Cancer as a Dynamical System – June 2nd to June 4th 2010, Tempe

A Mountain- Tempe Workshop - June 2010Understanding cancer in the context of evolutionary biology, how neoplasms evolve within the host organism, the nonlinear feedback between cancer cells and stroma, and how cancer behaves as a complex adaptive system. Emphasis will be on the application of dynamical systems theory, game theory, systems biology and related fields of inquiry to cancer and its progression to malignancy. The goal of the workshop is to determine how tumor growth, tissue invasion and metastasis might be understood and even controlled via these dynamical properties.

Listen to Audio Interviews and Read Transcripts

Audio Interviews from the Workshop

Interview Transcripts

Interview with Athena Aktipis

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Athena Aktipis: I’m Athena Aktipis I have a Ph.D. in Psychology. I studied evolutionary models of cooperation for my Ph.D. and now I’m applying those ideas to understanding cancer.

Pauline Davies: Well that’s quite a leap from psychology to cancer. Was it easy to make?

Athena Aktipis: Well I’m still making it. So I think there’s a lot of really important insights from thinking about both our psychology and how we perceive cancer, but then also thinking about what cancer is like in terms of its features as a social entity, because cancer cells are in contact with other cancer cells through sort of direct touch and also through lots and lots of signaling systems. So there’s actually quite a bit going on at the level of decision making in terms of the cancer cells themselves. So I think there is a wide-open arena for doing some interesting work.

Pauline Davies: I guess you had to learn a lot of biology before you could get on top of this subject?

Athena Aktipis: Yeah and I still am. So it’s a long process and I’m learning the pieces that are most relevant to the areas that I’m studying. So one of the things that I’m particularly interested in is migration and metastasis. So I’ve been trying to learn as much as I can about what makes cells gain the ability to move, what makes them disconnect from the cells that are near them to go on to a new environment, and what they’re responding to in their environment that causes those changes.

Pauline Davies: What are you going to be talking about today?

Athena Aktipis: Today I’m going to be talking about how on one hand we see cancer as being smart on some level, and that’s a result both of us ourselves being organisms that have evolved in a very social world so we see things as social; we see entities as having intention. So we see cancer, if it comes up inside us or if you’re a doctor and you see it in your patient, you have a tendency to think about it as a social entity that may be intelligent or smart or doing things in response to what you’re doing, and if we try to break that down and think “Well what is it that actually makes cancer look smart to us?” There are two fundamental things: one is that cancer is a population of billions of cells that are reproducing and they’re evolving constantly. So if we do things to a tumor, it’s going to look like it’s responding when really what’s happening is that selection is acting. So I think at the population level what we think we see is cancer being smart when really what we’re just seeing is evolution going on at the population level. But there’s another way that cancer cells might be smart and that’s in the fact that they can conditionally respond to their physical and social environments. So a single cell can change from being a sedentary cell to being a motile cell if it’s in a region that has low oxygen. So I think that it’s important when we’re thinking about cancer and we’re conceiving of it as smart, and we’re then trying to counteract what we think of as its dangerous effects, to really consider why are we seeing it as smart and then how do we interfere with the mechanisms that are actually leading to that particular kind of smart looking behavior on the part of the cancer cells.

Pauline Davies: So this is a rather new approach. How is this going down with cancer biologists?

Athena Aktipis: Yeah, so this is a new research program that I’m working on now with Carlo Maley and Steve Neuburg here at ASU and Virginia Kwan here at ASU also, and they’re both social psychologists. We’re trying to basically come up with a systematic research program to evaluate first of all what are the biases that shape how we think of cancer, and how do they relate to how patients perceive their cancer and how clinicians approach cancer, how researchers think about solutions to problems relating to cancer and then can we actually give researchers and clinicians tools that may improve the way they’re approaching cancer that take into account the fact that we have certain biases when we’re interpreting the behavior of cancer: to think about it as a social entity that’s smart, that may have a particular essence to it that we’re responding to and we may feel disgusted by it because its activating our disgust response system because it’s something that’s invading our bodily space. So I think there is a lot of potential but its work that’s really yet to be done.

