Dr Kat Arney on everything you need to know about cancer
Read the full transcript of our Science Focus Podcast interview with the Dr Kat Arney – listen to the full episode at the bottom of the page.
Dr Kat Arney: I am Dr. Kat Arney. I am a science writer and broadcaster. I am the author of the new book Rebel Cell: Cancer, Evolution and the Science of Life, which is out now. I am the founder and creative director of First Create the Media, which is a science communication consultancy.
Amy Barrett: Kat, what is cancer?
KA: Cancer is a complex biological phenomenon. So I've spent a lot of time working at Cancer Research UK in the Science Comms team, and I'd have to do a lot of the pieces that start, you know, what is cancer? And we sit down and start with a phrase like, cancer starts when a cell picks up genetic mutations and multiplies out of control and usually adding on to form a tumour.
So there are solid tumours and these come out of the solid tissues of the body and then there are blood cancers or liquid cancers. So these are things like leukaemias and lymphomas that affect the white blood cells. So we would sort of have this idea that cancer is basically a disease that happens when cells go wrong and they multiply out of control.
And that was something that I really wanted to explore in my my book Rebel Cell, which is all about kind of where did cancer come from and where is it going? Because we have this idea that it's a disease that just starts right when one cell goes wrong. And that's it. That's cancer. And it's coming to this sort of slightly more sophisticated idea that, like, there are lots of cells in your body with lots of mutations.
So this is work that was done recently by researchers at the Sanger Institute finding that by middle age, most of your tissue is a patchwork of mutation. So actually, if all your cells have got mutations and they're a bit damaged and sad in their own kind of way. But most of us will only develop cancer once or twice in a lifetime.
You know, cancer is a bit more complicated than just those cells have gone wrong. So it's not just about having cells with mutations and change genetic changes in them. It's also about having the tissue environment that allows those cells to emerge.
I use the analogy of sort of cheating in a society of cells. It allows these sort of damaged cells to cheat the cells around them, to grow out of control, to take more than they need to make a mess around them, to stop doing the jobs they're meant to be doing, not to die and get rid of themselves when they should.
So cancer is not just about cells that have gone wrong. It's really a more holistic tissue disease. It's cells that are faulty. Emerging out of a tissue where lots of things have gone wrong. And so we need to sort of understand cancer is like a tissue disease, not just as cells that have gone off on this specific mutational journey, although ultimately that is how we understand cancer. As you know, cells that have picked up genetic mutations and then pick up more and more or more as they progressed.
AB: So what is it about the tissue and the cell surroundings that causes it to become cancer?
KA: So this is a really interesting question because we spend a lot of time as biological scientists thinking about what's gone wrong and particularly in cancer. There's been an awful lot focus on the cancer itself, on the tumour, on the leukaemia cells. Like what? What's gone wrong in these in these cells?
And we don't really think about what goes right. We don't really know what does healthy tissue really look like?
How do we maintain tissue health? And there's some really interesting work. This sort of philosophy, it's called adaptive oncogenesis, which I explore a bit in the book. And it's this idea that we have evolved as a species to keep our tissues healthy through reproductive age, and after that. But at some point, you know, then evolution basically gives up on us. And as we age, we see that our tissues change. You know, you can look at yourself. I'm a woman in my 40s, like, you know, things things are going south. Basically, I am not the woman I once was.
You know, we change as we age. Our tissues become more inflamed. We don't really know how things like physical activity, how certain things in our diet actually keep our tissues healthy. We know that these things are important for health, but we don't really understand why. And at the same time, we know that obesity increases the risk of cancer and other diseases as well. But we don't really know why.
So is it in some ways affecting the tissue, like, affecting, we think increasingly inflammation, chronic inflammation in tissues is important for encouraging these rogue cells to emerge as cancers.
So we do need to sort of understand a lot more about what does healthy tissue look like? What is a healthy society of cells in different parts of the body? How does that change as we age? What can we do to slow that down or even reverse it? And that sort of starts to make you think properly about what really does prevent cancer.
In terms of preventing these rogue cells emerging rather than just going like, well, you know, don't smoke, don't do bad things. Also, of the kind of information we have, obviously, smoking does massively alter your tissue environment and gives you mutations as well. So that's a really bad idea.
