Professor Doug Hilton of the Walter and Eliza Hall Institute of Medical Research in Melbourne talks about identifying genes and treating genetic diseases.
Voice-over: Welcome to the National Health and Medical Research Council podcast series, a conversation with some of the great minds and leaders in Australian medical research. The NHMRC is Australia's leading funding body for health and medical research. We provide the government, health professionals and the community with expert and independent advice on a range of issues that directly affect the health and wellbeing of Australians.
Interviewer: Professor Doug Hilton is head of the molecular medical division at the Walter and Eliza Hall Institute of Medical Research in Melbourne. In 2007 he was awarded an Australian fellowship. His laboratory is primarily interested in understanding the molecular regulation of cell proliferation and differentiation. Doug, welcome to today's conversation.
Prof. Hilton: Thank you.
Interviewer: I thought we might begin by you describing this wondrous institution that you work in here in Melbourne.
Prof. Hilton: So we're sitting in my office on the fourth floor. It has a rather nice view. You can see we're next to Royal Park, so I have on one side a view of the park and on the other side a view of the Royal Melbourne Hospital and the university. And those two institutions are a really important part of the life of the Walter and Eliza Hall Institute.
Interviewer: Which is where we are today.
Prof. Hilton: Yes. Its nickname for the people who work here and a lot of people in medical research is ‘Wee-hi’, W-E-H-I ‑ so if I say that again, you'll know what I'm talking about. WEHI is one of the oldest medical research institutes in the country, it's about 90 years old, just over 90 years old; it has a history of doing research that matters, I guess. It's probably most famous for its work on blood cells, immunology, haematology and diseases of blood cells.
Interviewer: I noticed on your website, when it talks with the history it's got a quote from the person who opened it. I was reading that recently and thinking that those words are just as apt today as they were then.
Prof. Hilton: Yes, trying to create an institution in the Southern Hemisphere that would rival some of the great institutes that were around then in the Northern Hemisphere. And I think that's still a challenge. We're a long way away from a lot of the centres of medical research.
Interviewer: Yes, but this institution has made a huge mark in contribution to Australian research?
Prof. Hilton: Yes, it has. I think one of the exciting things about working in Melbourne, and one of the reasons the Hall Institute has been able to do well, is it's certainly not working in isolation. So essentially over the last 15, 20 years, there've been a number of institutes that have really risen quite dramatically in the quality and quantity of the research that they're doing and that's been just fabulous for WEHI as well.
Interviewer: It has to be a global effort, doesn't it?
Prof. Hilton: It does. And that critical mass of people thinking about the same sorts of problems, but maybe coming at it from a different angle is really important for the feel of the place ‑ the whole community. So there's a bit of a buzz down here.
Interviewer: There are lots of other institutions around here ‑ hospitals, and the Howard Florey institute just around the corner. So this area here is known as the Parkville strip.
Prof. Hilton: It is.
Interviewer: It is a real concentration ‑ you've got the Bio‑21 precinct next door and so forth.
Prof. Hilton: CSL up the road, so a mixture of hospitals, universities, medical research institutes, biotech companies, and it's very exciting.
Interviewer: Doug, what is your position within this institution. I mean, I understand you have a very interesting position?
Prof. Hilton: Yes, I'm the head of a newly created division in WEHI called the division of molecular medicine, and we can talk a little bit later about what that division is doing. I also have a chair at the University of Melbourne, an appointment at the University of Melbourne, which means that I can supervise some of the fabulous graduate students, the PhD students, that are coming across the road to us. And I have an NHMRC Australia fellowship, which is a new initiative of the NHMRC.
Interviewer: Yes, I see they were announced, was it last year?
Prof. Hilton: They were announced just a few months ago. So the initial round, the application round, started last year, and the announcements were made in the middle of the year.
Interviewer: Tell us what the rationale for creating these Australian fellowships was.