Pauline Davies: How are you enjoying this workshop?

Athena Aktipis: I think it’s wonderful. This is my favorite kind of environment to interact with other academics where you have presentations of information that are relatively short and lots of opportunities for discussion. Not just at the end but very readily being able to interrupt, when someone’s talking, ask a question. That’s a really nice way to get an exchange of ideas that really flows rather than have it be very structured.

Pauline Davies: It consists of lots of different people from different backgrounds. Is that a positive benefit for you?

Athena Aktipis: I think it’s great. I mean anytime you’re bringing people together who have lots of different background knowledge, occasionally you run into difficulties, but I think those difficulties are far outweighed by the benefits of having people with different perspectives, organizing frameworks and just asking different kinds of questions, I think that’s really valuable.

Pauline Davies: What’s been the question that’s caused you to think the most?

Athena Aktipis: The question that caused me to think the most. I think, what is really going on when cells in a tumor or micro-tumors that are nearby are interacting with one another in terms of the competition versus cooperativeness and in particular one of the suggestions that was made today was that perhaps we want to enhance the competition that’s going on within tumors or even between tumors. And I think it’s a really complex question, and its not really clear to me whether its better to sort of enhance the competition within tumors so they kill themselves off or whether we want to sort of take all the weapons away from all of the cancer cells for even fighting with one another. That’s a question that I think I’ll sort of be stewing on for quite a while and probably the answer will depend on the type of cancer and maybe the environment that the cancer evolved in.

Interview with Carlo Maley

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Carlo Maley: I’m Carlo Maley. I’m a evolutionary cancer biologist.

Pauline Davies: Did you start off as a biologist or did you come to this from a different field?

Carlo Maley:I actually started off as a computer scientist and an evolutionary biologist and then came into cancer after I got my Ph.D.

Pauline Davies: So tell me what you were talking about at this workshop?

Carlo Maley:We were talking about the mutability of cancer. How it changes over time when we apply therapy or other selective pressures to it.

Pauline Davies: By understanding that you hope to intervene in some way at some stage?

Carlo Maley:Well this has been the central challenge in curing cancer, is that every time you apply a drug to it you select for resistant cells just like spraying pesticide on a field and selecting for resistant pests. If you do that enough time pests will evolve that are resistant to your pesticide. When you do this in cancer you apply a drug to the tumor and you select out the resistant cells that are resistant to your therapy. So we are trying to understand how to avoid that. That’s the central problem in curing cancer these days.

Pauline Davies: As you said that is a problem but yet most patients are treated with chemotherapy. Is there something going on that shouldn’t be going on?

Carlo Maley:Well I would say there hasn’t been a lot of work yet in understanding the nature of the therapeutic resistance that evolves and then better strategies for avoiding that. That’s just starting now and a lot of the people at this workshop were discussing how to do this work better.

Pauline Davies: Have you got any ideas that you can tell me about?

Carlo Maley:Oh sure the simplest one is because this process of resistance to therapy is an evolutionary process, if you could slow down the rate of evolution you could actually slow down the rate of relapse and people could live much longer before their tumors emerge again, evolve, come back after therapy. So we’re thinking about what determines the rate of evolution, what interventions, what drugs, what kinds of things we could do to slow that rate.

Pauline Davies: What ideas have you got about slowing the rate of evolution?

Carlo Maley:Well one of the basic things that drives this rate of evolution is the mutation rate. So if you could slow down the mutation rate you could actually slow down this process and one of the things that causes mutations in cancer are exposures like smoking, but also we think inflammation causes mutation to the production of reactive oxygen species and oxygen radicals as you probably have heard. In some cancers it looks like taking anti-inflammatory drugs like aspirin seams to at least prevent cancers. There’s a whole other story here, which is the process of getting cancer is also an evolutionary process. So if you could slow that down we wouldn’t get cancer until our hundreds or hundred and twenties, whatever it is we could live to. So one path to reducing the mutation rate would actually be in reducing the inflammation, probably more important in early tumor development rather than in late stage cancer.

