Speaker 1: Welcome to Stuff to Blow Your Mind production of My
Speaker 1: Heart Radio. Hey are you welcome to Stuff to Blow
Speaker 1: Your Mind? My name is Robert Lamb and I'm Joe McCormick.
Speaker 1: And today we're bringing you another interview that I conducted
Speaker 1: last week while Robert was taking a break from work.
Speaker 1: That's right. Once a year, I like to bury myself
Speaker 1: in some sacred imported soil and allow my my body
Speaker 1: to break down and then reconstitute itself so that I
Speaker 1: can rise once more and be up to the challenges
Speaker 1: of podcasting in this day and age. Today we are
Speaker 1: going to be sharing the conversation that I had with
Speaker 1: the British geneticist and science communicator cat Arnie talking about
Speaker 1: her upcoming book, Rebel Cell Cancer Evolution in the New
Speaker 1: Science of Life's Oldest Betrayal. So a little bit of
Speaker 1: biographical information. Cat Arnie hosts the Genetta Unzipped podcast and
Speaker 1: she holds a PhD in developmental genetics from Cambridge University.
Speaker 1: She was a key part of the science communications team
Speaker 1: at Cancer Research UK from two thousand four to co
Speaker 1: founding the charity's award winning science blog and acting as
Speaker 1: a principal media spokesperson She's also the author of Hurting
Speaker 1: Hemmingway's Cats, Understanding How Our Genes Work and How to
Speaker 1: Code a Human and she's written for Wired, The Daily Mail, Nature, Mosaic,
Speaker 1: News Scientist and more, and has presented many BBC radio programs.
Speaker 1: You can find Cat Arnie on Twitter at at cat
Speaker 1: Underscore Arnie A r in E Y and UH. I
Speaker 1: should note that the book is coming out at different
Speaker 1: times in the UK in the US, so Rebel Cell
Speaker 1: can be found in the UK starting on August six,
Speaker 1: and then in the US I believe it's coming out
Speaker 1: on September twenty nine, but you can go ahead and
Speaker 1: preorder it online. All right, Well, I'm I'm in a
Speaker 1: rare position here because I am just like the listeners
Speaker 1: out there. I have not heard this interview yet myself,
Speaker 1: so I am excited, uh to to to listen in
Speaker 1: as she sheds light on this, uh, this fascinating topic.
Speaker 1: Cat Arnie, thanks so much for joining us today on
Speaker 1: the podcast. Thank you for having me. It's an absolute pleasure.
Speaker 1: It's a pleasure to have someone on the show who
Speaker 1: has not only written a great book, but you're actually
Speaker 1: a podcaster yourself, so you're so you're used to this
Speaker 1: whole game talking into the mic with alone by yourself
Speaker 1: in a room. Yeah, I've been making the Genetic sun
Speaker 1: Zipped podcast. I did have to say that through this
Speaker 1: time we've we've deliberately made it a COVID free zone,
Speaker 1: so it is currently a COVID free genetics podcast. So
Speaker 1: that's been that's been a nice thing to do during
Speaker 1: during this time. I gotta say I was listening to
Speaker 1: one of your episodes of the Genetics sun Zip podcast,
Speaker 1: the one about mount Sly and Pauline Gross, which I
Speaker 1: thought was fantastic. Of course it connects to the book
Speaker 1: that we're gonna be talking about today. So, uh, personal
Speaker 1: endorsement from me of your podcast. Don't really like it,
Speaker 1: thank you. Yeah, it's really fun. We we alternate. We
Speaker 1: do sort of interviews with scientists who are working now
Speaker 1: in genetics. But I also really like to go back
Speaker 1: through those stories and and dig out, particularly the untold
Speaker 1: women who were often they're doing the work, doing lots
Speaker 1: and lots of stuff, incredibly detailed observations and breeding experiments,
Speaker 1: and then basically didn't really get the credit for it
Speaker 1: because until the middle of the twentieth century or later,
Speaker 1: women weren't really respected as a scientist, so it's it's
Speaker 1: just a wonderful exploration you come up with all these
Speaker 1: incredible people, although, of course, in the early twentieth century
Speaker 1: lots of them do turn out to be eugenicists, but
Speaker 1: that's different. Podcast. Yeah, so I think maybe a good
Speaker 1: place to start when talking about cancer. Of course, your
Speaker 1: book is about cancer, and specifically a lot about the
Speaker 1: genetics of cancer. I wanted to maybe start off by
Speaker 1: talking about this strange kind of gut feeling or almost
Speaker 1: superstition that somehow, unlike other diseases, cancer is a modern synthetic,
Speaker 1: some kind of perversion in some way against nature, and
Speaker 1: that it sometimes comes with this odd edge of moralism,
Speaker 1: that cancer is not just unfortunate, but it's somehow decadent
Speaker 1: in an indicator of something wrong with our age. Parts
Speaker 1: of your book indicate to me that you've come up
Speaker 1: against this kind of thinking a lot as well. What
Speaker 1: do you think this sort of thinking signifies. I think
Speaker 1: it's absolutely fascinating. Cancer is not a new disease, and
Speaker 1: that really became abundantly clear to me. So, just as
Speaker 1: a little bit of background, I spent twelve years working
Speaker 1: at Cancer Research UK, the UK's biggest cancer charity, answering
Speaker 1: lots of questions from the public, and all the time
Speaker 1: this question comes up. It's like, why me, isn't it
Speaker 1: just a modern disease? Oh, it's all this stuff in
Speaker 1: the air, Oh it's stress. What what is it? And
Speaker 1: you start to look into what cancer really is, and
Speaker 1: it's it's ancient. It's hardwired into our biology because it's
Speaker 1: just cells doing what they're going to do. Cells multiplying,
Speaker 1: cells jostling for space, cells competing with the cells around them,
Speaker 1: obeying the processes of evolution. And so when you really
Speaker 1: start to look, it's not surprising that you find cancer
Speaker 1: going all the way back through human history, all the
Speaker 1: way back through the history of of animal life on
Speaker 1: this planet. But at the same time, when people start
Speaker 1: to become aware of cancer as a disease, they start
Speaker 1: to ask questions about, well, where did this come from?
Speaker 1: Why has it affected me? You start to get the
Speaker 1: Greek doctors, people like Hippocrates, who were writing about cancers
Speaker 1: in their patients and saying, well, what what has caused it?
Speaker 1: It must be the gods, it must be the humors.
Speaker 1: Something is out of whack in here, and then you
Speaker 1: start to get the slightly more religious thing of well
Speaker 1: it is it's sins visited on us, it is something
Speaker 1: to do with immorality, modern living. And then you bring
Speaker 1: up to today this we don't necessarily have such a
Speaker 1: strong religious view of it, but certainly the idea of
Speaker 1: almost wellness as a religion. You've done something toxic to
Speaker 1: yourself and that's why you you now have cancer, and
Speaker 1: you look back at the history of cancer as a
Speaker 1: biological phenomenon, and that's simply not true. You know. It's
Speaker 1: it's basically like the dark side of life rather than
Speaker 1: anything that we have particularly brought on ourselves in our
Speaker 1: modern life. Yeah, that's one of the things I really
Speaker 1: loved about your book was the way you how you
Speaker 1: show cancer to be so fundamentally integrated with with with
Speaker 1: life itself or I guess, multi cellular life. Um. And
Speaker 1: so so maybe we should focus on on a couple
Speaker 1: of these ideas in particular, one of them, I guess,
Speaker 1: is the idea of modernity, right, the idea that that
Speaker 1: cancer is something that was very rare until recently. You
Speaker 1: make an argument against and people have argued this, but
Speaker 1: you make an argument against this in the book, and
Speaker 1: you cite some both some reasoning about why a lot
Speaker 1: of cancers wouldn't necessarily show up in the kinds of
Speaker 1: remains we can examine, and then pointing out examples that
Speaker 1: we do find in fact, in the human record and
Speaker 1: physical remains of human society and prehistory. Yeah, it's the
Speaker 1: classic thing in biology that you find what you're looking for,
Speaker 1: and people have not been looking for signs of cancer
Speaker 1: in ancient remains. And the thing about cancer is that
Speaker 1: that when you're thinking about ancient remains that we find,
Speaker 1: mostly you're talking about bones, and particularly when you get
Speaker 1: very ancient, you're talking about fossilized bones. And not every
Speaker 1: cancer leaves its trace in the bones. So when you're
Speaker 1: thinking about cancers that affect the soft tissue, you may
Speaker 1: never see the traces of a cancer that killed someone. Also,
Speaker 1: you know, ancient remains don't turn up in beautifully age
Speaker 1: matched structured populations, so you can say, oh, this is
Speaker 1: exactly the population that was alive at the time, this
Speaker 1: is exactly the number of cancers in this population. I
Speaker 1: think some people have argued that the fact that cancers
Speaker 1: are rare in ancient humans is an argument that cancer
Speaker 1: was very very rare. But I slightly feel the other
Speaker 1: way around. I feel like the fact that the more
Speaker 1: people start looking for cancers in human and animal remains
Speaker 1: from from way way back, the more cancers they start
Speaker 1: to find suggest that it was more common. We will
Speaker 1: never know how how common it was, because you can't
Speaker 1: do you know, a lovely epidemiological study on the sort
Speaker 1: of stuff that you can get out of the ground.
