my 8 cores were positive adeno-carcinomas. When my feet touched the ground, I decided to find out about the best options for treatments decisions so I went to America . I went to Seattle to talk about brachytherapy. I sat in Starbucks in Los Angeles with people who'd had brachytherapy and people who'd had surgery. I thought about and talked to people about cryosurgery. I talked about external beam radiotherapy and also talked to people about active surveillance - just watching to see what happens. I'm looking hard at brachytherapy. I gather it's less invasive. It's got pretty good success rates and less side effects. So I am juggling between brachytherapy done by the right people who know what they are doing and have a well oiled machine or finding the right surgery for me.”
Professor Roger Kirby: That's a doctor, actually a psychiatrist. He illustrates the dilemma that we have, that many patients have, about choosing the right treatment for them. With more treatment options becoming available almost every week, that dilemma gets more difficult, not more easy. So he could have, for example, now gone for laparoscopic radical prostatectomy. The prostate can be removed pretty safely now through five small holes each a centimetre or two across.
The technology is there. Or he could go for the robotic radical prostatectomy. I just came back from a training course on robotic radical prostatectomy last week. The aim of the surgery is to remove the entire prostate and the entire tumour but preserve continence and most difficult of all, preserve potency as well, which is the tricky thing and maybe these new technologies will enable us to do that.
I'm just going to play you a little bit if this video - not the entire thing - just to give you an idea of what robotic surgery is about. That's a graph showing you the difference in a Scandinavian study. Again, everything in this area is a little bit controversial, between removing the prostate and just watching and waiting. I am sure Chris Parker will have something to say on that a little later.
Let me just show you this video clip.
“ Intuitive Surgical is changing the face of modern surgery with Da Vinci, a revolutionary robotic surgical system that takes surgery beyond the limits of the human hand.
Historically, patients have undergone open surgery, in which large incisions are made. More recently, minimally invasive surgery was introduced greatly reducing the trauma and pain. But although endoscopic surgery is less traumatic to the patient, it has many disadvantages. The surgeon's range of motions is restricted and unnatural, requiring counter-intuitive motion to execute instrument manoeuvres. Today, with Intuitive Surgicals, Da Vinci surgical system, robotic surgery offers the benefits of open surgery without the trauma to the patient, and the benefits of minimally invasive surgery without the restriction to the surgeon. ”
Professor Roger Kirby: That's quite a fun bit of marketing hype you'll appreciate. I like the soundtrack as well as the clips. I was playing with that a million and half pound machine in New York last week and I'll tell you it's an amazing bit of equipment I think it really will change things. There's a lot of pressure on the Trust to purchase this device.
What else have we got? Brachytherapy - you've heard mentioned before. This is the implantation of radioactive seeds into the prostate, now the fastest growing of treatments for localised prostate cancer. Technically not that easy to do as it needs a lot of practice to get used to the equipment, done under ultrasound control. A stepping device and a template that allows you to put the needle just exactly into the prostate and it takes quite a few weeks of intensive training to get people up to speed on this, but when they are good at it they can get the seeds into the prostate, each of those radioactive seeds, irradiating the prostate from inside to out rather than outside to in. Another new treatment that we've been using is cryotherapy - freezing the prostate. So this amazing organ, you can remove it, you can treat it with radiotherapy, you can freeze it and kill the cancer cells this way. You have to be careful because the rectum is so close behind the prostate that you don't damage the rectum and the ultrasound machines help you to avoid that, although there have been some complications with cryotherapy that you have to be aware of.
The thing that was in the Telegraph this time last year, I think maybe a little later, on the front page of the Telegraph, focused ultrasound, high intensity focus ultrasound – HIFU - where high intensity focused waves are focused on the prostate. You can see the transducer in the rectum there, and these little cavitations areas are used by heat in the prostate. The prostate is heated up by the ultrasound waves being focused within the gland. And it does look like a positive treatment, less invasive obviously than with surgery but with all these things there is a lot of marketing hype and interest in new treatments but what we need to do is wait for the longer term results. But so far it looks promising and side effects are certainly quite manageable.