Pauline Davies: You just mentioned though that it would be much better if we could prevent people getting cancers in the first place. Apart from the obvious things that we all know about, what sort of clever techniques are scientists coming up with?

Carlo Maley:Oh well I think the obvious things are still the most powerful, that is not smoking and eating diets that are rich in fruits and vegetables, exercising etcetera. People are trying to come up with drugs that will either kill early cancer cells or prevent the process from taking off. That’s still very early work although there is a lot of interest in that field. One of the big challenges is that you don’t know who would have gone to get cancer in the first place, so if your drugs have any kind of toxicity, if they cause any damage of their own, you might be doing more harm than good. So the bar is much higher in cancer prevention. In cancer therapy the person is going to die soon anyway unless you intervene so you can tolerate, its ok if your drug has some toxicity, its better than dying the next few months.

Pauline Davies: So I know that you were talking some clever science in the meeting. Can you just elaborate a little bit?

Carlo Maley:Sure I mean I think some of the most exciting things were actually discussed by John Pepper today, in terms of asking what it the immediate cause of death in a cancer patient, its not the cancer cells per se, its your immune system collapses and you get an infection or cancer seems to be triggering a starvation response called cachexia and there’s good arguments for intervening in the immediate cause of death, not trying to kill the cancer cells, just trying to prevent the death of the patient or the morbidity in the patient, the painful side effects of cancer. If you don’t kill the cancer cells then you don’t select for resistance and you might be able to live with cancer for decades and make it a chronic disease rather than an acute disease and I think that’s an exciting area that there’s been very little work on it and I think there’s strong reasons to believe we could make a lot of progress in that area.

Pauline Davies: Do you think that your background as something other than a cancer biologist is beneficial in your work nowadays?

Carlo Maley:Oh very much so. I think my big contribution, the reason I’m able to add anything to the conversation in the research about cancer is that I have an evolutionary biology background. Most of cancer researchers do not have an evolutionary biology background and so there’s been a blind spot in terms of addressing the evolutionary dynamics of the cells within tumors and its just now becoming recognized as an important field that we need to expand because this evolutionary process is fundamental both to how we get cancer and why we haven’t been able to cure it. So there are a lot of exciting tools from evolutionary biology that we can bring into cancer biology and cancer research.

Pauline Davies: I’ve been realizing that the chemotherapy regimes that are used at the moment seem to be very blunt instruments, that maybe we ought to take more care and look at each individual person and their cancer.

Carlo Maley:Yeah the traditional chemotherapies attempt to kill every proliferating cell in your body and because the cancer cells proliferate more that your normal cells that it has some therapeutic benefit, but your entire digestive track sloughs off and your hair falls out and as we all know its extremely painful and awful experience to go through. More modern therapies try to target the cancers cells particular mutations in cancer cells or particular aspects of the cancer cells that distinguish them from normal and are hopefully less toxic. Unfortunately both forms select for resistance, but one of the things that’s been talking about a lot is what’s called competitive release in ecology, that is if you kill off all of the competitors, in this case all the sensitive cells in a tumor, then its much easier for the resistant cells to proliferate because now they’re no longer limited by space or the resources that their competitors were taking up. So in some cases we think we see this in the clinic that after therapy patience relapse very quickly we can’t treat the relapse tumor very well.

Pauline Davies: How important do you think it is for cancer biologists to know something about evolution?

Carlo Maley:Oh actually I think its critical because it’s the fundamental process driving these hard problems in cancer and so in fact I think for everybody involved both patients and doctors and researchers, its important to understand and address these kinds of evolutionary processes and its an example of why evolution is relevant to our everyday lives and touches all of us, both in cancer as well as infectious disease.

Pauline Davies: What are you getting out of a workshop like this where they have people from different disciplines?

Carlo Maley: Oh it’s really a great environment to generate new ideas and bring ideas in from different fields that we hadn’t even heard of before and strike up new collaborations and open up whole new research fields that we hope can drive progress in defeating these diseases.