Prof. Hilton: I think from the NHMRC's viewpoint it was to highlight to the medical research community and to the general public and perhaps aspiring researchers that there was an opportunity to progress to a high level within medical research career in Australia and having identified, I guess, those high achieving medical researchers, to provide them with some additional funds to, I guess, increase the pace of their research.
Interviewer: That's fantastic.
Prof. Hilton: It was a really great honour and it's changed the way the lab's running, so it's been fabulous.
Interviewer: Now we walked through your lab on our way into your office here, and it seems to be very full ‑ lots of activity. Why don't you describe to us broadly the activities of your laboratory and then we'll focus on some of the current exciting stuff you're doing.
Prof. Hilton: Okay. So ever since I was an undergraduate student, I originally got into research by doing a summer project at the John Curtin School from Canberra, attached to ANU, and the lab that I went into was interested in how blood cells are produced and the genes that regulate the production of blood cells. And really for the last 22 years I've been working on the same thing. I found that very intriguing. So my goal has been to understand how we produce exactly the right number of blood cells every day. We need to produce trillions of blood cells. If we produce too few, we end up in trouble because we don't have enough red cells to carry the oxygen or white cells to fight infections. If we produce too many, then we can get diseases like leukaemia. So it was very clear that there has to be a balance and I've been very interested in how that balance has been achieved and that has led me down the track of trying to understand how cells talk to each other.
If you think of your body like a city, then for the city to function well all of the people in the city need to be communicating with each other, and that communication can occur at lots of different levels. So it can be, I like to call it the pillow talk level, where two very intimately associated people are talking at close proximity across a pillow or it can be mass media communication where a satellite is beaming Foxtel into many different homes in the city. And communication in the body occurs like that as well. So it can be very intimate, by two cells being next to each other, almost rubbing shoulders, or it can be a global message sent out by the body to all cells. And I'm interested in how those messages are sent and how they're received and how they're responded to.
Interviewer: And this process of production of blood cell types is called haemopoiesis.
Prof. Hilton: Haemopoiesis, and that occurs in your bone marrow.
Interviewer: Let's look at an illustration of what happens when you get an abnormal event, such as a leukaemia, occurring. Walk us through some of the signalling and communication that's going on in the body.
Prof. Hilton: Okay. So normally the body has ways of talking to the cells in the bone marrow, the cells that are responsible for production. So all of your different blood cells originate from a common precursor, almost like a great-great-grandfather cell. It's called a stem cell. That stem cell has a really important capacity, and that is it's capable of producing all of the cells you need today without exhausting your ability to produce cells you'll need tomorrow. And that, to me, is an amazing juggling act. And so that stem cell has to be regulated very carefully about the number of times that it and its progeny, its children, divide, because every time a cell divides you get twice the number of cells that you had before.
So a normal cell, a non‑leukaemic cell, has a very tight link between its division, its replication, and its differentiation ‑ and that's a fancy word for changing into a cell that does a specific job like carrying oxygen. That has to be very tightly coupled. If the cells keep dividing without differentiating, then you end up with a disease like leukaemia, whereas if the cell can divide and differentiate in unison, then you end up generating red blood cells to carry the oxygen.
Interviewer: Well, we'll talk about these stem cells to begin with. These are adult haemopoietic stem cells, I suppose is the correct phrase?
Prof. Hilton: Absolutely. And they've been known for 50 years. They are used medically, so people have stem cell transplants every time they have a bone marrow transplant, so there's nothing very controversial about those sorts of cells.
Interviewer: That's right. But now the neat thing is that those stem cells can produce, as you say, red blood cells which carry oxygen, platelets …
Prof. Hilton: Platelets that stop you bleeding to death.
Interviewer: The white cells, which are part of our immune system, and then the sub types of those.
Prof. Hilton: Yep.
Interviewer: What are those unique signals that tell a stem cell to produce one of those types?
