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Can we cure cancer?
Professor Brian Cox and our expert panel are discussing the future of cancer research and treatment.
With nearly 1 in 2 of us in the UK now expected to receive a cancer diagnosis in our lifetime, pursuing a cure is more important than ever.
Our panel brings expertise from the lab, the clinic and their own experiences to answer audience questions about lifestyle and genetic risks, treatment side effects, and what they see as the biggest areas for hope.
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A Question of Science is a podcast series of panel discussions where experts from different fields respond to your questions, sharing the scientific perspective on society’s most pressing questions. A Question of Science is BBC Studios production for the Francis Crick Institute.
Brian Cox: Hello, I'm Brian Cox and this is A Question of Science here at the Francis Crick Institute. This is a series in which we discuss the science that underpins pretty much all of the biggest challenges and opportunities we face as we make our way through the 21st century, AI, ageing populations, climate change, pandemic disease.
And in this episode, the latest understanding and research into cancer. We'll also be focusing on your questions, but the primary difference between this and other shows based on audience questions is that our panel have both opinions and expertise in the relevant subject. Radical.
Charlie Swanton: Lots of opinions.
Brian: Yeah.
Lauren Mahon: Many opinions.
Gerard Evan: Some -ese.
Brian: Yeah. Today, we will be discussing cancer. With nearly one in two people experiencing a cancer diagnosis in their lifetime in the UK, this is an issue that most of us will face in some way. For many, the word is a scary one, but today, treatments are rapidly advancing and institutions like the Crick are leading the way.
We'll be looking at where the latest research is heading, whether research is best focused on prevention rather than treatment, exploring what might explain the rise in rates of some cancers and what we could do to speed up the development of new treatments. Joining us to help answer the big question, can we cure cancer? I'm joined by a panel of experts who are all involved in the field of cancer research and they are...
Gerard: Hi, I'm Gerard Evan. I'm at Francis Crick Institute and King's College London, and I'm particularly interested in why cancer is so rare.
Kairbaan (Kebs) Hodivala-Dilke: And my name is Kairbaan Hodivala-Dilke. Everybody calls me Kebs. I'm from the Barts Cancer Institute and I'm a scientist interested in how our bodies help cancer grow.
Lauren: I'm Laura Mahon, I'm a cancer survivor. I used to do the podcast You, Me and the Big C, and I'm interested in what hope there is for people diagnosed with cancer in the future.
Charlie: Thank you, Lauren. I'm Charlie Swanton. I'm a lung oncologist, lung cancer doctor at University College London Hospitals and I'm a scientist here running a lab at the Crick, studying how cancers initiate and progress and develop drug resistance and we're getting very interested in how environmental carcinogens like air pollution trigger lung cancer initiation.
Brian: And this is our panel. Gerard, I couldn't help but ask because in the introduction I said, which is a correct statistic, one in two of us will have a cancer diagnosis. But your introduction was, you're interested in why cancer is so rare.
Gerard: I obviously can't count.
Brian: So, what do you mean?
Gerard: Well, cancers can arise in any cell in the body and there's a hundred thousand billion cells in your average human being. A bit more for you, a bit less for me. And in principle, let's say 10% of those cells could become a cancer cell if they got knocked about by the right cosmic rays and things that we shouldn't do, like smoke and drink and everything else.
And one of those cells could grow, and grow and then become a cancer. So actually, cancer is incredibly rare because it happens in one out of a hundred thousand billion times in 70 years of life, despite us doing everything we can to give ourselves cancer.
Brian: Yeah, so it's rare on a cellular basis statistically.
Gerard: On a cellular basis, it's rare and it just clones itself into mayhem.
Brian: And we used one term for cancer. So is that appropriate? Because clearly there's a range, a range of disease.
Lauren: For me, it was like, as somebody who isn't scientific or has that kind of knowledge, I've lumped cancer in as one big thing. So it's just been really educational for me being a sick person to find out how much more complex it is as a disease.
Brian: And did you know much before you were diagnosed? 'Cause I suppose many people will not think about it so much. So did you learn about it post-diagnosis essentially?
Lauren: Yeah, you become like an expert in your field in that respect. Like you know it inside out, it's a full-time job basically, but with no pay and no hair, which is like no fun for anybody.
Brian: And what is cancer? So if we go to the, let's say we start with the cellular level. How would you define it?
Kebs: So cancer is part of us. It's not something from outside. And it's when a cell like Gerard just said decides that it's gonna keep growing and growing and growing, multiplying and multiplying, doesn't have the brakes that normal cells have to stop growing. That's makes the lump and lump is cancer. Yeah.
Brian: And clinically, I mean, I go back to that previous question that it's a catchall term, but clinically speaking, is it really inappropriate to just to put everything into one box, isn't it?