Interview with Charley Lineweaver

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Charley Lineweaver: My name is Charley Lineweaver I am associate professor at the Australian National University and I have a joint appointment at the research school of astronomy and astrophysics and the research school of earth science is there. I consider myself to be an astrobiologist and a planetary scientist and a cosmologist.

Pauline Davies: So what does someone with your background have to bring to cancer research?

Charley Lineweaver: Well I guess one thing is data analysis. What I’ve been trained to do as a physicist is to take a data set and look for patterns in that data set, almost arbitrarily complex data sets and for example in astronomy we have elemental abundances and we want to know if a particular star has a certain elemental abundance, what types of stars contributed to that final product. Data analysis is really something that translates well, you can analyze exoplanets you can analyze cosmo microwave background fluctuations. Science in general relies on math in many ways and data analysis in almost every way and so cancer research is something where there’s an ever increasing data set that’s beautiful and getting every more and more sophisticated as gene sequencing techniques get cheaper and so they have a need for data analysts. So there are a lot of similarities. Chi-squared to fits for example is one of the simplest forms of data analysis that is everywhere in science.

Pauline Davies: Have you considered the problem of cancer before?

Charley Lineweaver: Not really except that I know that it’s a common problem and my mother died of cancer about three years ago but the details of cancer I was almost completely ignorant of until I got this invitation to contribute to this meeting and so I bought the best book I could on the biology of cancer and I’ve been studying hard to prepare myself for the jargon and the vocabulary that’s being used, you know d-differentiation for example and p-53 and tumor suppressors and all of the things we talked about today. I mean once you know the vocabulary you can at least try to pick out the hidden assumptions that sometimes they seem crazy and other times there are some reasons for them, I guess my job is to say that doesn’t make sense or this makes sense or some assumptions that I guess a reasonable scientist would be the first to question. I think in physics we question our assumption with much more rigor than biologists are used to and I think that’s probably one of the most helpful things that physical scientists are doing here.

Pauline Davies: Can you identify any barrier to communication between the different disciplines?

Charley Lineweaver: Yeah, as a theoretical physicist or a data analyst I mean we have a very objective stance that we take and we can afford to play around with ideas with a lot of freedom. I think the biologists, at least or the clinical oncologists here, are dealing with people who are dying tomorrow and they are throwing poorly thought out solutions but the best they can come up with at the problems because it has to be an immediate solution. You can afford to think laterally and have fun if you know somebody’s life doesn’t depend on it. So physical scientists are not used to having life threatening results coming out of their thoughts and so they have a certain flexibility to them. While if you’re really under pressure and tense and if, it’s kind of like you know choking, if you take a test and think, “Hey, this person is going to die if I fail,” well then you’re unable to come up with that weird solution that you might be if you say, “Oh well who cares, lets see it might be this is might be that,” and that’s also something I think that physical scientists can give to the more time constrained, well financed but essentially locked mindset of some of the oncologists.

Pauline Davies: What was the reaction to your talk?

Charley Lineweaver: Oh I thought it was a very positive reaction. The name of my talk was, The Perspective an Astrobiologist has on Cancer, and so it really was a big picture, here’s the evolution of life, here’s how multi-cellularity fits into that evolution and here’s how cancer fits into multi-cellularity. So really was a 30,000 feet view of what cancer is about and how it can be understood, and I guess the main insight, well one of the insights I think was because cancer dies and doesn’t continue, the apparent evolution of resistance of cancer is a limited thing. It cannot carry on because once the patient dies the next person that gets cancer does not have the advantage of all the resistance that the cancer could have evolved while it was in a previous individual. So the ability of cancer to evolve is severely limited, although it seems like its unlimited, that cannot be the case, and so I think that understanding that cancer is not a moving target because its not adaptive it gives people who are working on this very complicated problem I think hope that they will eventually solve it particularly given the incredible increase in the rate of data acquisition. I just have a few suggestions about what kind of data should be acquired, and I was you know appalled at the lack of the ability of people who are studying human cancers to understand that the study of cancer of other species not just mice models, but you know chimpanzees, primates in general, other multi-cellular creatures even fungi and plants that their adaptations or how they prevent cancer or why they do or do not get cancer those are questions that they haven’t even thought about because they’re so interested in solving human cancer and I think well to solve human cancer you need to have an understanding of what it is by comparing it to other types of cancer.