AB: But of course, there are people who who have never smoked, who never drank excessively, who who still get cancer.
KA: Exactly. You know, this is this is what I really wanted to get the idea. Cancer is is not a new disease.
It's not a uniquely human disease. It's not always caused by something you did. Cancer is basically an emergent property of life. It's kind of the dark side of life. And even if you lived an absolutely completely pure life, you know, you never did any of the things that we would consider to be, you know, bad for want of a better word. There would still be a chance that you would develop cancer because cancer develops in multicellular bodies, because no multicellular you know, there are cancers that have emerged in tiny, tiny Hydra. These are organisms that are basically tubes of cells with tentacles.
There's cancer across every single branch of the tree of life because where there are cells, where there is a society of cells and one starts to get the edge, one starts to cheat based on genetic changes that it's picked up. That can lead to cancer. So, you know, I've had some people say, well, like, well, why should we bother? You know, you may as well just smoke or drink, do whatever you want to your heart's content. It doesn't make a difference. Well, it does, because for a start, if you're exposing yourself to things that damage your genes, that cause mutations to carcinogens, you're increasing your mutational burden.
So you're increasing the sort of fuel that these cells have to go rogue. So, like, that's a bad idea. And at the same time, it's like you are adding to the damage potentially of the tissue environment. So you're creating sort of a nasty, toxic environment that these cells are bad cells, damaged cells are more likely to emerge from so in.
But even in any case, just the hurly burly of life of the processes of life within your body means that, like, you know, there is a chance for any single one of us and probably all of us. This interesting studies from autopsy studies that have been done of people who've died at all kinds of ages in road traffic accidents.
You know, loads of people have tiny lumps and bumps throughout their bodies. Things go wrong. Things start growing. But very, very few of those will actually develop into a frank cancer. So, you know that the sort of process of life and and the bustle of cells within your body is something that I think we really need to explore a bit more.
AB: Mm hmm. And the problem with cells who become cancerous is that, of course, they then can spread. Can you tell me about how cancer can spread around the body?
KA: So this is really what makes cancer so dangerous. So, you know, we can talk about, you know, cells growing out of control, forming a lump. That's a benign tumour. If it never breaks through the boundary, the sort that we call it like that, the membrane of all your tissues are covered with the kind of thick equivalent of molecular clingfilm. It's like basement membrane.
And so if cells don't ever break through that, then they cannot spread through the body. And the problem happens when cells do manage to break through that and they get into the blood supply. They get into the lymphatic system. This is sort of another sort of immune plumbing that's in your body. And they start to spread. And they set up home in other places.
And there's a lot we don't understand about why cancers spread to different places. Some cancers like to go to certain places like the brain or the bones or the liver. Others like to go to other places. We also know that cancers do start to spread very early on, but they're not always successful.
So you can think about the sort of migration of pioneer cells. Not all of them will manage to find somewhere that they can settle down at and thrive. So, you know, finding secondary tumours is is not a great sign. It does show that cancer is spread. But we need to really understand why does that happen? What are the signals that cells are sending out? How do they go on this journey? How do they decide where to settle down and and work out how that process happens?
AB: And you've mentioned the relationship between cancer and genes. How much of a genetic component component is there to cancer?
KA: So there's two kind of angles to come at this. So one is how much of a hereditary component of cancer is there?
And we do know that there are some genetic changes, some genetic variations that you can inherit or that can sort of you can be born with that do increase the risk of certain types of cancer. And lots of researchers are searching for lots of those. The classic example of that is the BRCA genes. You know, the Angelina Jolie gene where variations in these genes significantly increase the risk of things like breast cancer, ovarian cancer, prostate cancer and a few others.
And there are some hereditary bowel cancer genes that we know about as well, and sort of certain other types of cancer, too. So there is a component that we know is hereditary. It may not be relevant for everyone. We know that more subtly, all of us have genetic variations that influence how we come out and our risk of disease. So there's many, many hundreds or thousands of variations that might suddenly increase or decrease your risk. And also, of course, interact with your environment and the things that you do throughout life.
But I think what's a little bit more interesting is there's really been this idea that cancer is a genetic disease because it's all about the mutations. And this has led us to the idea that if we can just find the mutations in cancer cells, the faulty molecules that these faulty genes make and target them with drugs, then that's going to be the way that we cure cancer.