Charlie: Yeah, I think it is. I mean, it's a little bit like saying, you know, I've got an infection. You know, there are so many different types of infection. You know, you could have a staph aureus infection, you could have a flu infection, you could have Ebola, HIV, you know, there's so many different types of infections and cancer's not dissimilar, you know, there are hundreds of different types of cancer and it's mathematically impossible for two patients to have identical cancers.
Every cancer is different. There are commonalities and the commonalities are driven by the tissue from which they arise. And that governs to some extent the drugs that they'll be sensitive to and the types of treatment approaches they'll take, surgery, radiotherapy, immunotherapy, targeted therapy depending on the types of mutations present in that cancer.
Brian: Kairbaan, at the basic level and the fundamental level. Could you take us through what's actually happening, what we understand is the problem?
Kebs: Even within one type of cancer, there are lots of subtypes of cancers and they've got different molecular make-ups. And so, the drugs we make usually are targeting a molecule. We've got 30,000 of those and nature's quite clever, you know, you knock one on the head, another one pops up. So then we face this problem of resistance to therapy and that's like really trying to work out a needle in a haystack. 'Cause the cells in our body all talk to each other and the cells in the cancer all talk to each other and cells in the body talk to the cancers.
And so, when we think about therapy, we think about immunotherapy for example, trying to make our own immune system work against the cancers. Well, we want that to happen, but we don't want that to happen to everything else in our body, right? So we've gotta understand where that cancer is and its own microenvironment, just like an environment around us. The cancer's got its own microenvironment inside our bodies, but a microenvironment that's has the job to protect the cancer, throws this invisibility cloak over the cancer and now our drugs can't see the cancer anymore.
And trying to understand that relationship and trying to pick our way through that so that we can make drugs work better is really important, that's what we're all doing. That's what we're all working on.
Brian: And Gerard, Charlie referred to prevention, of course. So you referred to it, this almost, this miraculous idea that it doesn't happen very often. Do we know how we are almost, how most cells are protected most of the time?
Gerard: One of the things that I think is important to realise is that cancers don't really invent things. What they do is they wreck the control of things. So you've got usual processes that normally self-terminate, self-attenuating processes that no longer attenuate. But even if you push the system to its limits and make those cells, I mean, by the time people are 30 or 40, they're crawling with mutations in these genes that should be pushing these cells into being cancer cells but they still don't get cancer.
So there's still quite a lot to discover and quite a lot of difference that we can make. And actually, the difference is evident in the size of animals 'cause if cancer's just a risk depending on how many cells you have, then elephants should get more cancer than humans. And whales shouldn't even be whales, they just be floating tumours on the Pacific. And they're not, they're better protected per cell per unit time than our cells are. And we don't understand that either of them.
Brian: Well, we have a first question from the audience actually, which is a question about treatment.
Mathew D'Souza: Hello, I'm Mathew D'Souza, and my question is, what do you believe are the most promising areas of research or technological advancements that could lead to a universal cure or significantly improve treatments in the next decade? Thank you.
Gerard: You mentioned pan-cancer therapies. Well, there may never be pan-cancer therapies because the cancers come in so many types. But on the other hand, there are things that make every cancer in every patient different from every other cancer in every other patient, as Charlie has said.
There's also an awful lot of stuff going on in cancer cells that's the same as going on in normal cells. The problem is that we don't know how to target some of those guys, some of those particularly transcription factors that regulate gene expression and seem to be at the heart of how cancer, how cells switch into proliferation and switch out.
So one problem is that we can't make drugs that inhibit everything and there's still quite a tidy box full of toys out there that we could inhibit probably with good anti-cancer effect, but we just don't know how to inhibit them. So that's one little part of the story. Over to you.
Kebs: I think we need to think about not just the cancer cells, you know, the baddies. We need to also think about our own bodies and how our own cells could help attack that cancer. We need to think about the environment around us and I know Charlie knows a lot about that. And we need to combine efforts, right? So there's lots of combinations of therapy. I mean, those that you had. How many different types of drugs did you have?
Lauren: Chemo, radio, I'm on tamoxifen still.
Kebs: Yeah.
Lauren: Which is a hormone blocker, guys, 'cause I appreciate, not everybody knows what that is. Herceptin, it's interesting 'cause obviously through my work and my experience, I've met a lot of people in the cancer community and it's that minute where you find out you've both had breast cancer, you're like, "What drug did you have or what way round did you have? Did you have chemo first and then surgery, like what way round?" But it is so interesting 'cause drugs that have worked for me, as we said, haven't worked for other people in certain combinations, haven't been as kind.
I know there's a lot of research going on, especially around like melanated skins and radiotherapy, like the burns on like Black women that I've seen are terrible. So it's really interesting because I think from the outside looking in people are maybe like, "Oh, what are developments in treatment?" And they may be good for some, but not for everyone. And it's such, it's so complex. I don't know how you guys do it.