Speaker 1: You get what you get and you get on with it, basically.
Speaker 1: But I do think that cancer is not an exclusively
Speaker 1: modern disease. I will say, certainly it is more common
Speaker 1: as we live longer. So another of the things I
Speaker 1: go into later in the book is the idea that
Speaker 1: there's almost a sort of a shooting up point. After
Speaker 1: you have got to a certain age, your risk of
Speaker 1: cancer does significantly go up. So if you think about
Speaker 1: ancient populations when there were many, many, many more things
Speaker 1: that we're going to kill you, your chances of getting
Speaker 1: to an age where you could dive cancer before something
Speaker 1: else got you worse smaller. So it's not surprising we
Speaker 1: find fewer ancient remains with cancer. But when you think
Speaker 1: about some children have been found with types of cancer
Speaker 1: that are very very rare in populations, and the fact
Speaker 1: that we have found them at all suggests that this
Speaker 1: is a disease that has always been with us, and
Speaker 1: it's not exclusively a confection of modernity. It's it's basically,
Speaker 1: you know, it is with us and always has been.
Speaker 1: And what about the part of the misconception that views
Speaker 1: cancer is something that is uniquely kind of human and
Speaker 1: maybe associated with uh, with the synthetic products of human
Speaker 1: industry and all that. Like, this ties into the idea
Speaker 1: that sharks don't get cancer, right, that there's a widespread
Speaker 1: belief that that, for some reason, animals that don't engage,
Speaker 1: you know, don't live in cities and drive cars and
Speaker 1: eat processed food and stuff won't get cancer. But they do. Yeah,
Speaker 1: And this really my mind. I can see over on
Speaker 1: my bookshelf. I'm so tempted to go and grab it.
Speaker 1: But there's a book where someone has gone through all
Speaker 1: the different species that have been known to have cancer
Speaker 1: in In some cases it's many examples, in some it's
Speaker 1: just a few. But it's pages and pages and pages.
Speaker 1: It's everything from like odd wolves to zebras, and almost
Speaker 1: every branch of the animal kingdom develops cancer. There are
Speaker 1: a couple of really weird exceptions. So one is comb jellies.
Speaker 1: Comb jellyfish don't seem to get cancer, never been detected.
Speaker 1: And also sponges really weirdly resistant to sponges. There's this
Speaker 1: guy in in Arizona, guy called Carlo Malei, who is
Speaker 1: zapping sponges with enormous amounts of radiation like that would
Speaker 1: kill a human, and they're just fine. They just shrug
Speaker 1: it off. So there are some species that are cancer resistant,
Speaker 1: but pretty much everything else to a greater or lesser
Speaker 1: extent is and humans aren't even the most susceptible species.
Speaker 1: There are some that are much more susceptible to cancer
Speaker 1: than humans are. So this idea that it's it's just
Speaker 1: a modern disease, it's just a human disease, it just
Speaker 1: doesn't stack up. You know. Yes, there are things that
Speaker 1: we do in our modern lives that increase the risk
Speaker 1: of cancer, and our lovely living to a nice old
Speaker 1: age is a major risk factor. You know, Thank god
Speaker 1: we don't all die in childbirth and of infectious diseases
Speaker 1: before our tenth birthday. But you know, we are we
Speaker 1: are not, you know, unique and wonderful when it comes
Speaker 1: to cancer again, it's it is just part of life.
Speaker 1: There are some other interesting observations you mentioned in your
Speaker 1: book about what might create a specific propensity for cancer
Speaker 1: in certain species versus others. Are One that I recall
Speaker 1: is that you mentioned that it's cancer seems to be
Speaker 1: more prevalent in species that have been through a genetic
Speaker 1: bottleneck at some point in the relatively recent past. So like,
Speaker 1: if their breeding population was reduced to a pretty small
Speaker 1: number at some point, they tend to be more susceptible
Speaker 1: to cancer. Is that correct? Yes, So that does seem
Speaker 1: to be the case, which suggests that there are genetic
Speaker 1: factors at work. Because if you shrink a population down
Speaker 1: to a very small what's called an effective breeding size,
Speaker 1: you've got quite a small population that's all breeding with
Speaker 1: each other. You do start to get a pile up
Speaker 1: of mutations being passed from generation to generation, which might
Speaker 1: be increasing the risk of cancer. One of my favorite
Speaker 1: species in this case is the Syrian hamster, which all
Speaker 1: the Syrian hamsters pretty much that are in pets and
Speaker 1: labs all over the world are descended from one litter
Speaker 1: of hamsters, and they are incredibly cancer prone because they're
Speaker 1: just massively in bread um. But yeah, every every species,
Speaker 1: some more than others and some much less than others.
Speaker 1: So elephants very surprisingly, you'd think when you think about
Speaker 1: it logically, animals that are very very big, they have
Speaker 1: lots of cells that they live for a very very
Speaker 1: long time. You think that elephants should be riddled with
Speaker 1: cancer by the time they die, but they are not.
Speaker 1: They are amazingly resistant and really long lived animals like
Speaker 1: bowhead whales, even some of the really long lived bats,
Speaker 1: brand bats that live for forty years, very resistant to cancer.
Speaker 1: So they have evolved mechanisms that enable them to live
Speaker 1: these very long, luxury lifestyles and be resistant to cancer.
Speaker 1: Whereas you have very small rodents, things that live fast
Speaker 1: and die young. Why bother. You know, you're going to
Speaker 1: be around for a couple of breeding seasons and then
Speaker 1: you're out. And humans are kind of in the middle.
Speaker 1: You know, we live for many decades, we reach our
Speaker 1: child bearing years in between our sort of twenties to forties,
Speaker 1: hang around for a bit after, and then the risk
Speaker 1: of cancer does start to go up. So you know,
Speaker 1: this is when you put humans in the context of
Speaker 1: all of life, you start to understand how our evolution
Speaker 1: as a species is in trance tied to our as
Speaker 1: a species risk of cancer. But you do have to
Speaker 1: separate that from personal risk of cancer as well, and
Speaker 1: that's a that's kind of a bit hard to get
Speaker 1: your head around. So we're talking about evolutionary risks versus
Speaker 1: personal risks. So one of the most interesting ideas in
Speaker 1: your book that that you keep returning to is a
Speaker 1: framework for thinking about multicellular life through the analogy of
Speaker 1: a society, that a multicellular organism is a society of cells.