What else have we got? Well this is Nick James' area more than mine. I think Malcolm might mention this as well. What we're seeing as urologists is patients with hormone escape prostate cancer - relapsing cancer after hormones now having their lives prolonged by the use of chemotherapy. It's not something that I do, but I refer my patients to Chris Parker and Nick James and I am seeing patients survive for many, many months longer than they would have done by only being referred to palliative care with taxotere.
And I think that Zometa - we'll be talking about this in the symposium at 5.30 - Zometa and the use of biophosphonates, which is widely used in breast cancer, not much used in metastatic prostate cancer. But the data from a study recorded about two years ago show improved outcomes in terms of delay to events occurring in the skeleton which looks promising. So I think that's a new wave treatment that we need to consider.
So these are my conclusions. I'm going to hand over to Malcolm before the questions.
We are getting a better understanding of the disease thanks to teams like Norman 's up in Yorkshire . We've got better diagnostic tests. They need to be proven, they need to be refined, we need to work not only on diagnosis but on better staging. We need markers to tell us which of the cancers will progress and which won't. We're looking at gentler safer treatments. New technologies like robots and HIFU and cryotherapy and brachytherapy and we are looking at new hormonal and chemotherapy approaches. So I think that Ian Drury was right, we have reasons to be cheerful but we don't have reasons to be completely cheerful enough yet. Thank you very much.
Vivienne Parry: If you could just hold the questions I know you now have until the end and can we now hear from Malcolm.
Professor Malcolm Mason: Well, thank you very much indeed. It's always a challenge to follow Roger, and so this is a low technology presentation because the only video footage I had was of my skiing holiday and I lent it to Roger and what happens…
I'm going to be very selective because the scope is just enormous. So I thought I wanted to focus on three particular things which I've got here. They are not completely taken at random and there could have been others, so I hope you'll bear with me in my choice.
The first which, again following on from Rogers comment, is a real message of hope, is the question of: Can we cure patients who have metastases, who have secondary disease in the lymph glands? The conventional answer to that question when I was doing my exams many years ago would have been no.
The second question is: What can we envision happening from our improved understanding of our biology and the sorts of things Norman has told us about?
The third thing, which I think is a real problem for patients and healthcare professionals dealing with prostate cancer: How on earth can we get the new drugs quickly from the laboratory, from the design and into the clinic? And I am really just echoing Normans comments from earlier, it really is taking an enormously long time. Is there anyway we can shorten that timeframe?
Well let's think about the first thing, and think about conventional radiotherapy, external beam radiotherapy. I'm not talking about brachytherapy and the limitations of treating the lymph glands the lymph nodes which are the things involved in draining fluid from all of the tissues all around the body, and are important in the context of prostate cancer because they are a route whereby cancer cells can spread. One of the problems with conventional external beam radiotherapy is that if you look at the area that receives the highest dose, it's a kind of blob, and what that is is an image that's a section taken through the middle of a patient. The green blob shows where the prostate is, somewhere in the middle of all that and the intention is to treat an area around it.
But there are other areas - and you can see there it's almost like a complete slice - which are receiving some dose of radiation. And the problem is if you look at what is in that area, it includes many things that you don't want to receive a very large dose of radiation. It's the bladder to the left and the rectum, which is the back passage, which is to the right of the green blob. And that is a problem because if we are trying to give radiotherapy to the lymph glands, what limits the dose that we can give conventionally is the dose that would be received by these other tissues around it. We can't give as higher dose to the lymph glands as we might like, as that would involve unacceptable toxicity, unacceptable side effects, as regards, for example, the bowels.
Now despite that, there maybe some rather interesting data coming through. These are the early results of a trial published last year from the USA that was looking at the differences in outcome in patients who had radiotherapy just confined to the prostate gland, compared to radiotherapy given to the whole pelvis. A lower dose and then a larger dose to the prostate. And I am sorry I don't have a pointer, but if you look at the table and you look at the column that says “failures”, and just the first two figures, there were other things in this which I am not going to go into which were different ways of giving hormone therapy. The point is that in this very, very early look at the data it might just be that outcomes for some of these patients are better if we give what is after all a lowish dose, but give some dose to the lymph glands around the pelvis as well as the high dose to the prostate.