Prof. Hilton: So a stem cell will produce all of those types of cells all of the time, and the trick that the body has to play is to make sure that it produces enough of each type. So, for example, if you've just cut yourself and bled, the body will want you to produce more red cells. It might not need more white cells at that time. So, for example, the way it will stimulate the production of more red cells is through a hormone, which is a protein messenger, that secretes it by the kidney, and the secretion of that hormone is linked to the oxygen tension. So the lower the oxygen tension, the more hormone is produced, and therefore the more red cells the bone marrow will produce.
Interviewer: The name of that hormone is?
Prof. Hilton: EPO.
Interviewer: Which we might know about from some athletes. So erythropoietin is the correct name?
Prof. Hilton: That's exactly right.
Interviewer: So that's the red blood story. What about if I get an infection? What happens then?
Prof. Hilton: That works slightly differently. When you have an infection, what you want is more white cells than you would otherwise need. And the way the body senses an infection is by monitoring for particular products that are produced by bacteria, for example.
Interviewer: Or viruses?
Prof. Hilton: Or viruses, and those products are products that are unique to the invading pathogen and they can be self‑surface components, for example, lipopolysaccharide is a self‑surface component of bacteria.
Interviewer: Do these stick out of the cell?
Prof. Hilton: They stick out of the cell ‑ humans don't have them, so when one of your white cells sees them, it recognises it as being foreign. And viruses have the same sort of thing ‑ double‑stranded DNA is recognised as a viral product and the body senses that and knows that it has to respond to an infection. And one of the ways the body responds is by producing white cell hormones called colony stimulating factors. And one of those, granulocyte ‑ and granulocyte colony stimulating factor and granulocytes are one of those types of white blood cells ‑ circulates back to the bone marrow and stimulates the bone marrow to produce more granulocytes or neutrophils. And granulocyte colony stimulating factor is not so much used by athletes, but it's used in the clinic to stimulate white cell production for patients that are undergoing chemotherapy.
Interviewer: I believe the Walter and Eliza Hall had a very important role in this with this particular hormone?
Prof. Hilton: Absolutely. So the scientists that I did my undergraduate work with and my PhD work with ‑ Don Metcalf and Nick Nicola ‑ were the scientists that discovered G‑CSF and really showed that this was a hormone that regulated white cell production and also were involved with the clinical trials at the Royal Melbourne Hospital, which we can see out the window, that tested the ability of this hormone to stimulate cancer patients to produce white blood cells and therefore overcome some of the side effects of chemotherapy.
Interviewer: And it's been taken into the clinic, hasn't it?
Prof. Hilton: It's been used in more than 3 million patients now, so it's a really wonderful Australian success story.
Interviewer: Though not a very successful commercial story.
Prof. Hilton: Well, that's interesting. There are two sides to that coin, because Don and Nick discovered two CSFs ‑ GM‑CSF, granulocyte macrophage colony stimulating factor and G‑CSF. They discovered GM‑CSF with their colleagues at the Ludwig Institute, and that was very successfully patented and commercialised and has led to many millions of dollars of income back into the country. So that was a wonderful success. G‑CSF was a situation where three groups basically discovered it and the Hall Institute didn't end up with the patent. That's life. So one out of two is not too bad.
Interviewer: No, that's right. Now, coming back to this communication in the body, I'm interested to understand what are these little molecules that are important in mediating this communication, and there are different types of these.
Prof. Hilton: There are. So you could almost think for all of the different types of cells in the body there are a number of different messages that need to be received. In some ways, each message is packaged up in a particular protein called a cytokine or a growth factor or a hormone ‑ and there are lots of different names for them.
Interviewer: But they're basically communication molecules?
Prof. Hilton: Yes. They're sent by one cell and received by another. One of the things I've been interested in is how cells receive the molecule, receive the message and interpret the message and make the right decisions about how to respond to the message.
Interviewer: Okay, so these little proteins, molecules, they whiz around in the blood, they communicate with other cells, telling them what to do and getting the communication going. But because they bind to the outside of the cell as the first point of contact, the real communication happens, and a series of actions happens, inside the cell.