Speaker 1: Could you explain this way of thinking in some of
Speaker 1: the implications that extend from it. Yeah, this really really
Speaker 1: blew my mind when I started to understand this. So,
Speaker 1: this idea of cells as a society, it goes about
Speaker 1: quite a few decades. A lot of the things I
Speaker 1: discovered while I was researching the book are quite old
Speaker 1: ideas that have got, you know it, subsumed or left
Speaker 1: behind in this this rush to just understand cancer as
Speaker 1: a purely genetic disease. But the idea is that that
Speaker 1: cells and organisms and individuals in a species, they live
Speaker 1: in societies, and there are rules of societies at every
Speaker 1: single level. You know things like do the job you're
Speaker 1: meant to do, don't take more than you need, clean
Speaker 1: up after yourself, all these kinds of things. There are
Speaker 1: rules to societies that make societies work productively. And you
Speaker 1: start to look around at groups of cells that are
Speaker 1: in tissues and in organs in your body. You look
Speaker 1: at societies like ants and bees. You look at colonies,
Speaker 1: you look at troops of chimps and herds of deer,
Speaker 1: and you look at human societies and they all work
Speaker 1: in the same way. And this particularly an idea that
Speaker 1: I was influenced by. There's a researcher in Arizona called
Speaker 1: Athena Actipis, and she works a lot on social cooperation
Speaker 1: and cheating and the idea that cancer cells basically cheat
Speaker 1: in society. They are cheaters. They take more than they need,
Speaker 1: they produce waste, they proliferate out of control, they don't
Speaker 1: die when they're meant to. They are not good cells. Now,
Speaker 1: if every cell in your society was doing that, it
Speaker 1: would just be, you know, mad max style dystopia. Nothing
Speaker 1: would work, your body would not function. But you can
Speaker 1: get away with being a cancer cell and cheating and
Speaker 1: keeping going and keeping going because to a certain extent,
Speaker 1: cheaters do prosper, and it's the same in many animal societies.
Speaker 1: So one of the lovely examples that I found was
Speaker 1: these cape honey bees. So this just wonderful example. So
Speaker 1: cape honeybees, they have a classic honeybee population structure. You
Speaker 1: have the queen, and you have all the workers, the
Speaker 1: female workers, but the queen is the only one who
Speaker 1: gets to reproduce, and so all the workers are busy
Speaker 1: doing all the work in the hive, and the queen's
Speaker 1: just cleaning around basically like a um and you know,
Speaker 1: popping off to reproduce when she feels like it. But
Speaker 1: there is a genetic change, single genetic change that means
Speaker 1: that these worker bees can become queens and they start
Speaker 1: to just sit around, you know, queening it up, and
Speaker 1: eventually the hive starts to collapse under the weight of
Speaker 1: all these cheaters. And it's just a single genetic change
Speaker 1: that enables them to do this. And actually some of
Speaker 1: these queens will go off to other hives and start
Speaker 1: to infect them and turn them into cheaters as well.
Speaker 1: And it's almost like a bee cancer, I suppose, because
Speaker 1: ultimately it leads to the destruction of the hive, and
Speaker 1: you say, well, why would the bees have this, Why
Speaker 1: would it be so fragile that one genetic change can
Speaker 1: disrupt it like this? And it turns out that where
Speaker 1: the bees live it's very, very windy. So there's a
Speaker 1: risk that if you just have one queen and that's
Speaker 1: all you get, your queen could get blown off course
Speaker 1: and you might lose her totally, and then your hive
Speaker 1: would collapse anyway. So the ability to flip into queen
Speaker 1: mode it's really useful for the bees for their evolutionary survival,
Speaker 1: but it comes with a risk. And it's the same
Speaker 1: with cells. So we need to be able to make
Speaker 1: new cells. You need to regenerate millions of cells in
Speaker 1: your body every day, millions of cells in your skin,
Speaker 1: your blood, your bowel. You need to be able to
Speaker 1: heal yourself if you're wounded. You need to be able
Speaker 1: to grow from one cell into an adult human. Cells
Speaker 1: need to reproduce, they need to do stuff. Flip side
Speaker 1: of that is that they can sometimes go out of
Speaker 1: control because it's the same mechanisms that make cells grow
Speaker 1: and multiply in the right way that they kind of
Speaker 1: harness and hijack when they decide to cheat and grow
Speaker 1: out of control in the wrong way. So that's interesting.
Speaker 1: You're sort of showing how cancer is one side of
Speaker 1: an evolutionary balance where on one hand, you've got you know,
Speaker 1: as your ability to do something good goes up, the
Speaker 1: risks associated with those same genes that code for that
Speaker 1: also go up. So we know on one side what
Speaker 1: the downside is. We can see tumors in cancer, and
Speaker 1: you're saying that the the the goods that make those
Speaker 1: risks worthwhile are basically being able to proliferate quickly in
Speaker 1: cell growth. And this would have to do not just
Speaker 1: with growth in youth, but in healing and things like that. Yeah, exactly,
Speaker 1: And you see this. This starts to explain the differences
Speaker 1: across species because if you if you cut a mouse,
Speaker 1: mice heal amazingly fast. Their cells just basically knit themselves
Speaker 1: back together. It's it's absolutely incredible. Um. One of the
Speaker 1: stories that I discovered when I was talking to a
Speaker 1: researcher in Santa Barbara who's trying to work with the
Speaker 1: animals in the zoo to understand their cancer risks. She's
Speaker 1: she went to the zoo and said, can I get
Speaker 1: a little bit of skin from your giant tortoise, and
Speaker 1: they were like, hell, no, cut a tortoise. It takes
Speaker 1: a year to heal, and tortoises live for a very
Speaker 1: long time. They are incredibly cancer resistance, but they the
Speaker 1: flip side of that is that they don't heal very easily.
Speaker 1: So humans again somewhere in the middle. We don't heal
Speaker 1: as fast as mice. We live much longer than mice.
Speaker 1: So there's there's all of this stuff is a trade
Speaker 1: off about the evolutionary journey that your species has taken.
Speaker 1: And one of the things that I sort of took
Speaker 1: this to its logical conclusion, and I was like, if
Speaker 1: there's aliens, aliens would get cancer, that there's very unlikely
Speaker 1: that they would not if they obey the general rules
Speaker 1: of evolution, and this idea that like cells, organisms living
Speaker 1: in a society behave according to the rules of that
Speaker 1: we know make a good society. I don't think there's
Speaker 1: any reason why aliens wouldn't get cancer. She's like, that's
Speaker 1: a bit of a that was a bit of a
Speaker 1: sort of late night thought. I think, because all that's
Speaker 1: necessary is that they exist by cell division, right, I mean,
Speaker 1: that's pretty much it. Yeah, yeah, exactly, if you have
Speaker 1: cells and your cells are doing cell division, and also
Speaker 1: if you have evolution by natural selection, which is basically
Speaker 1: the engine that drives cells to to proliferate and be
Speaker 1: selected for and to keep going, and species to keep
Speaker 1: proliferating and keeping going, then yeah, you probably could get cancer.
Speaker 1: And that's what we generally see across the entire animal kingdom. Well,
Speaker 1: thinking about aliens getting cancer makes me think of another
Speaker 1: interesting part of your book, which was about difficulties in
Speaker 1: classifying what appears to be some form of uncontrolled cell
Speaker 1: growth in animals or even not animals, other organisms that
Speaker 1: are very different from us. So can you look at
Speaker 1: what's going on in a clam and say that it
Speaker 1: has cancer? Yeah? Probably, But what about a mushroom or
Speaker 1: in an algae or something? Yeah, this was this was interesting.
Speaker 1: So you know, what is cancer and n is cancer?
Speaker 1: Is an interesting question. And when you get to more
Speaker 1: organized animals and particularly mammals, we define invasive cancers as
Speaker 1: cancers that kind of break through the sort of molecular
Speaker 1: I guess you'd call it like saran wrap that's around
Speaker 1: your organs and your tissues. They break through this membrane,
Speaker 1: and that's what we call invasive cancer. But really, you know,
Speaker 1: the phenomenon of cells growing out of control is all
Speaker 1: over the place. You can see it in plants when
Speaker 1: they get ghouls, you can see it in in fungi.