That's extremely interesting. Why? Well because we have the technology to do rather better than that, and Paul mentioned it earlier – IMRT - Intensity Modulated Radiotherapy. I have to try and keep up with Roger in some of the gadgets. We oncologist like gadgets as well, and this one is actually rather important. And it's a way of changing the high dose area we treat from just being a blob to being able to be curved. And the picture that's there, it's actually curving around the spinal cord which is an area we desperately do not want to give radiotherapy to.
So we now have the technology whereby we may well be able to give a high dose to the prostate and a high dose to the lymph glands and the pelvis. And that's really important because I actually personally believe - and my belief is not highest level evidence - I believe we can cure patients with lymph node metastatic disease as Paul has indicated. We need those studies to show who those patients are and how to do it the best way and how often we can do it, and I think that's a real source of hope.
And now to something completely different. What about the new biology and really to look at the issue of, well can I focus on these three points: we need to hit multiple targets. One of the principles that we just can't get away from is the era whereby there will be one drug and one cure. And perhaps I could add to Norman 's guidelines when you read about the latest bold advance, I'd be very, very surprised if there is a single drug that is going to cure prostate cancer. I think the answer is going to be some sort of combination therapy.
Second question to which the answer I guess is obvious: Should we be targeting prostate cancer stem cells? Because I had a sneaky suspicion Norman would say something about it and I believe very strongly the answer is yes, and if so the question is how?
This is a slide I showed last year - so apologies to those who have seen it before - but I still think its important. The control of what makes cells divide is immensely complicated. At the centre of it is DNA, the things that make up the genes. They are they things that control whether cells divide, how they divide, how cells behave, and in this diagram I have shown three possible things that might influence DNA in the context of prostate cancer. One is testosterone. Second is something called EGF (Epidermal Growth Factor), and the third is something called IGF 1, or Insulin like Growth Factor. And these are three things that I have selected as being probably rather important in the context of controlling how prostate cancer cells grow and divide.
The point is that you can't think in isolation. All our conventional hormone treatments for all the good that they do - and they do a tremendous amount of good - are only basically targeting one of those pathways: testosterone. What about the other pathways? And it's equally wrong to produce a wonderful new drug that's going to target the epidermal growth factor receptor and put that into patients and be surprised if it doesn't give the results we would like it to give. Well if it so happens, that in order for that to work you have to have the other pathways blocked off as well, that would be no surprise at all. So my guess is that we are going to need to block multiple pathways. I'm not saying that these three are the particular ones.
But there's another aspect to it which I think could link into new therapies, whether or not it links into stem cells I don't know because I don't know enough about the biology I would have to ask Norman . And that's this concept of program cell death or apoptosis. What is apoptosis? Well did you know that most of the cells in your body are capable of committing suicide? They are capable of killing themselves and that's the process of apoptosis. It happens in a very highly regulated manner because as you get to the end of the day you come to the conclusion that all the cells in your body haven't actually committed suicide. And I am still hoping to make it to lunchtime despite my excessive toxic waste. It is almost self evident that if cells survive despite being given anti-cancer treatment, they are probably resistant to apoptosis, as we now believe that apoptosis is a very important process in the response to anti- cancer treatments. So why? And what can we do about it?
And here is the beginning of my biology lesson. It's impertinent of a clinician to give you a biology lesson when there is an eminent biologist in the audience, so I hope that he will forgive me for this.
These are some of the slides which I show to the students and on your left you'll see a cell dying by what is called a necrosis, that is, the conventional, sort of thing that will happen if a cell is machine gunned basically. If you cut off its oxygen supply, something happens just so catastrophic that there is nothing the cell can do about it. It just looks like a ghastly mess. Looks like it's been dropped from the top of the post office tower and been splattered on the pavement.