Charlie: So I'm gonna answer that question in a slightly different way, which is what we are interested in now is having studied late stage disease to the extent where I've got a little bit depressed about the possibility of ever curing advanced stage four cancers. We're going right back to the beginning and asking Gerard's question, which is how does this all start in the first place? And can we prevent more cancers than we're preventing? And obviously, their lifestyle choices don't drink. Most importantly don't smoke. If you do one thing in the audience, you can possibly do is just don't smoke. Above everything else, that is the one risk factor that increase your risk of cancer by about 30 fold.
Lauren: Yeah.
Charlie: So there's lifestyle choices, but I'm very interested in molecular cancer prevention and feeding into the signalling pathways that we all accumulate as we age that cause chronic inflammation that aren't just driving cancer initiation but are also doing other things like driving cardiovascular disease and dementia and other illnesses we associate with ageing. And we are getting closer to this idea that there is a sort of, there are a few pathways that are activated as you age that cause multiple ageing pathologies. And if we knew what they were and we had drugs against them and there are some examples, we could actually start to target those pathways and slow the ageing process down and reduce your risk of cancer, cardiovascular disease, and maybe even dementia. So that's what we're beginning to get more interested in now. So prevention is better than cure.
Brian: Actually, our next question builds on that and the challenges posed by different cancers.
Jo Bland: Hi, I'm Jo Bland, and my question is, are there any cancer types that you believe won't get a cure for a much longer time, if at all? And should research go into developing cures for all the different types or aim for a universal cure for all cancers?
Brian: Well, who wants to start off?
Charlie: So I've got a few ideas on this. I mean, one of the biggest challenges right now targeting cancers which don't have cell surface receptors that are easy to hit with small molecules or antibodies. 'Cause antibodies can bind on the surface of the cell and inhibit, you know, this particular activated protein in a cancer from working, it's a bit like a traffic light that's gone from red to green and it's constantly telling the cell to divide. If that traffic light's on the surface of the cell, you can hit it with a small molecule or an antibody to stop it from working and switch it back to red again.
The challenge comes from some of the mesenchymal tumours as we call them, they're called sarcomas, soft tissue tumours, which have these transcription factors that are deeply embedded in the cell that activates gene expression in the nucleus that switch on programs telling the cells to divide and switch on hundreds of genes. And they're intrinsically very difficult to target for reasons I won't bore you with. And there are lots of different types of these sarcomas, all with different transcription factors. And we have to potentially, unless Gerard comes up with a solution which he's very close to doing. Potentially target multiple different transcription factors in all these rare sarcomas.
And the problem is, A, they're very difficult to target. B, very few individuals are affected with these individual types of sarcoma, which means commercially, pharma companies don't invest in developing drugs against these diseases. And it's similar for paediatric tumours as well, similar problem. But there are new technologies emerging that are looking scalable, looking like we might be able to start doing this much, much faster and much more cheaply than ever before. So there is hope, but it's taking time.
Kebs: I think you also asked about a cure for all. I think there's little evidence that that's gonna really happen. Although we all want it. We'd like an aspirin for cancer. Yeah.
Lauren: So would I.
Kebs: Yeah.
Lauren: Mm.
Kebs: I think we all would.
Lauren: Yeah.
Kebs: But I think if it's there, we would've found it by now. And I think it just goes right back to the beginning of the discussion that all cancers are a bit different and in different people, different cancers are also different. But what's hard is in, you know, working in the lab and Charlie works in the hospital and he works in the lab, working in the lab like I do, we also need to have really good models to be able to understand how to understand that rare cancer. And even getting that sort of material is hard to get because it's a rare cancer.
So it's a circular problem. It's a really circular, but it doesn't mean it's not important. And there are funding bodies who are particularly interested in making sure that research happens in rare cancers. So it will happen, but it hasn't happened yet.
Gerard: So I respectfully disagree. I think there's no... The way that cells get the information what to do proliferate for example, comes through the fact they have receptors on their surfaces, the binds, signals that tell the cell to proliferate or differentiate or die or live or anything else like that. And they're very important in trying to understand, they're the things that differ from cell type to cell type.
But the pathway that connects all of that to the nucleus, for example, which has the final say in deciding whether a cell is gonna divide or not has a certain shape. And one of the shapes they seem to have, and this isn't fully explored, is they're shaped like a hourglass. So there's lots and lots of signals going along, measuring this, measuring that, assessing all sorts of states for the cell and it's a microenvironment and everything, but in the end, that has to be distilled down into a yes/no binary decision, proliferate or don't proliferate, live, die.
And we don't really know where those switches are that consolidate all of this upstream information. And there's not much hope at the moment of designing drugs that will inhibit them. But if you could design drugs that would inhibit them, and we don't have any at the moment, you would find I think, which we're trying to see that that's what we're working on. I think you would see a much more vigorous pan-response against many different types of cancer.