Pauline Davies: Now you said that you’ve read the text books in preparation for this meeting, do you think you’ll go home to Australia and consider cancer more?

Charley Lineweaver: I’m definitely getting an education here. I came here with a bunch of half-baked ideas and now that bunch has been narrowed down to a few and they’re now more baked, they’re more developed and more sophisticated and I know how to express them. I know what is known and what is not known about, well at least I have a better idea of what is known and what is not known. I also have a better idea of some of the insight and myopia of people who are practicing oncology.

Pauline Davies: So will you continue?

Charley Lineweaver: Oh yeah definitely, in fact I’m going to my room right after this and finish reading this textbook, Biology of Cancer by Weinburg, and it’s a very good textbook, I’m learning a lot and I think it will help me later on understand, I mean heck what fraction of all people die of cancer, maybe I’ll die of cancer and at least I’ll know what I’m dying of, when it happens. So that’s a little bit of an advantage – maybe it is, maybe its not. It’s definitely an important problem and in physics we’re not used to dealing with problems that have so much influence and impact on people. We’re used to dealing with problems with electrons and protons and dead things and to have applications of your expertise in ways that can be possibly meaningful is kind of rewarding.

Interview with Tibor Antal

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Tibor Antal: My name is Tibor Antal and I’m a statistical physicist by training and I started working on cancer a couple of years ago and I am interested in stochastic models of tumor progression.

Pauline Davies: What are stochastic models?

Tibor Antal: Stochastic models are models where randomness had a big role. And most people believe that in cancer and tumor progression, randomness has a huge role . With each mutation you get, when did you get these mutations.

Pauline Davies: How does statistics help us understand cancer?

Tibor Antal: Statistics is typically knowing some average and not knowing the details and in physics, statistical physicists use this thing and they know things; they can think about a gas and know averages like knowing the pressure and the temperature of this gas but not know how individual little molecules are moving. And in cancer you have many cells, millions, billions of cells, and knowing, assuming some rules as to how the cells behave, one can try to understand how the whole tumor behaves, and know something about the whole tumor without following individual little cells.

Pauline Davies: Are you looking at some particular property of cancer cells?

Tibor Antal: I’m looking at how tumors are turning from a benign state to a malignant state and how they evolve and how they acquire new mutations and how this turns the tumor to malignant cancer.

Pauline Davies: Describe the process of your study, you presumably don’t get the sample yourself to play with, do you?

Tibor Antal: Right, I work with experimentalists and we discuss and we try to set up models and then try to work on these models and solve these models and then try to compare the predictions of these models to what they see in clinical data or in experiments.

Pauline Davies: So you’re playing around with numbers on the computer to design a system that looks a little bit similar to what they’re discovering in patients?

Tibor Antal: That’s right. Or try to do it even on a piece of paper with a pen next to playing on a computer.

Pauline Davies: What sort of insights have you got?

Tibor Antal: I think the main benefit is, if you find a model, which explains a couple of features of tumor progression, it helps you think about this whole process and you have like a model in your head and it helps you think and helps you predict things and compare other things. So we are in the process of building a model and I think that’s the biggest insight by now in that it gives you a model to think about these problems.

Pauline Davies: Does your model have any particular features that you can describe to me?

Tibor Antal: Yes. We find that this tumors as they are evolving, they are getting worse and worse at an increasing rate. So at the beginning, from initiation of the tumor, you might have ten years or twenty years until it evolved into a cancer but as it starts evolving, this evolution is speeding up, it’s exponentially getting faster and faster. So at the beginning its evolving slower and then it starts evolving faster and faster and that’s clear from the model and that’s what you also see in clinical data. In a model it would be very easy to cure cancer because you just change a couple of parameters and cancer would be cured. The question is which parameters or how to change these parameters what other side-effects are there and so that’s a much more complicated program but its still I think helps thinking about the problem.