Speaker 1: You can see it in all sorts of things. And
Speaker 1: what are the interesting questions is you know something like endometriosis,
Speaker 1: which is a condition where you get rogue tissue within
Speaker 1: the body and it's sort of it grows and its
Speaker 1: spreads and it bleeds and it's very very painful. It's like,
Speaker 1: but that's not cancer, it's not invasive. But actually, when
Speaker 1: you look at that kind of tissue, it has lots
Speaker 1: and lots of the kind of mutations and changes we'd
Speaker 1: expect to find in cancer. But that's not cancer, and
Speaker 1: that's in humans. So this this idea that mutations it's
Speaker 1: not just what makes cancer. Uncontrolled cell growth is not
Speaker 1: just what makes cancer. It's it's sort of this this invasive, aggressive,
Speaker 1: evolving characteristic that really is what we can classify as
Speaker 1: as cancer. All Right, we're gonna take a quick break,
Speaker 1: but we'll be right back, and we're back. So maybe
Speaker 1: we should shift to talking about the history of our
Speaker 1: understanding of the proximate causes or maybe better to say,
Speaker 1: the risk factors for cancer where it comes from, whether
Speaker 1: that's there's a hereditary component and an environmental component. There's
Speaker 1: a part in the book where you mentioned this thing
Speaker 1: that was called the Daily Mail Oncology Ontology blog, which
Speaker 1: I've really appreciated because so the idea was this was
Speaker 1: an attempted list of all the things that either cause
Speaker 1: or cure cancer, according to the Daily Mail, And that
Speaker 1: made me say, I've got to it's something I read
Speaker 1: a lot of science and medical news from my work,
Speaker 1: and I have all but completely turned off my recognition
Speaker 1: system for articles about, you know, new supposed causes or
Speaker 1: cures for cancer, because this was already like a cliche
Speaker 1: to the point of being a hack joke for comedians
Speaker 1: in the nineteen nineties. Is there something we should learn
Speaker 1: from this, like the way that we get this conditioned
Speaker 1: kind of num reaction to these types of news stories. Yeah,
Speaker 1: that's we used to get a lot of that when
Speaker 1: I was at Cancer Research k. You know, I think
Speaker 1: that the stupidest one was that water gives you cancer,
Speaker 1: and also that turning on turning on the light at
Speaker 1: night to go to the bathroom, gives you cancer. So
Speaker 1: you know, this is this is really really frustrating. So
Speaker 1: there's kind of a couple of there's a couple of
Speaker 1: things to dissect because it's also comes down to like
Speaker 1: what what is actually the nature of cancer? And the
Speaker 1: way that cancer has been thought about for a very
Speaker 1: long time is according to what scientists like to call
Speaker 1: the somatic mutation theory of cancer. So this is this
Speaker 1: idea that cells pick up changes in their DNA in
Speaker 1: their genome that the instructions that they use to do
Speaker 1: what they do, they pick up these changes, these mutations,
Speaker 1: and that enables them to do more bad things. And
Speaker 1: then they pick up more and they do more bad things.
Speaker 1: So it's this gradual accumulation of nasty mutations terms nice
Speaker 1: well behaved cells into aggressive cancer cells. And we can
Speaker 1: start to see some of the characteristic fingerprints that different
Speaker 1: agents leave in the genome. So we can see, for example,
Speaker 1: cigarette smoke or ultra violet light from the sun, we
Speaker 1: can see those characteristic fingerprints of damage in the genome.
Speaker 1: What that doesn't necessarily tell us because when you start
Speaker 1: looking closely at a cancer or even in fact at
Speaker 1: normal tissue, you start to see these changes and mutations everywhere.
Speaker 1: So this kind of simplistic model that it's a hit
Speaker 1: in this gena hit in this gena hit in this street,
Speaker 1: and a hit in the street in a bang there,
Speaker 1: you've got a cancer cell is nonsense. Because loads of
Speaker 1: healthy cells such a peppered with mutations and loads of
Speaker 1: things do damage our DNA. And that's kind of like
Speaker 1: it's mostly fine. So it's a bit more of a
Speaker 1: sophisticated understanding of yes, there are things that damage DNA.
Speaker 1: A lot of them we know about, some of them
Speaker 1: we don't know about yet. Researchers are trying to figure out,
Speaker 1: you know, how do we match up these signatures of
Speaker 1: damage to things that are in the environment alas Mostly
Speaker 1: the most single, most damaging thing you can do for
Speaker 1: your DNA is a breathe oxygen. Literally, just being alive.
Speaker 1: The processes of life in your cells damage your DNA unfortunately.
Speaker 1: But then if all your cells are to some extent,
Speaker 1: you know, more or less messed up. Everyone's got a
Speaker 1: few mutations here and there, some more than others. What
Speaker 1: is it then that tips the cell into becoming a
Speaker 1: cancer cell? If everyone's a bit weird, what makes that
Speaker 1: cheating cell kind of slip the bonds of good society
Speaker 1: and really start going for it. And that really is
Speaker 1: is an evolutionary question that cell has involved the capacity
Speaker 1: to do that, and so I think it's it's far
Speaker 1: too simplistic to say, oh, well, you know your cancer
Speaker 1: was absolutely caused by smoking, that was it. It's like, well,
Speaker 1: that was a risk factor and it certainly didn't help,
Speaker 1: but there were many other things. And also many people
Speaker 1: who do smoke don't get cancer. So it's like we've
Speaker 1: got to be more sophisticated in understanding what makes normal
Speaker 1: cells become damaged and what makes kind of sad cells
Speaker 1: become really bad cells. Yeah, this is an important point
Speaker 1: about thinking about risk factors instead of causes. And I
Speaker 1: know that that's it's in fure creating to people especially.
Speaker 1: I think if you don't have a lot of like
Speaker 1: training in a statistics oriented field, that it just doesn't
Speaker 1: feel very comfortable to think about, especially something that's a
Speaker 1: really important life and death issue like cancer in terms
Speaker 1: of probabilities. You want to know like what it was
Speaker 1: or what what did it? Yeah, exactly. I think the
Speaker 1: best analogy that I really came up with is and
Speaker 1: this is spoilers now if anyone's seen Agatha Christie's murder
Speaker 1: on the Orient Express where and I am this is
Speaker 1: a massive spoiler, but come on, the books like really
Speaker 1: old you should have read about now see the movie
Speaker 1: with Albert Finning too. It's great, but it's a murder,
Speaker 1: but all the people involved they all have a stab,
Speaker 1: so you never know who actually was the murderer. So
Speaker 1: it's it's kind of like this. So you know, we
Speaker 1: have lots and lots of genes that we know are
Speaker 1: implicated in cancer. There are lots of things that can
Speaker 1: damage our DNA. There are lots of things that can
Speaker 1: like impre of the environment of our tissues or not.
Speaker 1: We know that things like you know, keeping keeping well
Speaker 1: and healthy and doing all the boring healthy living stuff
Speaker 1: that helps to keep your your body healthy makes yourselves
Speaker 1: more likely to fall into line. But saying exactly like
Speaker 1: it was that thing, you know it was, it was
Speaker 1: that sunny holiday in Marbea in that damage that skin
Speaker 1: cell that gave you cancer. As I know that's that's
Speaker 1: simply not possible. So trying to say oh it's this,
Speaker 1: oh it's that, do this, don't do that, I think
Speaker 1: is not terribly helpful, because at some point we've just
Speaker 1: got to get on and live and try and negotiate
Speaker 1: the risks that we're happy with taking. Right though, at
Speaker 1: the same time, you do point out how there are
Speaker 1: certain factors that increase your likelihood so far above the
Speaker 1: baseline that maybe at that point it even though you
Speaker 1: still can't quite say it's a cause, it's something closer
Speaker 1: to a cause. What I think one common example given
Speaker 1: would be tobacco. Remember you mentioned another example in the
Speaker 1: book about just chronic exposure dermal exposure to soot in
Speaker 1: chimney sweeps. I believe it was. Yeah, this was the
Speaker 1: first example of someone actually showing that something, a substance
Speaker 1: in the environment could increase the risk of cancer. And
Speaker 1: this is an English surgeon called Percival Pot who had
Speaker 1: a purely professional interest in the scrotums of young boys,
Speaker 1: purely professional because he was interested in chimney sweeps in London.