The cell in the middle which is undergoing apoptosis looks different. Now you'd be surprised I can remember when this concept of apoptosis first came out. Nobody believed it - cells committing suicide? And the people who first put that theory forward were really thought to be weirdos - completely crazy ideas. But it really does happen and it's a highly ordered program.
Now pay attention there's a biology test later and only the people who pass the test will get lunch!
It is very complicated and I just want to point out a couple of things here. One is you are welcome to read the whole diagram but this is showing part of what controls apoptosis, and at the bottom right hand corner you have these things which are called caspases. They are enzymes which actually start destroying the cells in a very specific way, in a highly ordered way. So they are the executioners. And the important control is to make sure that the executioners are not actually switched on. So there are powerful ways of making sure that executioners get switched off and are kept switched off. The other culprit in this or the other player, are these things called the mitochondrion. And those of you who have done A' Level biology will remember that mitochondria are little things that look funny and are rod shaped things inside cells. They are inside all cells and they are extremely important. And it turns out that things that get the least from the mitochondrion actually trigger the events that lead to the apoptosis.
So why am I telling you this apart from the fact that it's extraordinarily interesting? Well it turns out that there are all sorts of things involved in controlling apoptosis and it's not just a matter of keeping everything switched off and its all or nothing. It's probably much more like, well it depends on the balance of certain things, which are promoting apoptosis and certain things which are inhibiting it. And what happens to an individual, let's say prostate cancer cell, is going to depend on how that balance is working out. So if the balance is heavily in favour of activity of these things which are anti-apoptotic and we have something there, BCL2 which Norman mentioned earlier, and we have these other things IAPs, Inhibitors of Apoptosis and if there's a lot of activity from those things then cells are going to be resistant to undergoing programmed cell death. So it may be if we insult them they will survive because they are programmed to survive. On the other hand there are other things in there which might promote apoptosis and it's probably a balance between the two.
Well the key question is: Can we target this mechanism in cancer therapy and in prostate cancer therapy? And the reason why I highlighted those two things, BCL2, our old friend from earlier, is responsible because it sits in that mitochondria. And it's probably acting very early on in that pathway and the IAPs are probably acting later on in that pathway at the point when these caspases, or executioners, get activated. The logical thing to try and do would be to try and block both of those, and it's not a completely random selection. Because in the one case I am talking about a therapy which is on trial at the moment in prostate cancer and in the other case it's a therapy which is shortly going to be put into trial in cancer patients in general and I think maybe prostate cancer would be one suitable model.
How can you do this? All sorts of ways. And just for a change instead of talking nonsense like I usually do, I'll talk about anti-sense, which is slightly different. Now those of you if you have your chemistry sets ready would you like to get busy - that's what you need to make!
I talked about DNA. DNA is like the software in a computer program. It provides all the information of what has to be done. What DNA is going to do is produce a template called RNA. And that template is used in order to make a protein. And that protein could be PSA, or BCL2 or could be anything.
The way that the anti-sense works is that it has a sequence that will binned to the template and destroy it like I nearly destroyed that microphone. So it's a way of preventing the signal from the gene from getting through. Now it's so cutting edge that there are no results from it. Is it going to be hype? Maybe. But it's the sort of area and if that's not the right agent then I think we may be heading towards the right target.
What else can we do? Well maybe we can use conventional things. And one of the frustrations for me is that we have actually quite an old treatment in the form of Strontium 89, radioactive Strontium that gets into the bone which gives a very high dose of radiation to bone and particularly to damaged bone; bone that has been damaged by secondaries from prostate cancer. This is a form of therapy which is very underused in the UK and we really need to have trials to look at its use earlier on and in different combinations. And Professor James, who is sitting in the audience, has been leading the way in trying to develop these sorts of studies.
And maybe if these stem cells are resistant to radiation, maybe if we knew why that was, it might still have a place in treatment. And maybe the same thing is true of docetaxol. Maybe if there are specific reasons, like if we can work out how these pumps are getting rid of drugs, maybe there's a way of putting this in combination in a way that will target the very cells that we need to target.