And actually, when you start thinking about cancer as a disease of tissue, you realise that actually some, you know, for a start, a lot of normal tissue has mutations and changes in it, that if we found them in cancer, we would say that is a cancer gene. That is a cancer driver gene.
So it's like, well, that throws that idea about out in window. And then also there's been experiments done where you can take healthy cells and put them into a tumour, into the context of a tumour, and they will start to go wrong. There are sort of all sorts of influences, the actual cells. This idea of a cellular society, the tissue that's going on in there, and also you can go the other way round. You can take cancer cells and put them in the context of healthy tissue, and they will behave.
So it's not quite as simple as just saying it's just about the genes. I wrote my first book all about genetics. It's like, oh, I thought this was just going to be a book about cancer genetics. Like, there's a bit there's more to it than the genes. Definitely.
AB: And what makes something a carcinogen?
KA: So the definition of a carcinogen is something that induces cancer. Carcinogenesis is the process of cancer forming. So, there are sort of two types. So one is things that actually directly damage DNA. So these would be things like some of the chemicals in tobacco smoke, these polycyclic hydrocarbons. And we can see now with DNA sequencing techniques, we can actually see the scars in the genome that chemicals leave things like ultraviolet light from the Sun, X-rays.
Some of the fundamental biological processes of life are, alas, inherently carcinogenic, like breathing oxygen. It's carcinogenic. Just being alive damages your DNA. Every time you replicate your DNA, you get mistakes in it.
So there's some really there's a really interesting project called the Mutographs of Cancer. This is one of Cancer Research UK's Grand Challenge projects. It's being run at the Sanger Institute by Mike Stratton. And they're really looking at what are the signatures of damage that different chemicals leave. And then if we go and look at people's cancers all across the world, can we find these scars in the genomes of people's tumours and then try and work out what might have caused them?
So, you know, all their environmental exposures are their chemicals that people don't realise. Are there other things in regional diets or regional behaviours? But also there are things that accelerate cancer or like I said, damage the tissue environment that don't damage DNA but still accelerate the process of cancer.
So things that cause inflammation, this process of sort of tissue inflammation, that's normally a response to infection or some kind of damage, but it can also encourage cancer cells to grow. So there's sort of two different ways that that you can disrupt the tissue environment and allow these sort of cheating cells to get an edge. So one is directly damaging the DNA. And the other is by disrupting the environment of the tissue.
AB: And why is it that some cancers like leukaemia more prevalent in children, whereas others are more common in adults or elderly?
KA: So there's a real distinction between the actual disease that is cancer in children and cancer in older people. So most cancers happen in people over the age of 60, and that's quite a sharp uptick.
So through most of our lives, our cancer risk is generally quite low. And then it does start to rise after the age of 60. You sort of there's there's some kind of suppressive effect in all tissues that's keeping us healthy for quite a long time. And then basically, evolution gives up on us.
But cancers in elderly people, in older people and in adults more generally are very different from the cancers in babies, in children and in teenagers. And that's because the cancers in younger people, they're kind of a developmental process that has gone awry. So as you're developing as a baby in the womb, your cells are specialising. They're turning into different types of tissue.
And this is all under a genetic programme and it's looking like four different types of cancer. They turn up at exquisitely precise times in life. So there's a type of kidney cancer called Wilms' tumour in children. It turns up a very specific age.
There are different types of leukaemias that turn up really specific ages. And that's because the cells have kind of got to a certain point and then got stuck. They've gone on their developmental journey and then something has gone wrong genetically that have, like, made them get stuck there. And so they're proliferating in the wrong kind of way and not fully differentiating and doing what they're meant to be doing.
And so these are very different cancers. This is almost like - always want a different word for it. This is sort of a disease of differentiation, if you like, or lack of differentiation, lack of correct developmental pathway. And so they need treating in quite different ways and understanding in quite different ways to cancers in adults.
AB: And in terms of treatments at the moment, what do we know about how to treat cancer?
KA: So the thing that I wanted to get across in the book is that we do have a lot of information about how to treat cancer. So we already know in some cases how to cure some cancers. The best cure for cancer is to find it early and cut it out before it has spread around the body.