Pauline Davies: So it sounds like you’ll be kept in business for a long time to come?

Tibor Antal: Yeah I will have things to do for the next hundred years.

Pauline Davies: What attracted you to studying cancer?

Tibor Antal: One thing is that I think it is an important question. The other thing is that I think that I can use my expertise on these systems because I work always on stochastic models and many times stochastic discrete models, and here cancer is very stochastic and so very random and also discrete, so there you have cells which are individual cells which is a discrete process. So it’s a discrete stochastic process, so it fits into the line of work I was always doing.

Interview with Jasmine Foo

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Jasmine Foo: My name is Jasmine Foo and I am a postdoctoral scholar at the Sloan Kettering Institute, and I study mathematical models of cancer evolution.

Pauline Davies: Did you start off as a mathematician?

Jasmine Foo: Yes I started out as an applied mathematician and got into cancer about two years ago.

Pauline Davies: So what brought you to cancer study?

Jasmine Foo: Well I guess mainly two factors. One, as a mathematician a lot of times you work on problems that are really obscure and maybe only ten or fifteen people in the world understand or care about. So I was interested in getting into mathematical biology to work on more applied problems, ones that would be more relevant to our society. The other reason is that, when I was in graduate school my mom was diagnosed with and past away due to lung cancer and you know when I found out that there were opportunities to apply mathematics to helping to solve the cancer problem I was really interesting in getting involved with that.

Pauline Davies: What exactly are you working on?

Jasmine Foo: So one of the things I’m really interested in is using mathematics to kind of quantitatively and rationally design treatment scheduling for the goal of either your debulking of tumors most efficiently or to prevent or delay the emergence of resistance.

Pauline Davies: Are you making much progress?

Jasmine Foo: Well I hope so. One of the things that’s a major barrier to what we’re doing is the lack of data about parameters to inform our mathematical models. A lot of times biologists don’t necessarily do a lot of cell counting or quantitative measurements in their experiments so this requires sort of an extra level of effort, which we’re lucky enough to be involved with some collaborators now who are really excited about helping us to measure these parameters.

Pauline Davies: What do you think of this new initiative, the physics and oncology initiative, started by the NCI?

Jasmine Foo: I think it’s really great. It’s really been an eye opening experience for me to listen to all of the sometimes wild and crazy ideas that mathematicians and physicists come up with, with regard to approaching cancer. I think it’s exactly what’s needed to bring new ideas to the field.

Pauline Davies: You gave a talk today, what did you talk about?

Jasmine Foo: I actually talked about the idea of using treatment schedules or designing better treatment schedules to prevent or delay treatment resistance to targeted therapies. The main point I wanted to make was that resistance is only a problem if it occurs prior to the depletion of the sensitive cells in a tumor or prior to patience death due to other causes. So if we can delay resistance long enough than it won’t even be an issue.

Pauline Davies: There was a lot of very lively discussion afterwards. What sort of point resonated particularly well with the other people in the group?

Jasmine Foo: I only remember the points that didn’t resonate well. I think that one of the ideas that’s been batted around a lot that a lot of people seem to think is really important is the idea of heterogeneity in a tumor and the fact that you are going to have sensitive and resistant cell co-existing in a tumor, and its really important to quantify you know what are the selective pressures that are going to cause a more fit type of cell to out-compete and eliminate a lower fitness cell type.

Pauline Davies: That really hasn’t been studied by oncologists so much in the past?

Jasmine Foo: It really hasn’t been. You know when I got into the field that was one of the questions I kept asking people, you know how do we quantify resource limitation in tumors, and I think it’s really difficult to measure and so I think some of the other talks that we saw like the talk by Jim Elser, these people who are ecosystem ecologists, might have something really interesting going on measuring the amount of nutrient in a system quantitatively and seeing if we can get at what nutrients are limiting that way.

Pauline Davies: It seems that we shouldn’t be treating cancer as one disease, even one disease like lung cancer or colon cancer or pancreatic cancer, it’s a host of very different diseases with very little overlap it seems, genetically anyhow.