Brian: Well, we have, yeah, so you've been stood there for about half an hour. We have the next question from the audience.
Simren Bal: Hi, I'm Simren Bal, and my question is, is there a possibility of coming up with a cure for cancer that is less invasive than chemo and radiotherapy?
Brian: So as you said, like an aspirin for cancer.
Kebs: Yeah, so I think... So we've got a huge armoury of drugs to cancer and some of them are cytotoxic so they kill cells. Radiotherapy will try and kill cells that are dividing and if we use them at high enough doses, they'll kill everything, right? They'll kill everything. And then sometimes we have to wonder whether the treatment is actually worse than having the cancer because the treatment can be so toxic to the poor patient. So a lot of the work that we are doing is trying to really dial that down and work out ways to use the least possible amount of therapy, least amount of chemotherapy, the least amount of immunotherapy, but try and get it right into the cancer so that we can protect other organs and protect how, you know, how we breathe or getting rashes and all of that sort of nonsense. You just don't need it.
And I think sometimes when I talk to my clinical friends, it's quite interesting. They say, oh no, no, no, that chemo is really, that's really great and then there's almost no side effects. And then a friend of mine who's got breast cancer has it, she can't even take her kids to school because she's completely wiped out. Okay, her arms aren't dropping off but, you know, she's sick from the chemotherapy. And I think there are ways that we can learn to really dial that down so that we can use what we've got, use it better and use it precisely in the cancer.
Brian: It sounds to me, it's almost... The idea that the treatment is the thing that you actually feel-
Lauren: Yeah.
Brian: It feels very different from other diseases where, you know, if you're taking antibiotics, you're taking them because you feel absolutely terrible.
Lauren: Oh yeah, no, I was running around Glastonbury like two months before I got sick. I was living the time of my life and I had tumour in my boob the whole time. Do you know what I mean? I didn't feel sick. It was weird, like I got diagnosed with cancer and then I didn't start treatment for like a month or so because I had eggs harvested and stuff. Another thing you don't know, I was 31 and I got taken into room and got told you've got cancer, do you want kids? And I was like, "I don't even get swiped right on the Hinge. I don't know." Do you know what I mean? I don't know what I want.
But it was that weird moment of walking around and everything in my life was normal but everything had changed completely. And it was actually only when I started to undergo like medical proceedings that I felt poorly. The thing is what's really hard I think as a cancer patient is I love sitting here with you guys. Like, you know how much I admire you and think you're awesome and we talk about cancer as like cellular and that is part of us, but that is like a human.
And when you enter into the system to start getting treated, it's almost like a car going into a mechanic's where you like and, rightly so, the doctor's job is like, right, we need to get rid of that. So we're gonna do this and we're gonna move this and we're gonna put this here. But the whole time you are just othered completely from your body. It's a bit of a lose-lose. Well, it's a win-win and a lose-lose 'cause you're gonna get better and you're going to, most people, you know, survive it. But it means that my mum always said, you have to get sick to get better. Which is so crazy, 'cause normally it's like you take a drug to feel less crap.
Brian: And Charlie, the question was about this possibility of treatment becoming less invasive over time.
Charlie: No, it's a great question and there's huge excitement now. In the last five years, I've seen stuff that I just would never have believed possible. The combination of chemistry with AI and deep learning is just, I mean, it's mind blowing. Five years ago, you'd have thought this was science fiction.I mean, there are academic groups and companies now that are almost imaging proteins in real time. And these mutant proteins that cause cancer will for nanoseconds reveal a little pocket that is there in the mutant protein that's not there in the normal protein in your body that the chemist can just shove a drug into and block in that nanosecond and block it and block it permanently and switch it off. So we'll only hit the mutant protein but not the normal one.
And that's where we get into kind of treatments and now, there are new technologies like molecular glues and degraders where we can give, you know, chemical compounds that get into the cell and allow, we're talking about these rare sarcomas that can sort of bind these mutant transcription factors and essentially address them to the cellular machinery that acts as a dust bin and degrade them.
It's just miraculous and that's all extremely specific and it's come about through, it's a combination of a better understanding of biology, exquisitely extraordinary chemistry and AI and deep learning tools. So there's massive hope here now, I think.
Lauren: Charlie, oh sorry, I was just gonna say, I think you should start on OnlyFans 'cause I was getting hot under the collar hearing all that hope. I was like, "Oh, talk data to me, Charlie."
Charlie: What's OnlyFans?
Brian: Does anybody want to take it?
Lauren: Sorry, Bri.
Brian: Let's not get Charlie talking data hopefully. The next question from the audience.
Lucy Wojciow: Hello, I'm Lucy Wojciow, and my question is, does cancer risk come from lifestyle or our genetics? I've heard about blue zones where people in certain parts of the world have different diets and live longer. Can eating certain foods help protect against cancer? Thank you.