That is basically a cure. And by cure, I mean that the cancer is not going to come back and it's not going to sort of shorten someone's lifespan shorter than they might be expected to live. So and a cure is a sort of tricky word. We can maybe talk about that later. But, you know, we are pretty good at treating particularly early stage cancers. And here in the UK today, around half of all people who are diagnosed with cancer will survive at least 10 years after their diagnosis. And that's a figure that's doubled in my own lifetime. So, you know, we have made significant progress.
But where we've made much less progress is in later stage cancers. So these are cancers where they really have started to spread through the body. And there are a couple where they are re weirdly sensitive to treatments that testicular cancer, even testicular cancer that spread through the body is really sensitive to chemotherapy. No one knows why, but it is. So that's great.
So, you know, more than 99 percent of men with testicular cancer are effectively cured. And that is brilliant. But, you know, a lot of the other ones, breast cancer, bowel cancer, you know, people can be treated. But then the cancer can come back months or years later. And that's because there will still be cells left after that first treatment that they are resistant to the therapy. They've evolved resistance.
And then they start growing again. And this is really the challenge, the sort of evolutionary challenge of cancer is understanding how are these cells as populations of cells that all kinds of genetic diversity in there? How are they responding to the selective pressures of treatment, of the tissue of whatever's going on and evolving and changing, becoming resistant to therapy? And how do we tackle that? And that is still a really big challenge.
AB: And how long have we been plagued by cancer? Is it something the on sisters that are hominid ancestors were suffering with?
KA: Yeah. Cancer is a very, very old disease. I think sometimes we can get the idea that cancers it's a modern disease. It's a human disease. And, you know, I kind of knew that it wasn't. When I worked at Cancer Research UK, I would write pieces talking about cancers that's been found in mummies and then in fossils and things.
But when I started to really look at it and research it for the book, it was realising the sheer extent of that. You know, there's a a 240 million year old turtle fossil with a tumour in it. Just the week that the book came out, there's a 77 million-year-old dinosaur fossil with an osteosarcoma, a bone tumour. Pretty much everywhere we look across the animal kingdom, we find cancers. Almost every single branch.
The exceptions are jellyfish and sponges. So no one knows what that's about. But, you know, in fish. In birds and bats. Yes, in sharks. Yes, occasionally, in naked mole rats. All the animals that we say never get cancer. Yeah, they do. Everywhere you look, we find cancer. This is a deep, deep process of life. It's not just human and it's not just modern.
AB: But do we see it happen more in humans than in other animals?
KA: So actually, when you look at cancer risk across species, humans are actually somewhere in the middle. So it kind of weight for weight. The really big, long lived species. Things like elephants, whales. So bucking that trend slightly, bats, they have very, very low rates of cancer for their size. And this is all.
This is called Peto's paradox after Richard Peto, the epidemiologist, because he realised. Right. Right. If if you're a bigger organism, you've got more cells. You can have more cell divisions in your life. and so you should have more cancer. Right. That makes sense. You know, the longer you live, the more cells you have, the more cancer you should get.
But actually, these big, long-lived animals have far fewer cancers. And then, like small animals, particularly small rodents, they have loads of cancer, you know. But it's all about their evolutionary history as a species. So, you know, small rodents, they kind of live fast, die young. They don't invest a lot in repairing their tissues.
Elephants have evolved multiple copies of a gene called p53 that protects their cells against damage, like as soon as an elephant cells damaged. They just die. It's like really powerful protection mechanism. And other big animals have solved it in different ways. Capybaras, biggest rodents that those giant guinea pigs. They got really powerful immune systems that just mop up damaged cells.
Brandt's bats. These are tiny bats that live for like 40 years. They have changes in the way they maintain the telomeres, the kind of the ends of their chromosomes act as a kind of clock and a cancer protection mechanism inside their cells. So lots of animals have evolved protective mechanisms and humans, when you look at the grand sweep of things, if you take away the obviously bad stuff we do like smoking, we're kind of in the middle. So we're not uniquely cancer-prone. But obviously, we do do things in our lives that don't help us very much.
AB: Are things that we can do to try and prevent or protect us against cancer?
KA: So understanding cancer as as a disease of tissue and as a disease of like mutated cells in damaged tissue tells us there's two ways of preventing cancer. So one is to not add to that mutational burden. So, yeah, we absolutely should be understanding what does damage DNA, how do we try to reduce our exposures to those things? So the obvious things are things like, you know, toxic chemicals in the environment, X-rays, ultraviolet light from the Sun, the toxic chemicals in tobacco smoke, all these kind of things that we know damage DNA. Yeah. Reduce your mutational burden for sure.