Speaker 1: Now this was in the seventeen hundreds and chimney sweeps
Speaker 1: were basically sent naked up the chimneys by gangmasters to
Speaker 1: clean the chimneys. So they were exposed to a lot
Speaker 1: of soot and they noticed that they started to get
Speaker 1: these cancers in their genitals and they were called soot warps,
Speaker 1: and these were very very very nasty cancers, really horrible
Speaker 1: kind of stuff. And Pot realized that it was the
Speaker 1: soot that these boys were being exposed to that was
Speaker 1: causing these cancers. And he said, right, you know, we
Speaker 1: gotta get nice in Germany that all the chimney sweeps
Speaker 1: had these nice kind of tight fitting uniforms so they
Speaker 1: weren't being directly exposed on their skin. And he was like, right,
Speaker 1: we've got to get those in. I got to protect
Speaker 1: these boys, stop sending them naked up your chimneys. Um Alas,
Speaker 1: it took over a hundred years for people to actually
Speaker 1: change in Britain because the gang masters were like, no,
Speaker 1: those those uniforms are too expensive. They'll make our sweeps
Speaker 1: too expensive. You know, they're they're cheap. We don't really care.
Speaker 1: So that was really tragic that they managed to link
Speaker 1: this cause to these very horrible cancers. And there was
Speaker 1: something that everyone knew could be done that was helping
Speaker 1: in other countries. And nope, nope, it didn't happen for
Speaker 1: a very long time. Um but yes, that Percival part
Speaker 1: is kind of the father of this idea of external
Speaker 1: sources of of carcinogenic chemicals, I think, but I think
Speaker 1: it has stuck in the imagination that like it's all external,
Speaker 1: it's all from from something you've done, or something you've got,
Speaker 1: or something you've touched or eaten or being exposed to. Well,
Speaker 1: to go to the other side. So there's a part
Speaker 1: of your book where you explored I think we actually
Speaker 1: mentioned this earlier about your podcast episode about Maud Sly
Speaker 1: and Pauline gross and in the role for example of
Speaker 1: the research of maud Sly in establishing that there is
Speaker 1: a hereditary component to cancer that I think at the
Speaker 1: time you say that, you know, the primary argument was
Speaker 1: about two different major theories of external causes, whether cancer
Speaker 1: was caused primarily by inflammation or by infectious agents and parasites.
Speaker 1: Is that correct? Yea. So at the beginning of the
Speaker 1: twentieth century, the early twentieth century, there was this idea
Speaker 1: that cancer was either all caused by external things like
Speaker 1: certain things in the environment, or it was viruses. Mostly.
Speaker 1: There were a couple of good examples in animals where
Speaker 1: you could take viruses, exposed the animals to them and
Speaker 1: they would develop certain types of cancer. So the first
Speaker 1: one were as a guy called Peyton Rouse who discovered
Speaker 1: a virus that caused cancer and chickens. So by the
Speaker 1: sixties everyone was just obsessed with the idea that it
Speaker 1: was viruses. And now, you know, we really understand that
Speaker 1: there are families that are affected by multiple cases of cancer,
Speaker 1: that cancer can be to some extent influenced by the
Speaker 1: genes we inherit. But really this was almost a completely separate,
Speaker 1: parallel strand running up through the first half of the
Speaker 1: twentieth century, and it was work in mice in families.
Speaker 1: In the podcast, we talk about the story of Maud
Speaker 1: Sly who bred all these mice together to show cancer
Speaker 1: could be inherited. And then the story of Pauline Gross,
Speaker 1: who was a seamstress who meant a scientist and she said,
Speaker 1: you know, I'm going to die young, and he mapped
Speaker 1: out all her family because so many members of her
Speaker 1: family were affected by the same types of cancer. And
Speaker 1: it took, you know, decades until they pinned down the
Speaker 1: particular gene fault that was responsible. But yeah, they're all
Speaker 1: these lines were like running a completely separate to each
Speaker 1: other until it all started to coalesce together in this
Speaker 1: understanding that you know, there are things that damage our genes.
Speaker 1: There are genes in our cells that make ourselves replicate
Speaker 1: that that stop ourselves from dying. This is good normally,
Speaker 1: but they can go wrong. They can be mutated, they
Speaker 1: can be changed, We can inherit versions that affect their function.
Speaker 1: And it all sort of started to coalesce into this
Speaker 1: very sensible idea of of how cancer starts. But I
Speaker 1: think it just became very very focused on the genes
Speaker 1: and the cells, just yes, single genes, shopping lists of
Speaker 1: genes and changes, and forgot to look at this broader
Speaker 1: picture of the environment in which cells are, the society
Speaker 1: in which they're living, how they can interact with each
Speaker 1: other cheap, overcome expand push against each other. This more.
Speaker 1: I hate to use the word holistic because it sounds
Speaker 1: really kind of hippie dip it, but you know, it's
Speaker 1: it's part of our bodies. It's not an external alien thing.
Speaker 1: These cells obey the rules of our bodies to to
Speaker 1: a certain extent, they cheat the rules to another extent,
Speaker 1: but it's all kind of part of one piece. And
Speaker 1: we've just focused on on genes and molecules for the
Speaker 1: past couple of decades, I think far, far too much.
Speaker 1: All Right, we're going to take a quick break. We'll
Speaker 1: be right back with more than than all right, we're back.
Speaker 1: So you mentioned in the book that you believe that
Speaker 1: the future of our resistance against cancer and medical treatments
Speaker 1: of cancer are going to rely on quote shifting towards
Speaker 1: a new way of evolutionary and ecological thinking about cancer.
Speaker 1: So I assume there you're connecting to the ideas you
Speaker 1: were just articulating. But could you expand on what you
Speaker 1: mean by that. Yeah, So, as all the sort of
Speaker 1: strands of cancer research over the past that one years
Speaker 1: started to coalesce on this eye dear that that cancer
Speaker 1: starts when cells pick up certain genetic mutations and they
Speaker 1: go out of control. And then we started to get
Speaker 1: to this idea that then, well, the way you treat
Speaker 1: them is you find the molecules the genes that are
Speaker 1: making them go out of control, and you target them
Speaker 1: with drugs. And that's going to be the way we're
Speaker 1: going to cure cancer. And there's been so much, so
Speaker 1: much effort, money, research, time, patients, lives in clinical trials
Speaker 1: have gone into testing these very molecularly targeted drugs, and
Speaker 1: you know, some in some cases there have been incredible
Speaker 1: success stories. So, for example, a drug called gliveck for
Speaker 1: treating a certain type of leukemia is incredibly successful. It
Speaker 1: targets a very specific genetic fault in the cancer cells,
Speaker 1: and it is it was game changing, and it continues
Speaker 1: to be game changing. But lots and lots of the
Speaker 1: other drugs that have been developed along these lines, they
Speaker 1: have not transformed survival in the way that we would
Speaker 1: hope they've They've eked out, you know, in some cases months,
Speaker 1: in some cases, you know, a few years. In one case,
Speaker 1: I saw a paper that said nine days increase in
Speaker 1: survival with this particular incredibly expensive targeted drug. And you're like,
Speaker 1: these are not cures. The these are these are the
Speaker 1: magic bullets that we were promised, and they are not cures.
Speaker 1: And in virtually all these cases, the cancer comes back.
Speaker 1: And why does it come back? Because of Charles Flipping Darwin.