I hope Nick James will forgive me again if I stray into another area. This is a trial that I talked about last year that has now been started in the UK and is being led again by Nick James but modesty forbids me to tell you where the first patient in the UK was entered from. It couldn't possibly have been from a centre outside of England, Scotland or Northern Ireland .
The idea behind Stampede is that we are looking at multiple combinations of drugs. It's a very complicated regime. They all said patients will never be able to cope with this. They will never be able to understand it. I believe that they will be able to cope with it and they will be able to understand it. This is going to be a very powerful way of looking at a number if different drug combinations in a much more speedy fashion than we have ever done before. I won't go into all the details of exactly how the trial design is made up and why it is done in different stages, but I ‘m going to come back to it.
Again, last year I had three wishes, because I thought I was only allowed three. And the first one of them was understanding the biological basis of what is significant as opposed to insignificant disease. The tiger and the pussy cat - how can we tell the difference between the two?
The second was understanding the biological basis of hormone resistance because that the thing that in the clinic frustrates us, that's the thing which we find difficult to treat.
And the third thing was to find a surrogate end point for overall survival, because that's the conventional measure of efficacy in treatments. But it takes a long time, because in some prostate cancer patients we may need to follow them for 10 or even 20 years to get that answer. The case of Stampede, I hope, is going to be a shorter time, but even then it's probably going to be 8 to 10 years.
So how have we done? End of term report. I think we have made some progress in understanding the biology of the disease and Norman 's team have been a key part of this. I think we have made some progress in understanding the biology of hormone resistance, but in terms of finding a different end point I think we still have a bit of a battle.
I am going re-visit a bit of the debate that we had last year. Thinking about how we might think about drugs differently, how we might get them into the clinic more quickly. My own thinking has changed a little bit, but there are still some formidable challenges here. What I would like to see - and this is a purely personal view - is a situation where if we have patients who are about to be treated by Roger or somebody like Roger with a radical prostatectomy, that we are able to treat those patients with a test drug for a short period of time. Then when the prostate is removed at surgery we are able to access the tissue from those patients and we ask two questions and only two questions of that tissue sample. The first one is: Is that drug getting to the cancer? If you measure the levels of the drug in the cancer, is the drug able to get there?
And the second question: If the drug is supposed to be hitting a target, is it actually hitting that target? And that says nothing about whether it's effective or not, because I don't want to know that, I just want to know the answer to those two questions.
Now is that controversial? Well yes possibly it is, because in many ways the patients here are not patients with much more advanced prostate cancer who are having a clinical trial to see whether the treatment benefits them, they are almost like volunteers. Helping us is a very different approach. I don't know if it's the right one. I think it could be an approach. And what do you do? I think the key point is if you get positive answers to those two questions and if you also know that the drug is giveable, so there have to be toxicity studies that are currently done, I'd like to see them plugged into that sort of Stampede trial design where you are lining up different drug combinations against each other, as a way of finding out how these things might work.
That really is difficult because what you are talking about here is a challenge, not only to the clinical community and the Government for the appropriate funding and the appropriate support for that, because of course you need them, but it is also a challenge to the pharmaceutical industry. Because what we are asking them to do is to put up a new drug, that as Norman has said, they may have invested hundreds of millions of pounds in, and you are asking them to put it up against their competitor's drugs, singularly or in combination with the prospect that in a short period of time they might lose that drug because it might be shown to be ineffective. One of the by products of this, which we would have to think about, would be that if they bought into this model, new drugs might become much more expensive. I think it happens to be that that's the case, and I have a belief that there is no point in the pharmaceutical industry not being able to recoup the cost of developing drugs because if they can't they won't develop new drugs and we need them to do that. But I think that is a problem that we all have to face and we all have to think about.
With that I am going to finish. Can we tame the tiger without drowning the pussy cat? Can we tell the difference between the prostate cancers which are significant and those which aren't? And can we selectively treat the ones that matter? I think we have made some progress towards that. So whether that's a sunset on an old era or a sunrise on a new era, I shall leave you to judge. Thank you very much.