But then it is also trying to figure out and understand what are the things that disrupt our tissue environment. And what are the things that make a more healthy tissue environment and can even repair it. So I think that this is going to turn out to be a really important area. It's understanding things like the role of inflammation in our tissues, understanding how conditions like obesity contribute to tissue damage.
Understanding how exercise actually is good for us. We don't really know why exercise is good for us. But my suspicion strongly is that it's going to turn out to be very beneficial for our tissue environment. So, you know, I think we're all very obsessed about from the outside, looking 10 years younger, everyone's trying to look younger.
But I want to know about, like, how to make my tissues inside look younger, because the younger and healthier your tissues are, the less likely it is that rogue cells will emerge. And if we can even push this, you know, 10, 15 years further down the road, you can make your tissues 10 years younger than that will stave off the emergence of cancer by a significant time. And that could be really transformative.
AB: So if it's something that happens in tissues, we'll always have tissues. Does this mean we'll never not get cancer?
KA: Yeah, that's right. It's a bummer, isn't there? And so, you know, this is sort of idea. And having worked for a cancer charity, you know, you sort of have this idea that we will find the cure and we will eradicate cancer and we will live in a world free from cancer.
And the more I look and understand cancer as a biological phenomenon, that is basically that the flip side of multicellularity. Well, I know it's it just emerges wherever there is society, cheats are there. And it's not just in all tissues. It's like every society you look at. There are some stories in the book I talk about sort of cheating amoebas and cheating bees. Where there are societies with rules, cheats will emerge.
So if you even if you did lived an absolutely perfect, perfectly healthy life, there's still a chance that you could develop cancer and for all of humanity, I think, you know, because we are multicellular. It's still going to happen.
So then the important thing is, is how do we, A, push that back in terms of timing, you know, make it as late an event as possible in our lives, and then, B, once it does emerge, how do we detect it as quickly as possible, treat it as effectively as possible? And if it's not detected and treated early, how do we understand its evolution, its resistance to therapy and try and control it much more effectively or even potentially - I kind of get to this at the end of the book - potentially drive it to extinction within the body.
But alas, you know the positive news will not be there that we will eradicate cancer and never have it with us. It's it's an intrinsic part of of all life and certainly an intrinsic part of human life.
AB: And, of course, we can do cervical screening. We do breast screening. Are there any other widespread programmes that we could be doing to try and catch these cell abnormalities early?
KA: This is where it gets really challenging because I think there's a sort of a mantra that like cancer screening, cancer screening, cancer screening, cancer screening. And obviously I have to said that the key is to detect cancer early and treat early.
But, you know, earlier I was talking about like we are full of kind of weird lumps and bumps and cells going wrong and doing their thing, but not actually developing into cancer. So the key thing is with any screening is, is this clump of cells that we found actually on the road to becoming a cancer. Is this actually going to be a cancer? And certainly with with breast screening, we're finding a lot of very, very small tumours.
And they're not even called kind of cancer. They're called ductal carcinoma in situ. And we don't really know of any of them. Which ones are the dangerous ones? And so some people treat them, some people don't treat them. Some people watch and wait. And all of this is incredibly worrying. If you're someone who's going through this and that's what we really need to understand is what are the triggers that turn these kind of sad cells into actually bad cells?
And it's looking like the sort of the idea that there are kind of chromosomal catastrophes, some kind of catastrophic event that happens to cells that really starts them down the road to cancer. So it's like, how do we actually understand what tips sad cells into being bad cells? And then when we find lumps and bumps and things like that.
Being able to distinguish what's safe to leave, what's safe to ignore, what's safe to just watch and wait, and what actually if we got rid of this now, that would really be like life saving. But right now, we don't really know that. Cervical screening, I think, is a slight exception to that, because certainly when you look at the data, it's really obvious that cervical screening does absolutely save lives.
And I'm fairly convinced by the evidence on bowel screening, but certainly like widespread unstratified breast screening of the entire population, like all women over a certain age, I think I'm not convinced that's a good idea. So it's again, it's understanding who will benefit, who's more likely, who's most at risk and will benefit from screening, whereas he's actually a lot less at risk.