Speaker 1: You know, it's it's evolution. You hit something, you get
Speaker 1: rid of most of the cells that are sensitive, and
Speaker 1: you've still got a core of resistance because you've got
Speaker 1: so much genetic diversity in that population. Of cancer cells,
Speaker 1: and so they start growing again, and this time they're
Speaker 1: resistant to the drug. So maybe you try another drug,
Speaker 1: same thing happens. You get rid of the sensitive cells,
Speaker 1: you've still got a core war of resistance, and they
Speaker 1: grow back, and eventually you run out of options, and
Speaker 1: there's time now to think about cancer in a much
Speaker 1: more evolutionary and ecological way, as you say, thinking about, well,
Speaker 1: if we know that this process of evolution is at work,
Speaker 1: that if you get rid of the sensitive cells, the
Speaker 1: resistant ones come back, Like, well, why don't we try
Speaker 1: and approach this in a different way. Why don't we
Speaker 1: try not to knock them all out? Why don't we
Speaker 1: try and balance these populations, keep them suppressed, keep them
Speaker 1: under control, much in the way that say a farmer
Speaker 1: would try and control the pests in his crop, rather
Speaker 1: than completely trying to nuke them all from orbit or
Speaker 1: eradicate every single last grasshopper. You know, and understanding the
Speaker 1: ecology the tissue biology, so you know, are you actually
Speaker 1: causing more damage two tissues by treating with drugs or
Speaker 1: radiotherapy or surgery. How can we minimize that so that
Speaker 1: it doesn't encourage cells to to cheat even more In
Speaker 1: a damaged environment. So it's this this idea is starting
Speaker 1: to come through, But I think I think it does
Speaker 1: take a bit of a subtle and sophisticated understanding of
Speaker 1: cancer as an evolutionary process within the tissue environment of
Speaker 1: the body, rather than just like, these are some rogue
Speaker 1: cells that have gone wrong and they're growing out of control,
Speaker 1: and we just need to hit them with enough magic
Speaker 1: bullets and they'll go away. You know, the classic cure
Speaker 1: for cancer that that we've almost been sold. It's I
Speaker 1: don't think it's it should look like that, um because
Speaker 1: we've tried that and it's not really working. So I
Speaker 1: think we need to try a different approach. This way
Speaker 1: of talking about tumors is reminding me of something you
Speaker 1: mentioned earlier in the book actually, which I thought was
Speaker 1: really interesting image that stuck with me. The idea of
Speaker 1: a hypothetical hyper tumor. I'd never considered this before, but
Speaker 1: the idea that a tumor can get a tumor. Yeah.
Speaker 1: So again, it's the thing that really jumped out at
Speaker 1: me researching this book is that cancer is a microcosm
Speaker 1: of evolution. It's it's a crucible of evolution, a dumpster
Speaker 1: fire of evolution is probably the best way of putting it.
Speaker 1: Cancer is a dumpster fire of evolution. Then you go, um,
Speaker 1: but yeah, everything every innovation of life that you see
Speaker 1: on Earth, cancer can evolve because you have a very large,
Speaker 1: genetically diverse population of cells that have got lots of
Speaker 1: opportunity to try stuff out. So you know, it's not
Speaker 1: surprising that even within a horrible cheating atmosphere of a
Speaker 1: cancer you might get some really really badass cells that
Speaker 1: will start proliferating even more and actually suppress the original
Speaker 1: tumor by just out competing them in a Darwinian sense.
Speaker 1: And then there's some really wild things, um that I discovered.
Speaker 1: So the most crazy innovation is that a guy is
Speaker 1: a guy called Kenneth Pienta in Baltimore has discovered that
Speaker 1: cancer cells have invented how to have sex. This this
Speaker 1: really blew my mind because the implications are massive. Here.
Speaker 1: We have this idea that cancer cells they just they
Speaker 1: reproduce basically by splitting into that's fine. You know, you
Speaker 1: have one cancer cell, it becomes two, it becomes for
Speaker 1: all of that kind of thing. There's no transfer of
Speaker 1: information between cells and after that. But he's discovered with
Speaker 1: these prostate cancer cells that they fuse together and become
Speaker 1: resistant to treatments, and then they start kind of budding
Speaker 1: off little cells that are resistant to treatment. And you're like,
Speaker 1: what you know that looks like sex, I mean, for
Speaker 1: a very poor value of sex, but that you know,
Speaker 1: that's the biological process of Sex's two cells fusing to
Speaker 1: other and and creating more. And you're like, whoa, because
Speaker 1: that's a way of genetically combining forces. And again, it's
Speaker 1: an evolutionary innovation. Sex has evolved on this planet multiple times.
Speaker 1: You know, it's not unheard of. And if you have
Speaker 1: enough rolls of that dice, as might happen in in
Speaker 1: a cancer you know, weird, weird, weird, our stuff is
Speaker 1: going to happen in there. Um. It's just it really
Speaker 1: is mind blowing every innovation of life. Cancer cells, you know,
Speaker 1: at some point somewhere might have a go at. And
Speaker 1: so when I realized this, when I realized that, you know,
Speaker 1: cells can have sex, cells can do all these kind
Speaker 1: of crazy evolutionary things. They can smash their chromosomes out,
Speaker 1: they can glue themselves back together. It's all kind of crazy.
Speaker 1: And then I started learning about the thing that was
Speaker 1: just really incredible. So, right, imagine there's a disaster movie happening. Right,
Speaker 1: you know what happens in a disaster movie. Everything's going wrong.
Speaker 1: You've got the guy and you've got the girl, and
Speaker 1: what do you do when your world's ending, right, you
Speaker 1: have sex basically, So that's like a last ditch attempt
Speaker 1: for cancer cells to try and come up with some
Speaker 1: kind of evolutionary innovations that are going to get them
Speaker 1: out of trouble. But then there's one more thing that
Speaker 1: happens at the end of a disaster movie, right, you
Speaker 1: leave the planet. Sure, yeah, and like and cancer cells
Speaker 1: do this, and this is absolutely incredible. So so so
Speaker 1: this is where we get to infectious cancer, the idea
Speaker 1: that it could actually be contagious. Yeah, so this is
Speaker 1: this is kind of spooky and scary because it's a
Speaker 1: very medieval idea that cancer is contagious, that you catch
Speaker 1: it from someone. And I will say that in certainly
Speaker 1: in humans, there's no contagious cancers that we know of.
Speaker 1: But the first example was the Tasmanian Devils. So this
Speaker 1: was back in the nineties nineties. The Tasmanian Devils, they're
Speaker 1: all in Tasmania. Southern Australia. They're very cute animals, but
Speaker 1: like they're evil. They they're very you know, they're they're
Speaker 1: placid more or less around humans, but they absolutely hate
Speaker 1: each other. So when you get two Tasmanian devils together,
Speaker 1: they're just like, really, go for it now, biting each
Speaker 1: other's faces. And researchers started to notice that these animals
Speaker 1: were getting big tumors in their faces and in some
Speaker 1: cases it was killing them, and that they're already endangered
Speaker 1: as it is, and this cancer started sweeping through the
Speaker 1: populations and I was like, oh no, what we're going
Speaker 1: to do. And a woman in Australia, she was working
Speaker 1: for the for the government in a hospital. She she
Speaker 1: was looking at cancer samples from humans and looking at
Speaker 1: the chromosomes. It was a way back then of identifying
Speaker 1: the kind of cancer you might have. And so she
Speaker 1: started looking at these Tasmania devil cancer samples. Now, the
Speaker 1: thing about human cancers is every human cancer is a
Speaker 1: one off. It's a unique evolutionary event. It starts in you,
Speaker 1: it grows in new it evolves in you, and it
Speaker 1: it dies in you one way or the other. When
Speaker 1: she was looking at these devil cancers, like they're all
Speaker 1: the same from every animal. The chromosomes were absolutely the same,
Speaker 1: and it's like that does not happen. That is that
Speaker 1: she was like, this is a contagious cancer and U
Speaker 1: and eventually they kind of pinned it down and it said, yes,
Speaker 1: it was cancer cells transmitting from one devil to another
Speaker 1: through that mechanism of biting and fighting and scratching. So
Speaker 1: it's a you need with a contagious cancer. You need
Speaker 1: to have a mechanism of transfer to get the cells
Speaker 1: from one organism to the other. So with the devils,
Speaker 1: it was it was biting and fighting. Um. And then
Speaker 1: there was another cancer, contagious cancer. Which are we allowed
Speaker 1: to talk about dog genitals? Oh? Yeah, I just I
Speaker 1: just did. Um. Yeah. So there's a dog genital cancer
Speaker 1: called canine venereal tumor as CTBT and so yeah, it's
Speaker 1: again when when dogs have sex, it's not pretty, but
Speaker 1: they get kind of tied together in the the gentleman
Speaker 1: and lady department and that can cause some injury. So
Speaker 1: again you have a mechanism for cancer cells to transfer
Speaker 1: from one dog to the other. And this cancer it
Speaker 1: transmits through populations. And there's a woman called Elizabeth Murchison
Speaker 1: who's in Cambridge University. She started studying the devils and
Speaker 1: then she started studying these dogs and they discovered that
Speaker 1: these cancer cells in the dogs have been around for
Speaker 1: thousands of years. The first dog with that cancer lived
Speaker 1: and died thousands of years ago, and it's gone all
Speaker 1: over the world. And that's like, it's like the oldest
Speaker 1: I don't know, it's like the oldest mammal. I suppose.