Kebs: There's a lot out there. There's a lot of information about different sorts of foods and bacteria and kimchi and all that delicious stuff. But we don't really know and I don't think it's been tested properly. I think we need to be a bit cautious about the claims that are sometimes made for some of those things.
Lauren: Mm-hmm. Yeah. Can I just ask as well, because there's this real thing in the cancer community almost like you've caused your cancer or you've caused your cancer to come back. And it breaks my heart because you'll listen to certain people on podcasts. I'm not gonna name names who have had cancer, but you know, they're like, "I've just cut out sugar and I'm now eating this and I'm now eating that."
But there's no proof, but by talking like that, what they're saying is, you, of course, it feels like you're shaming people who have had cancer because I got cancer at 31 and I was like having a drink. I was being a normal 31-year-old. There are millions and billions of 31-year-olds who don't get cancer. But I think maybe my family and my genetics more predisposed. So if we knew more about people's predispositions to diseases, then I think would lifestyle factors be a fair thing, to like chalk it up to?
Charlie: Yeah, it's a massive question this. It's a question that is, it causes a lot of controversy amongst scientists. Nobody can make their minds up. I mean, it wasn't so long ago, I guess seven or eight years ago when there were two articles published back-to-back, well, within about six months of each other.
One very famous scientist saying only about 30% of cancers were preventable through lifestyle choices. And another very famous scientist publishing an article six months later saying about 70% of cancers were avoidable through altering lifestyle factors. And of course, what ends up happening is it just sows massive confusion if two preeminent scientists can't even make their minds up about this problem, what hope is there for people listening to your podcast, for example.
This is highly controversial and part of the problem is that we are all humans, we're all genetically diverse. We all have different lifestyles and we all have different memories when it comes. If you ask me what food I had last week, I would have no idea.
Lauren: Yeah.
Charlie: And yet a lot of these epidemiological studies are based on memory, you know? What's your diet like? Tell us about your diet in a typical week. And then we put this all together with sort of 400, 500,000 individuals and we expect something to come out of it that's intelligible. And often it's not because you put rubbish in, rubbish data in, you get rubbish data out. You know, that cancer to some extent is a Swiss cheese effect. It's a series of bad events, some of which frankly is just unlucky.
Lauren: Mm-Hmm.
Charlie: And the point you make about patients blaming themselves and their diets and what have you, you know, it brings tears to your eyes.
Lauren: Yeah.
Charlie: It's totally unfair 'cause a lot of it is complete nonsense. And there is just bad luck.
Lauren: Yeah.
Charlie: That we don't really understand the role of.
Gerard: And treating it like a battle.
Charlie: Yes, that's right.
Gerard: Or a race or something else like that. I think the other thing that I've always had problems with, and I think a lot of people do, which is you can report statistically on an enhanced risk of something else or other happening 'cause you've done done a lifetime of not eating broccoli. But what people wanna know is they wanna know, is it gonna happen to me?
Lauren: Yeah.
Gerard: Or my mum.
Charlie: Yes, yes.
Gerard: Or my brother or my best friend and we can't tell. 'Cause there's so many variables and some of it is just statistical luck.
Charlie: Yeah.
Brian: We have another question from the audience.
Odhora Islam: Hello, I'm Odhora Islam, and my question is, how much of cancer research has historically focused on limited demographics and what progress has been made towards including more diverse populations in clinical trials and studies? Thank you.
Kebs: Yeah, I think I can take this one. So it's a really, really important and interesting question. So I think historically, there hasn't been enough research being done. It's coming to light now that people from different ethnic backgrounds might have different susceptibilities.
For example, women of South Asian descent, women of Afro-Caribbean descent have a higher risk of getting breast cancers at a much earlier age than Caucasian women of the same disease. And we don't really know why. And a lot of that has stemmed from thinking, well, it has been researched, not like it hasn't been researched, but a lot of it has been done comparing populations in different parts of the world. And that gets complicated because people in different parts of the world have different socioeconomic factors. They've got better healthcare in one part of the world, worse healthcare in another part of the world. They've got access to early detection and they don't have access to early detection. So all of that can muddy the waters.
We're now doing some really interesting biology to really understand that there are biological differences. And it's probably because of our genetic background, right? Which means that a white woman and brown woman or a Black woman might not be ready for the same sort of treatment. And we are starting to scratch on the surface of that and I think it's going to be really important. The technology now that we've got to be able to look at all our different sorts of cells at the same time and work out what's different is fantastic.
Brian: Okay, well, we have another, I think we have another question, do we? Yeah, another question.
Nashita Noor: Hello, I'm Nashita Noor, and my question is, is the rate of cancer increasing or is it that diagnosis is more common and how can you tell what is causing this?
Charlie: Well.
Brian: Who would like to start?
Gerard: It's the easy ones.