And if you found something like, well, that's you know, then you're just plunging someone into this sort of world of dilemma. So really understanding what do is dangerous cells look like? What do dangerous cells look like and what should we do about them? I think before we just go screening for everything for everyone is. And, you know, sometimes I see I think it's particularly in the US. You could do things like just pay to have a full body MRI scan.
You know, like an MOT, like do not do that. You do not know what you will find in there. That's such a bad idea.
AB: But it seems like there's so, so little we know about cancer and so much we don't yet have answers to. Is it that it's been understudied? Is it that there's only recent developments that are allowing us to do that?
KA: I think anyone who knows about the history of cancer research will say, well, it's certainly not be an understanding. And anyone who works in any other disease just kind of looks at cancer, goes like, I think you've had enough money.
So it's certainly not a disease that's been understudied. I think that there has been in recent years, I think there's been an over-focus on just looking at the faulty genes in tumours and kind of this huge shopping list of mutations that you can find in a cancer. And just trying to develop drugs that target them. And that has its place and it can be useful.
But I think it's quite narrow focus it understanding a disease that is a complex biological phenomenon. So it's not that it's been underfunded and certainly not. And recent advances in genetics and genomics are really, really powerful and I think are going to help us actually understand the kind of the evolution in the evolutionary playbook of cancer.
So I certainly think it is useful. I think that we do need to be a bit smarter. I think we have got to a very genetic reductionist view of the diseases. Like let's just focus on the cells, focus on the mutations in the cells and not focussing on the wider tissue and then even the wider body.
You know, I'm really keen to reclaim the word holistic from kind of alternative medicine because this is a disease in a human body. It's part of us. It comes from us. It emerges from our tissues. It's soaked in the hormones soup that we we swim in, that our cells swim, in is subject to our circadian rhythms. The day and night body clock, you know.
We feed cancers with the foods that we eat. It's exposed to the things that we expose ourselves to. So this is a not something that's kind of almost like weird an alien mutant cells inside us. This has come from us. So putting it more in that context of of the whole body rather than sort of very granular, reductionist thing, I think is is an exciting way forward.
AB: Mm hmm. And you and people talk about cancer. They talk about different stages. What are the stages of cancer?
KA: So there's sort of various ways of staging different types of cancer. And it's all about how. Certainly for solid tumours. It's about how much has it started to spread? Is it just all in one place? Are these is cancer cells just a lump in one place? Have they started to break through the membrane that surrounds the tissue?
That's sort of the second stage. Have they started to spread to other sites? Have they started to go to the lymph nodes? For example, the nearest lymph nodes to where the original tumour started? Or have they started to spread to much wider sites? So other organs like the bones or the liver or the brain. And we are the earlier you can detect cancer. So that kind of stage, one or two, you are much more likely to have a successful long term outcome and even potentially a cure, depending on the type of cancer. And depending on the cancer itself, how aggressive it is.
So, you know, there's this definitely is a call to try and work out how do we genuinely diagnose cancer at an earlier stage. But, yeah, it's more about sort of the progression of stages and how far and how how much it has spread throughout the body. Actually, there's some something I talk a bit about in the book is it's thinking not just about this, but also about kind of I call it the eco evo index. So it's like the Ecology Evolution Index way of thinking about cancer.
And this is an idea that's driven by particular by researchers like Carlo Maley at Arizona State University. And so it's thinking about what is this cancer actually like? Like how mutated is it? How much diversity is there in there? And what is the ecology of the tissue like, you know? Is this very toxic messed up tissue? Is this relatively fit tissue?
Are these cells are there not many different populations of cells in there? Or is there just complete wild diversity of all sorts of things in there? And that impacts on the kind of evolutionary feel for the cancer and will also inform maybe your best strategy for treating it.
AB: What is it that happens that makes a cancer fatal? How does it actually kill someone?
KA: This is a this is a really tricky one because in some cases. So, for example, in the case of a brain tumour, its cells that are growing in a confined space and that's ultimately at some point going to be incompatible with a normal function of your brain. So really, at the end of life, it is basically when these cells become incompatible with the normal functioning of your body.