Speaker 1: It's just incredible. Um this they've worked out what kind
Speaker 1: of dog it was. It was, you know, a little
Speaker 1: kind of dog with like pointiers and a sandy coat,
Speaker 1: and it's amazing. So when you're saying it's the oldest mammal,
Speaker 1: in a way, you're saying that the tumor is, in
Speaker 1: a sense a part of that original dog. It is
Speaker 1: that dog. It is that dog's body exactly. The tumor
Speaker 1: arose in the dog. It's got the genome of the
Speaker 1: original dog. Like seriously messed up, I mean, and these
Speaker 1: cancers are now evolving independently in different dog populations all
Speaker 1: over the world. But yeah, it's it's an incredibly long
Speaker 1: lived organism. I suppose. So that that was one devil
Speaker 1: cancer which was relatively recent a dog cancer, and then
Speaker 1: they found a new second devil tumor that had arisen
Speaker 1: even more recently. So that's very unlucky for the devil's
Speaker 1: and they think it's because again they're an inbred population.
Speaker 1: So with this this fight e bity mechanism of transfer,
Speaker 1: so you've got quite a high probability that this might happen.
Speaker 1: And then there's all these weird shellfish that have cancer
Speaker 1: and seem to transfer it between each other by shedding
Speaker 1: cancer cells into the sea, which is just disgusting. Um
Speaker 1: has made me rethink my idea of swimming. But there's
Speaker 1: some really incredible examples of transmissible cancers in nature. And
Speaker 1: again I think the more we look, the more we're
Speaker 1: going to find. You know, each one of these papers
Speaker 1: just gets published and less and less impressive turn or
Speaker 1: is more and more more and more turn up. But
Speaker 1: there are some examples in humans, and I talk about
Speaker 1: a couple in the book. So there's one which is
Speaker 1: they're absolutely horrendous. Is a guy called Chester Southam who
Speaker 1: was in New York, I think in the fifties, and
Speaker 1: he was doing experiments on prisoners, mostly black prisoners in
Speaker 1: the US people in care homes can existing cancer patients.
Speaker 1: People are very desperate and not consenting to these experiments properly.
Speaker 1: And he was putting cancer cells into them and in
Speaker 1: some cases they did developed humors. Mostly they didn't, which
Speaker 1: shows the human immune system will fight these cells off,
Speaker 1: but some of them did. And also there's a very
Speaker 1: sad story of a woman who developed melanoma. And at
Speaker 1: the time, this is around about this the sixties. I
Speaker 1: think it was an idea that you could transplant some
Speaker 1: cancer cells into someone to get an immune reaction going uh,
Speaker 1: and then give that kind of blood back to the
Speaker 1: patient and it would help to treat their cancer. It's
Speaker 1: sort of an early idea immunotherapy, so basically getting someone's
Speaker 1: donor immune system to generate some antibodies to neutralize the
Speaker 1: cancer when you donated them. And so this woman's mother said,
Speaker 1: all right, I'll do this. You transplant me with a
Speaker 1: bit of my daughter's cancer. I'll generate the antibodies, and
Speaker 1: then you can take my blood and give it to her.
Speaker 1: And unfortunately, the daughter actually passed away very quickly, and
Speaker 1: a few weeks later it was discovered that the mother
Speaker 1: actually did have the cancer growing in her, and and
Speaker 1: then shortly after that the mother passed away from the
Speaker 1: cancer that had killed her daughter. And you're like, it's
Speaker 1: rare and probably because they were related. You overcome the
Speaker 1: problems of immune rejection, but you're like, ohhs, well, it
Speaker 1: could happen. Ah. And then there's the most absolutely disgusting one,
Speaker 1: which is this is really sad and awful but also gross. Um. So,
Speaker 1: there was a man who walks into an HIV clinic
Speaker 1: in Colombia complaining of feeling very unwell and so HIV
Speaker 1: for a long time, so his immune system was very suppressed.
Speaker 1: He hadn't been taking his medication, and he was feeling
Speaker 1: very unwell. And they looked in his body and they
Speaker 1: found all these little nodules in his body and and
Speaker 1: they were like, well, these don't look like human cells.
Speaker 1: This is very weird. And they were well, maybe it's
Speaker 1: a parasite or something. And they gave him some some treatment,
Speaker 1: and he went away and and he came back in
Speaker 1: his life, it's still no better, and there's more and
Speaker 1: more of these weird things. And they looked more closely,
Speaker 1: they got them analyzed, and it was he'd been infected
Speaker 1: by tapeworm. But the tape worm had a cancer and
Speaker 1: the cancer had infected the man, and you're like, whoa,
Speaker 1: that is a just the stuff of nightmares. Um, be
Speaker 1: highlights how powerful the human immune system is at the
Speaker 1: best of times. And see is like, oh my god.
Speaker 1: You know, also tape worms can get cancer, so it
Speaker 1: sort of highlights a lot of the principles at work here.
Speaker 1: And very sad for that man, but unfortunately he couldn't
Speaker 1: be treated in the time. Um but it's like, this
Speaker 1: is an incredible biological phenomenon really, that we were only
Speaker 1: just starting to understand. Yeah, I mean, these are all
Speaker 1: just unbelievable examples and and go in the column of
Speaker 1: you know, the case you make that we should shift
Speaker 1: towards that thinking of cancer in an evolutionary and ecological
Speaker 1: way instead of a purely molecular way. So if that's
Speaker 1: the dark side, what about thinking about cancer in an
Speaker 1: evolutionary and ecological way gives you hope? Do you see
Speaker 1: lines of research extending from that framework that give you
Speaker 1: hope for the future and of cancer treatment and and
Speaker 1: the fight against cancer? Yeah, so you know, you can
Speaker 1: get very sort of nihilistic about this, and I oh yeah,
Speaker 1: resistance always emerges. Evolution is so powerful. But then I
Speaker 1: look at the kind of researchers that are really getting
Speaker 1: to grips with evolutionary therapy, and it's a growing bunch.
Speaker 1: It's all started, particularly, I think, from the Mopic Cancer
Speaker 1: Center in Tampa and Florida and a man called Bob
Speaker 1: Gattenby and his team there, and they are just really
Speaker 1: incredible people. So, I mean, I'm a biologist, I am biased,
Speaker 1: I will say against mathematicians and physicists. But it turns
Speaker 1: out the secret the secret weapon in the war on
Speaker 1: cancer is maths. So there you go. So he's brought
Speaker 1: together all these mathematicians and biologists and they're actually doing
Speaker 1: evolutionary modeling on cancer populations, trying to understand the rise
Speaker 1: of the fall of resistant and sensitive cells, trying to go, Okay,
Speaker 1: if if resistance is going to emerge when you treat,
Speaker 1: can we predict how that's going to happen? How do
Speaker 1: we kind of let cell populations balance them cells out
Speaker 1: and stay in control rather than just you know, nuke
Speaker 1: it from orbit, which is kind of the conventional idea
Speaker 1: about cancer therapy. And so they've they've done a most
Speaker 1: successful clinical trial so far is in prostate cancer. And
Speaker 1: it's it's an absolutely fascinating trial of an approach that
Speaker 1: they call adaptive therapy. And the way it works is
Speaker 1: you assume that within any cancer at any size, there
Speaker 1: are going to be sensitive cells to the drug and
Speaker 1: there's going to be resistant cells to the drug. And
Speaker 1: it's a drug called abbiratarone that they use, and so
Speaker 1: what you do is you you also have to have
Speaker 1: a marker that will tell you how much tumor is
Speaker 1: in anyone's body at any given time. And for prostate cancer,
Speaker 1: we have quite a good marker. It's called p s A.