Jasmine Foo: Yes I totally agree. I think that every patience tumor is genetically different from the next patient and a patience response to a drug is different a patience metabolism of a drug is different. I definitely wouldn’t consider cancer to be one disease.

Pauline Davies: Finally how are you finding the meeting?

Jasmine Foo: I think the meeting’s been really great. I’ve really had my eyes open to a lot of interesting and new ways to think of things and especially for me coming from sort of a more of a traditional cancer research institute, where certain approaches to cancer are sort of pervasive, its been really fun for me to listen to people coming from completely different fields and listen to other peoples ideas and approaches.

Pauline Davies: Not too many of them being crazy ideas or maybe they are.

Jasmine Foo: I think crazy ideas are what we need and we’ve heard a couple and it’s been really fun.

Interview with Rory Staunton

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Rory Staunton: I’m Rory Staunton. I’m a first year physics Ph.D. student at ASU in the lab of Dr. Robert Ros and we’re studying cancer cells, the mechanics of cancer cells.

Pauline Davies What got you interested in studying cancer?

Rory Staunton: Well it’s something that impacts everyone. Everyone you know is dramatically affected by it and it’s a disease that also enables us to learn about regular physiology. How the pathology of cancer can illuminate fundamental biological principles of how life works.

Pauline Davies Did you learn much biology in your physics degree?

Rory Staunton: Not so much. I did take a biophysics course, but primarily the biology I’m just kind of learning a long the way as I go. There’s tons of it out there to discover and try and keep track of.

Pauline Davies What do you think physicists can bring to the study of biology?

Rory Staunton: I think physics is fundamental to all science and so the perspective of a physicist is really broad and general. Anything that demands quantitative analysis, physics is right there to try and make those descriptions accessible. The way that they think is actually applicable to pretty much all problems that are faced in science, including cancer.

Pauline Davies So are you enjoying learning about physics and cancer?

Rory Staunton: Definitely yea, I think there’s a lot of promise in this field so I feel like I’m right in the middle of this huge growth and convergence of different science and it seems like a good place to be.

Pauline Davies Tell me about your own project, what are you doing?

Rory Staunton: Well in a nutshell we’re looking at how stiff a cancer cell is and the main reason for that is because when a cell is soft it makes it easier for a cell to escape from is neighbors and one of the key points to metastasis, when cancer spread in your body, is that cells from a tumor have to leave that tumor and circulate through either the blood stream or the lymphatic system and when they do that then they can land and start a new tumor and that’s how cancer is thought to spread.

Pauline Davies So you need to actually study the stiffness of cells to see what’s going on?

Rory Staunton: Right. The stiffness of cells is important for a number of reasons for example a stem cell in a developing embryo is actually very soft and as the cells differentiate they become stiffer. So if you think an analogy between a stem cell and a cancer cell, the softer a cell is may be very importantly related to a cells ability to change its environment such as adapting to a different organ system. So there might be more than just the physical advantages of being soft in order to metastasize but also to adapt to new environments within the body that’s associated with that softness.

Pauline Davies So how do you go about measuring the stiffness of a cancer cell?

Rory Staunton: What we use is basically a tiny needle. It’s almost like a fancy record player, a very expensive one I might add. This needle is brought down onto the cell and basically used to poke it and our equipment basically tells us how stiff it is depending on how much force is applied, which we can measure with extreme precision, relating that to how far into a cell the needle travels.

Pauline Davies So this is very fundamental research, do you think it can ever be useful in treatment?

Rory Staunton: It would probably a little ways down the road before measuring the stiffness of cells directly from someone’s body would have practical diagnostic applications, but we are starting to see some connections as far as finding different drugs that might be especially effective in targeting cells that are softer in these regards that might make good targets in cancer therapies.

Pauline Davies What’s the best thing about your job?

Rory Staunton: I think the best part of the job is getting to work with the microscope and just it amazes me everyday to see cells and look at them as they grow even as they divide I’m actually probing them and imaging them, I like where I am, it’s a lot of fun and its challenging.

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