So for systemic cancer that spread through the body, it may be because there's just so many cancer cells in organs like your liver, in the brain, in the bones that your body cannot function properly anymore. And this is obviously very, very difficult for people to watch. There's also a there's a syndrome called cachexia, spelled C A C H E X I A, which is this kind of wasting, extreme wasting that some cancer patients experience at the end of life.
And we don't exactly know what causes it, but it's it's sort of these are the the cancer cells just consuming the body. And so it's really at that point where the burden of cancer within the body becomes incompatible with the systems of life itself.
AB: What do we know about why cancer is on the rise?
KA: So we do know that rates of cancer are increasing and the a lot of that is driven by our ageing population. So we know that the risk of cancer significantly goes up in the sixth, seventh decade of life because our tissues age, our tissues change. We've picked up in our future mutations in in our cells. So that does explain it.
There are also other specific cancers and specific incidences that are affected by some things that we know about in the environment. So obviously, like the link between lung cancer and smoking we know about very well. We do know that, for example, changing reproductive patterns, particularly for women, influence the risk of things like breast cancers. And there is a link to show that, you know, things like hormone replacement therapy can increase the risk of breast cancer.
So, you know, there are some specific risks that we know about. I personally feel like the kind of the major driver is our ageing population. And that's obviously something that we really need to think about. How do we actually maintain our healthy bodies, our healthy tissues? If we're all going to be living longer, you know, if we're going to be living to like 85 or 90, how do we actually keep all tissues really healthy through our 60s or 70s or 80s? And that that's sort of a challenge as well.
AB: And in terms of the future of cancer research, what is giving you hope right now?
KA: I am really excited right now about the move to think about cancer more as an evolutionary phenomenon. So I am really excited by the ideas of people like Bob Gatenby, who's at the Moffitt Cancer Centre in Florida. The work of people at the Centre for Cancer Evolution, led by Mel Greeves at the Institute of Cancer Research down in Sutton in Surrey, who are really thinking about cancer as an evolutionary phenomenon.
And for example, in Florida, Bob is running clinical trials of something called adaptive therapy, which is. Pretty different to the way we normally treat cancer, which is just to, you know, just nuke it from orbit, like go in with big doses of drugs, try and get rid of every last cancer cell. He's thinking about using it, using mathematics, using modelling, understanding what populations of cells in there, and then using strategies that kind of balance the different populations of cells in a tumour resistant cells versus sensitive cells kind of riding this like rollercoaster of letting different populations of cells grow shrink. Fight it out between themselves rather than just trying to get rid of everything and call it done.
And so in that kind of approach, like that's really contrary to what we think of as a cure. But in some cases, he has the trial that's currently published is the one about prostate cancer. You know, he has men who have ridden this rollercoaster for for more than four years when the average time to progression for that cancer would be about 18 months. So, like, if this was a new drug, it would be amazing. Everyone will be falling over themselves.
And so they're trying to work out how can we do trials like this in other types of cancer? And then the other thing that really excites me is once you kind of accept that there is lots of genetic diversity within tumours, there's different populations of cells. They can respond to different drugs in different ways. And now we have the genetic tools to start to unpick that we can start devising proper extinction strategies.
So not just controlling cancer in the long term, but working out in the same way that like animal populations are driven extinct by. It's never just one thing, it's catastrophe after catastrophe, after catastrophe. Plus, you know, just some gradual whittling down, shrinking of habitat. So thinking about those kinds of evolutionary population based strategies for really driving cancers to extinction in the body. And when can you drive that population of cells so small that effectively it will just collapse or it will just be controlled?
Listen to more episodes of the Science Focus Podcast:
- Matt Parker, Helen Arney and Steve Mould: What links coffee, snowflakes and frogs?
- Professor Catharina Svanborg: Is the cure for cancer hiding in human breast milk?
- Is gene editing inspiring or terrifying? – Nessa Carey
- Can we slow down the ageing process? – Sue Armstrong
- Eating for your genes – Giles Yeo
- How to get a good night’s sleep – Alice Gregory
Amy is the Editorial Assistant at BBC Science Focus. Her BA degree specialised in science publishing and she has been working as a journalist since graduating in 2018. In 2020, Amy was named Editorial Assistant of the Year by the British Society of Magazine Editors. She looks after all things books, culture and media. Her interests range from natural history and wildlife, to women in STEM and accessibility tech.