So how long have we got? 45 minutes. So partly, cancer incidence or the rise in cancer diagnosis is a result of the fact that we're living longer. But you've probably heard in the press as well that there are other cancers that are coming on in a younger age, we call them early onset cancers under the age of 50. One of which is colorectal cancer. And that is absolutely true. I mean, without a shadow of a doubt. And that's not just because of screening, because actually, we don't screen the under 50s. These are new diagnoses and patients who present with symptoms who are without a doubt suffering from colorectal cancer and we're seeing many more of these individuals.
So the question is why, why are we seeing more early onset colorectal cancers? And this comes back to the sort of discussions we're having earlier around lifestyle. There are lots of theories which include changes in the diets, exposure to different bacteria in our guts that might be causing mutations in the epithelium, earlier antibiotic use potentially. Some people even suggested more caesarean sections that have occurred in the under 50s than in the 70 or 80-year-old age group. But it could be many other things including air pollution or microplastics or ultra processed foods, which is what I think is the most likely, if you were to ask me. I think it's ultra processed foods is perhaps the most likely of all.
Why do I say that? Take two populations, South Korea and Japan. Ethnically not too dissimilar, pretty close to each other, but the rates of colorectal cancer, the under 50s is staying pretty level in Japan, but in South Korea is rising quite rapidly. So that really suggests to me there's some dietary impact here that's having an effect. The truth is we don't know. Cancer Research UK have just funded a group called Team PROSPECT. They've given them $25 million to get to the bottom of this problem to really get the grips with what's causing colorectal cancer in the under 50s. And hopefully, in the next five years, we'll have an answer.
Brian: Yes, because part of the question was how can we tell, which is a broader question about the research. So maybe you could give us an example of how you, as a scientist researching this area, how you go about trying to understand or answer a question like that? Does this particular thing lead to a higher incidence of cancer?
Kebs: There is research being done on microplastics, ultra processed foods.
Gerard: Yeah.
Kebs: Yeah, you start by playing with cells in a petri dish and chucking these things at them. And you can see that there are changes happening. And then you just go up from there.
Gerard: But it's still difficult to associate. I mean, a lot of things could be quite toxic to cells in a dish.
Kebs: Exactly.
Gerard: And I mean, the sulfuric acid's a very good example of the, you know, but, yeah, you know, it's not clear that those necessarily are causing the problem. I mean, I'd be interested in Charlie, why he feels so strongly about processed foods, which I love.
Kebs: Why would you say that?
Charlie: Well, yeah, in general-
Kebs: You've gotta cut that.
Charlie: Yeah. So, yes. I mean, if something tastes that good, there's gotta be a problem with it.
Gerard: Yeah.
Charlie: No, but I think yeah, the other bits about that question, Brian, I think you're alluding to was this issue of are we diagnosing more cancers? And there is certainly an element of that. So when, I mean, there was a period in the US where they were doing a lot of PSA screening for prostate cancer and of course, the number of prostate cancers shot up. And the minute they stopped PSA screening, 'cause everybody thought it was bad, the number of prostate cancer diagnoses dropped off. And there's this whole that points this issue of overdiagnosis.
A lot of men will die with prostate cancer but won't die of prostate cancer. I mean, there've been lots of studies looking at this that you know, you've slice a prostate at death that you will find prostate cancers in many men over the age of 70, 75, but they will never die of prostate cancer. And this is one of the challenges of screening because you know, we have this issue of overdiagnosis, you can detect a cancer, you can diagnose a cancer, you can treat a cancer, but that patient may never have died of that cancer.
Gerard: I think, you know, one of the things that's most surprised me, and I think a lot of us in the field is just how full of chockablock full of pre-tumours we are by the time we're 50 or 60, we've got lesions all over the place. Pancreas, thyroid, you name it. They just don't go anywhere.
Charlie: Yeah.
Gerard: And we don't really understand that.
Charlie: I heard this amazing statistic from James DeGregori, who works in Colorado who's calculated that of the 30 trillion cells in our body in a 60-year-old, 100 billion of them will have one or more cancer mutations in.
Gerard: Yeah.
Charlie: And to your point, that tells you that cancer at cellular level is incredibly rare. Even though you've got a hundred billion cells with cancer mutations in, your lifetime risk of cancer is only one in two. That's extraordinary.
Gerard: Mm.
Brian: Another question. Again, you've been stood there for the best part of 45 minutes. Another question from the audience.
Paul Gredley: Hello, I'm Paul Gredley, and my question is, do you think future cancer research is better spent on finding a cure or preventing it developing in the first place? Thank you.
Kebs: Can I take that one? I think that we are getting better and better and better at treating early stages of cancer.
Lauren: Mm-hmm.