Speaker 1: So you can look at someone's p s A level
Speaker 1: in their bloodstream and say, okay, that's a proxy for
Speaker 1: how much cancer is in their body. And so they
Speaker 1: start eating this these men with prostate cancer advanced prostate cancer,
Speaker 1: so they're there. Probably their their life expectancy is about
Speaker 1: eighteen months on this drug before it starts to get
Speaker 1: really gnarly for them. And and they treat them with
Speaker 1: this drug and it starts to work and their tumors
Speaker 1: start to shrink, and then the difficult bit is you
Speaker 1: wait till it's shrunk to half the size it was
Speaker 1: and then you stop treating and you wait. So the
Speaker 1: idea is you've knocked down all the sensitive cells, or
Speaker 1: as many of them as you. You feel the urge too,
Speaker 1: and there's still some sensitive cells there which are keeping
Speaker 1: the resistant cells in check. And then you wait and
Speaker 1: you wait for them to grow back. But because being
Speaker 1: resistant to the drug is kind of it's it's it's
Speaker 1: not very good for you, these cells are less fit,
Speaker 1: they struggled to grow as much. So it's the sensitive
Speaker 1: cells that grow back as so you treat them again.
Speaker 1: And so you ride this kind of roller coaster of
Speaker 1: start the drug, let the tumor shrink, stop the drug,
Speaker 1: let the tumor grow. Start the drug, let the tumor shrink.
Speaker 1: And they have men who have been on this regime
Speaker 1: for four years. I mean gradually in the end the
Speaker 1: tumor does, the cancer does start to evolve because that
Speaker 1: population of resistance cells does start to get bigger, very
Speaker 1: slightly every time. But this is you know, if this
Speaker 1: was a drug and you were saying, I've gone from
Speaker 1: average eighteen months through to four years, you know, if
Speaker 1: this was a drug, the industry would just be throwing
Speaker 1: itself at trying to to get this you know, get
Speaker 1: this to the clinic, get this to work, get this
Speaker 1: to everyone. So that was that was a really powerful
Speaker 1: demonstration of an evolutionary therapy of understanding and accepting you've
Speaker 1: got these cell populations in there and they're kind of
Speaker 1: how to balance them. There are other sort of adaptive strategies,
Speaker 1: evolutionary strategies. There's one called the Suckers gambit, which is
Speaker 1: where you treat cancer cells with a drug that you
Speaker 1: want them to develop evolved resistance too. But you know
Speaker 1: that for them to have evolved resistance, they have to
Speaker 1: have activated certain molecular pathways, they have to have gone
Speaker 1: down an evolutionary route in one direction, and then you
Speaker 1: hit them with another drug that they can't get out of,
Speaker 1: so you're sort of you you get them into a
Speaker 1: blind evolutionary end. It's like a double punch, yeah, exactly.
Speaker 1: You know, there's there's lots of ideas out there about
Speaker 1: using the drugs we have, maybe even using drugs that
Speaker 1: are less you know, less good. I suppose less potent, less,
Speaker 1: less toxic, because you don't want to just nuke everything.
Speaker 1: You want to start thinking about how to balance cells,
Speaker 1: how to control cell populations. But this comes to the
Speaker 1: really difficult thing, which is the psychological element of this,
Speaker 1: because this is not the cure for cancer that we
Speaker 1: were promised. This is not the magic bullet. This is
Speaker 1: not eradicated from your body. There may be some approaches
Speaker 1: where we actually can and you know, the earlier you
Speaker 1: can diagnose cancer if you can treat it with surgery. Um,
Speaker 1: some cancers can be treated really effectively and cured at
Speaker 1: an early stage. But for cancers, once that evolutionary process
Speaker 1: is really kicked off, you have to approach them with
Speaker 1: an evolutionary mindset, and that may mean driving them to
Speaker 1: extinction with the right combination of sort of extinction events
Speaker 1: at the right time. Um. But it's a it's not
Speaker 1: going to be this kind of perfect cure that I
Speaker 1: think people want that we've been led to expect, and
Speaker 1: it certainly won't be one magic bullet drug that like, Yep,
Speaker 1: that's it, that's that's the cure. That's it. We can
Speaker 1: now sell this and give it to everyone because as
Speaker 1: I said, you know, every every individual cancer is a
Speaker 1: is a one off, it's a special snowflake. It's an
Speaker 1: individual evolutionary event. So we need to understand that where
Speaker 1: is it going what's it doing, what are what are
Speaker 1: the contingencies in there? And how can we either drive
Speaker 1: this cancer to extinction or drive it to a place
Speaker 1: where we can control it for the rest of someone's
Speaker 1: natural lifespan. And you know, that's not a cure for cancer,
Speaker 1: but to me, that's you know, I think that's getting there. Yeah,
Speaker 1: I really like that thinking of the body, not like
Speaker 1: as a malfunctioning car with a part that needs to
Speaker 1: be replaced or fixed, but as an environment with natural
Speaker 1: populations within it that in the relationships between them need
Speaker 1: to be managed. Yeah, sort of tending the garden is
Speaker 1: the idea, but you can take the ecological thing further.
Speaker 1: There are different sorts of cancers. You know. Some are lush,
Speaker 1: exotic rainforests that are really going for its summer arid deserts.
Speaker 1: Some are more like, you know, kind of neatly tendered gardens.
Speaker 1: But we've got to understand what each person's cancer is
Speaker 1: really like and how it's behaving, not just a shopping
Speaker 1: list of mutations that you can try and fire magic
Speaker 1: bullets at, but a much more holistic understanding and accepting
Speaker 1: that evolution is going to happen, always has done. That's
Speaker 1: why we're here, that's why the diversity of life is here.
Speaker 1: But if we can harness it and work with it,
Speaker 1: then I really think we can start to make some
Speaker 1: progress in in some of these most difficult advanced cancers. Alright,
Speaker 1: I guess we will wrap it up there. But again,
Speaker 1: the book is Rebel Cell. It's a fantastic reed. We
Speaker 1: we really think you'll like it. And also you can
Speaker 1: check out cats podcast, the Genetics Unzipped podcast. Is there
Speaker 1: anywhere else they should look for your work right now,
Speaker 1: Cat um, my first book, Herding Hemmingway's Cats, is available.
Speaker 1: I've got another book called How to Code a Human
Speaker 1: and you can find me at on Twitter. I'm Cat
Speaker 1: underscore Arnie. Pretty much yeah, every everything is pretty much there.
Speaker 1: All right, Well, that does it. Thanks again to Cat
Speaker 1: Arnie for joining us for this discussion. Again, if you're
Speaker 1: trying to look her up, you can find her on
Speaker 1: Twitter at at k A T Underscore A R N.
Speaker 1: E Y. And if you're looking for her book, Rebel
Speaker 1: Cell Cancer Evolution and the New Science of Life's Oldest Betrayal. Uh.
Speaker 1: The UK version is coming out on August six. The
Speaker 1: US version is coming out on September twenty nine. You
Speaker 1: can pre order now, I believe, If not, keep an
Speaker 1: eye out for it, and you can also look it
Speaker 1: up on her website at Rebel cell book dot com
Speaker 1: or check out her work on the Genetics on Zipped
Speaker 1: podcast at Genetics n zipped dot com. It's just such
Speaker 1: a great book title. I just keep coming back to
Speaker 1: how much I love that book title. It really is
Speaker 1: great and uh and it has some resonance throughout the
Speaker 1: book with some other themes and metaphors she discusses in there,
Speaker 1: such as the Society of Cells. So, Robert, I really
Speaker 1: do recommend you read it if you get a chance.
Speaker 1: I I really enjoyed this one, all right. I'll have
Speaker 1: to look for in September. In the meantime, Yeah, everyone
Speaker 1: out there would like to listen to additional episodes of
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Speaker 1: Huge thanks as always to our excellent audio producer Seth
Speaker 1: Nicholas Johnson. If you would like to get in touch
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