Vivienne Parry: While they come up, can I just ask you take a straw poll here? If you were a person about to undertake a radical prostatectomy and you were asked to take a drug for the good of other men, which of you would be ready to do that, be happy to do that? That's pretty overwhelming. Anybody here who wouldn't be willing to do that? Anybody's wives? Ah Sandy, why wouldn't you do that?
Sandy : My choice would be not to do it, I think because you've got to remember for those who have had a radical prostatectomy, what those 4 or 5 weeks were like before it, and I think most of us would not have wanted any other stress.
Vivienne Parry: Any wives here, girlfriends, mistresses even, would you let the man in your life do that?
Audience: (she says definitely would).
Vivienne Parry: Now I am sure you've got some questions for our dynamic duo.
Audience: I had a conventional radical prostatectomy and I am very glad that I did as I thought that the surgeon had some more elbow room and could be more accurate, and I would feel very uneasy about the keyhole operation.
Vivienne Parry: 10 years ago I did a documentary on robotic prostate surgery. I had to be called in because actually the male producer had fainted, so it was girls that had to be there!
Professor Roger Kirby: You are right. The open prostate removal is still a very good operation. In fact, a group of surgeons using the robot last week managed to drop the needle inside and they spent two and half hours looking for it. And because you haven't got an easy access it makes it harder to get. They did find it, so you make a good point.
Professor Nick James: It was a comment on your earlier question: Would men take part in a study upstream of having a prostatectomy? And we've done such a study with our gene therapy work where we've invited men to have virus injections in their prostate prior to their prostatectomy. And the answer is that 1 in 3 of the men that we approached actually underwent the treatment. So yes, men can and will do this. So I think it's actually a very good way of assessing new treatments. I'd agree with Malcolm.
Audience: I had conformal radiotherapy about three years ago. I think the biggest question I've got from hearing the two of you speak is the extent to which drugs versus alternative therapies is the right way for people who've got prostate cancer to consider. These new techniques like HIFU and cryotherapy sound as if they don't need supporting drugs. To what extent are drugs or the complicating process of verifying how combinations of drugs work, which is the most hopeful direction for the future?
Vivienne Parry: So are you asking, sir, whether it's really drugs only, or is it a combination? Are we going towards the combination? I mean from that earlier data we are going towards combinations treatments.
Professor Malcolm Mason: I think we probably are. And can I just echo what Norman said earlier - that all men are different. And in many ways what we would be doing form the sort of drugs studies I talked about, would be giving the drugs to men again who predominately probably don't need it, in order to gauge whether it was a drug that was likely to be effective in the men who do need it. Newer technologies, HIFU, robotic surgeries, cryotherapy, laparoscopic, phenomenally interesting and extremlely important; but important to men whose disease is limited to the prostate gland. To men who have disease that has spread else where, drugs are going to be immensely important when we find the right ones.
Vivienne Parry: One more question down here.
Audience: I live near Basingstoke and I believe that the Ark Centre and Pelican Cancer Foundation are doing a lot into the rather more robotic technologies. Now if you don't live near Basingstoke and you want this how do you get it?
Professor Roger Kirby: Very good question. The problem with developing these new technologies is not only the expense - the robots cost over a million and a half pounds - it's the training that the surgical teams need. These devices do more harm than good unless you have good training behind it. A lot of it's financially driven. In the States, there are 256 Da Vinci robots around. In the UK there are 4 - populations a quarter and there are 252 more. It's a big, big problem. Basingstoke is a good centre as is Edinburgh, but there are many others. The new website, the UK Prostate Link website, and The Prostate Cancer Charity - all these websites are there for good sources of information.
Audience: If you have that treatment does that mean that you don't lose potency - you don't become impotent?
Professor Roger Kirby: What we are hoping is that the new technology - with the use of the robot because you get 10 times the magnification of the nerves, very close to the prostate - it will be better at potency preservation. The early data suggested this, although there is a lot of marketing hype, and the surgeons who use it tend to promote their own work so there are lots of uncertainties, but it looks very promising and if we can remove the prostate safely without damaging any of the sexual functioning that would be terrific.
Vivienne Parry: We are going to have to move on now, so can we thank both of you - the dynamic duo.