Kebs: If you look at prevention apart from smoking, you don't really know how to prevent it very well. Early stages of cancer, we can actually treat really well and then we've got late stages of cancer, which gives us a this bell-shaped curve. And I think we need to flatten that curve. We need to be able to bring those two sides up
So we need to be able to prevent better. And if we can prevent everything, we won't need to be able to treat late stage cancers. But we still have people in the world now who are going to get aggressive cancers, got people in our hospitals with aggressive cancers. We've gotta be able to find ways of being able to treat them better. So I think we need to invest in both.
Brian: You must have a view on this, Lauren.
Lauren: Yeah.
Brian: 'Cause it's clearly I think most of us would say, well, prevention-
Lauren: Yeah.
Brian: Would be preferable.
Lauren: Yeah, definitely. I mean, I've lost a lot of friends to cancer that really should still be here. And it's been a case of too late really catching the disease. Really, for me, personally, I'm really interested in the genetics of it all and our predispositions. 'Cause I feel like if there was more investment into us and our genetics and understanding our like family lineage and you know, who's had cancer in the family and coming at it from that angle, you know, we'd probably be able to say, okay, rather than screening being over a certain age, maybe it's like, well, you have a predisposition to cancer, therefore, we should be screening you for these things. Like really and truly, I shouldn't have had my first smear test at 21, but because I was sexually active (show off) 'cause I was sexually active and my mom had had cervical cancer.
My GP was amazing and he was like, we're gonna get you in early. I think having that kind of knowledge can only be beneficial. And in my mind, I'm like, that is probably like a little gateway maybe into prevention that, you know, isn't just lifestyle and all this testing, maybe it's genetic.
Brian: And you mentioned earlier that tools, machine learning and so on, and this idea that each individual can be-
Lauren: Yeah, yeah.
Brian: Screened essentially.
Charlie: So actually, Lauren reminded me of quite an important point, which is the one cancer where there is a... Well, there are two actually, but one where there's an approved treatment for prevention is breast cancer.
Lauren: Yeah, BRCA.
Charlie: Yeah, that's right.
Lauren: Yeah.
Charlie: Patients who are at at high genetic risk of breast cancer can be offered tamoxifen if they're premenopausal and aromatase inhibitors if they're postmenopausal. The problem is the uptake has been very poor. And you know, if you speak to most primary care physicians, either they don't know the data or they don't tend to prescribe them or if they do prescribe them, patients don't stay on. Because they're not patients because they're not sick, so they don't stay on the drugs for very long. This is the challenge.
Gerard: This is why the question is difficult, right? Because the question is basically making assumptions. With the state of play at the moment where chemotherapy is pretty uncomfortable and no cure for cancer when people have it, which you are saying which is best. Well, actually people want both. But I'd go for, you know, if you had a cure cancer drug that cured every cancer, imagine going to hospital, having a diagnosis of cancer and then being told to go home and enjoy your holiday 'cause it'll be gone by next Thursday.
Lauren: Mm.
Charlie: Yeah.
Gerard: That's what I want.
Lauren: Mm.
Charlie: Yeah.
Lauren: That's true and-
Gerard: I want a cure.
Lauren: Yeah.
Charlie: Yeah.
Gerard: A cure for them all and then I don't have to worry about prevention, but meanwhile, prevention's a good way of preventing a lot of people from getting ill.
Lauren: Yeah, but it doesn't help those at stage four.
Charlie: No.
Gerard: No.
Lauren: No.
Kebs: Or think about living with cancer.
Charlie: Yeah, right.
Lauren: Yeah.
Kebs: So that we turn it into a cold, we turn it into a common cold.
Gerard: Yeah.
Kebs: I mean, that's also a massive objective. Cancer Research UK has putting a lot of money into learning how to live with cancer.
Brian: One more question.
Karen Donald: Hello, I'm Karen Donald, and my question is, what can the public do to ensure all this amazing science becomes new medicines and gets on the NHS fast track for funding and into clinician's hands? Thank you.
Charlie Swanton: So first of all, I'm sure many of you give money to Cancer Research UK and other worthy charities. And I just want to put a shout out to Cancer Research UK. I'm a little bit conflicted 'cause I work for Cancer Research UK and Cancer Research UK pay for a lot of the work that goes on in this building. So if you take that conflict of interest into account, when I give my answer. I mean, the work they do is really phenomenal.
I mean, they invest in fundamental discovery research, which pharma companies tend not to, to the same extent because pharma companies have a much sort of shorter horizon when it comes to, you know, I guess the profit motive and drugs into the clinic and making money from those drugs. Whereas Cancer Research UK will fund scientists to pursue curiosity driven research for, you know, almost a career. I mean, Gerard has been funded by Cancer Research UK on and off for a few years. I've been funded for a few years less than him. But you know, as long as you carry on-
Gerard: Not that many.
Charlie: Yeah, not that many, you know, not that many. But as long as you carry on doing interesting stuff and you know, some of the major breakthroughs have come about in science by funding curiosity driven scientists for decades and then suddenly something amazing happens.
I'll give you an example. Jim Allison, who discovered checkpoint inhibitors and won a Nobel Prize from this. I mean, he was studying the immune system and how the immune system could fight back against cancers. For years and years and years of his career, long after many research funders in the US, UK and Europe stopped funding this research 'cause they just thought it was futile and not going anywhere. But he carried on ploughing this furrow over a career until suddenly he made a major breakthrough.
And bingo, suddenly, almost overnight, melanoma, advanced melanoma was transformed from a disease where the best drug we had was DTIC that had a response rate of 4%. Four patients out of a hundred would respond, all patients with develop resistance and tragically all would die to a disease where well over half of patients, well over 50% of patients now, because of this molecule that he found that could reactivate the immune system. Now, we have drugs that can target that pathway, reactivate the immune system, recognise the cancer and cure over 50% of patients with melanoma in the last 15 years.
It's extraordinary. So again, to your point, I think the answer is carry on supporting discovery research, curiosity driven research funded by the Medical Research Council, Wellcome Trust, Cancer Research UK, all the people that fund this institute. I'm totally conflicted. But it is the most amazing place to do science here.
Brian: Yeah, I think you're so right there. I get asked this a lot in my field, and the answer to which research should we fund to make a big breakthrough is we're not smart enough to know.
Charlie: No, we don't know.
Brian: It's not possible to know. Absolutely.
Gerard: I mean, I think it's very simple, which is cancer research is done by scientists and clinicians, but it's also done by all the people.
Kebs: Yeah.
Charlie: Yeah.
Gerard: And you know, I say that there are two qualities that they're going to be looked at, trust and courage. We have to trust you. No, you have to trust us. That's the right way around. You have to trust us to do the great experiments and the things that are weird and strange and out of the box. And we have to have the courage to do those things and not just pause and just do the same old thing, turn the handle, crank the handle, but to share our excitement and share what I think is the inevitable result, which is cancers will become things of the past largely in the future.
Charlie: And I think you what you also point out, without patient participation in clinical trials, we'd have none of these breakthroughs.
Kebs: No, yeah. And that's really important when we go back to that ethnic diversity point. It's really important that everybody is represented properly.
Gerard: Yeah.
Kebs: In those sorts of clinical trials. 'Cause then, well, otherwise, we'll work in the dark.
Lauren: Yeah.
Brian: You know, we've got a huge number of questions from the audience. We're almost out of time. And just one last very quick question. We haven't really covered it, so I just... From Fabian Maxwell Drake, who's asking about a test. Will you find a universal test for cancer as accessible as standard blood tests?
Lauren: Mm.
Charlie: Well we're doing a big trial in the UK that I'm involved they called the NHS-Galleri Trial, where we're taking blood from 140,000 individuals. We spin it down and we look for cancer DNA, and those results will be published this time next year. So hold your breath.
Brian: I just want I to end with that. You've been quite optimistic, I think in your vision of the future. There is that question, that final question, which is, do you foresee a time when, as you said, it will be disease like a common cold or taking antibiotics? It's just something that everybody deals with and then it goes away. And I suppose that it's an unfair question, but if so, could you hazard a guess? I mean, I know it's unfair, but 10 years, 20 years, 30 years.
Kebs: In our lifetime?
Charlie: Not much in our lifetime is my guess, but for all cancers. But I think we will have more examples.
Kebs: Not in our scientific lifetime, but maybe in our actual lifetime.
Gerard: It'll be incremental.
Charlie: Are you planning on retiring?
Gerard: It'll be incremental. Probably tumour type by tumour type. I mean, there are always these outliers like pancreatic cancer that are bastards, sorry. You know, I mean, pancreatic cancer driven by the same molecular lesions as drive lung cancer can be a much more horrible disease. We don't understand that.
Charlie: Yeah.
Gerard: We don't understand why RAS proteins get mutated in most cancers, but very rarely in breast. Who said that had to happen? These are pretty weird stuff that we don't understand.
Kebs: But we are already curing cancers.
Gerard: Yeah.
Charlie: Yeah, I think there'll be many more examples of cancers like melanoma, for instance. One minute are totally incurable, the next minute are very curable.
Gerard: Turn on the dime. Yeah.
Charlie: And that's a beauty about science. It gives a lot of hope, number one. And number two, what's happening today may be very different tomorrow. And literally, almost overnight things can change. And that's what I love about this job.
Gerard: Yeah, and the people in it.
Kebs: Yeah.
Charlie: And the people in it. Absolutely.
Lauren: You're miracle workers, guys. You're miracle workers.
Brian: I think that's the perfect way to end, isn't it?
Charlie: Yeah, absolutely.
Brian: So thank you to all our wonderful question askers and to our fantastic panel, Gerard Evan, Kairbaan Hodivala-Dilke, Charlie Swanton, and Lauren Mahon.