Prof. Hilton: That's right.
Interviewer: This is where, I think, it gets more complicated.
Prof. Hilton: It gets a little bit trickier. So, for example, all of the different messengers are different shapes, and a cell can know that it needs to respond to a particular message by having a receptor on the cell surface that's matched to the shape of the message. So, for example, erythropoietin, EPO, the red cell hormone that we spoke about just before, has receptors in the cells in the bone marrow that are capable of producing red cells. So the white cells in the bone marrow don't have this receptor. So they know they can ignore that message. The cells that produce red cells, the precursor to the red cells, have the receptor. Therefore, when there's erythropoietin in the circulation, they can respond to the message and they can divide, produce more red cells. So in some ways it's pretty simple. And it's the same thing that occurs again in societies. Not everybody is responding to every message that's sent. There has to be some way of specifically sending the message to the person that you want to respond. We use that by having addresses on envelopes. Cells use it by having receptors on the cell surface. It's like a private mail box.
Interviewer: Now what happens when you open the mail box inside the cell and we start to decode the message that's being sent?
Prof. Hilton: That's a really interesting question, because from a cell's point of view there's a very, very long way between the surface of the cell and, in a sense, the brains of the cell, which is the nucleus, where the DNA is. And a lot of the mechanism by which the cell responds is by changing which genes are being used in the cell and therefore which proteins are being synthesised.
Interviewer: Okay, so we've got a protein binding to the cell, telling the cell that it's now going to actually communicate with its DNA.
Prof. Hilton: Yes.
Interviewer: Now, this is neat.
Prof. Hilton: This is neat. So there's a big gap between the surface of the cell and the nucleus where the DNA lives. And that gap is bridged by proteins that shuttle from the cell surface into the nucleus, and these are really the sensors between the outside environments and the inside environments of the cell. So as the cytokine or the hormone binds to its receptor, it changes the shape of the receptor inside the cell, and that can be done by bringing, for example, two receptors together in a process of dimerisation, and that change of shape inside the cell is recognised by these transcription factors.
Interviewer: You've mentioned a new word there, transcription factors. So these are the things inside the cell which then interact with the DNA; is that right?
Prof. Hilton: Exactly. So the transcription factors bind to particular parts of the DNA and turn parts of the DNA on.
Interviewer: Or offer?
Prof. Hilton: Or off. So that turning on or off of genes is how a cell ultimately responds to a signal. And the turning on of genes might be, for example, 'Please synthesise more proteins that are used to fight infection.' So it could be a very simple message.
Interviewer: Or more erythropoietin?
Prof. Hilton: Or 'Please turn on the proteins that will allow me to divide in a cell'.
Interviewer: So a lot more detail in that process and that's really what you're trying to tease out in many respects?
Prof. Hilton: Yes. So over the last 10 years, for example, one of the questions that we've been interested in answering is when a cell receives a signal, how long does it respond to that signal for, so how is the duration of the response controlled. And we found 10 years ago a really intriguing set of proteins that turned the signals off.
Interviewer: What are they called?
Prof. Hilton: They're called SOCS, or suppressors of cytokine signalling. So they turn one specific set of messages off.
Interviewer: So this is a feedback loop that's happening now?
Prof. Hilton: That's exactly right. It's a feedback loop. And it has some really important effects. I'll give you one example. One of the hormones that probably people will have heard of ‑ again because it's been used in sport ‑ is growth hormone. This is the hormone that is important for setting your final body size. So if you're a human being and you have a mutation in your growth hormone gene, you'll end up with short stature syndrome. If you have too much hormone, you'll end up having gigantism. So it's really important in setting the body size. What we did was to create a mouse that lacked the feedback regulator for growth hormone, and that feedback regulator is called SOCS‑2. What we found was when we deleted the SOCS‑2 gene in the mouth that it grew 1.5 to 2 times bigger, which is pretty spectacular. It may not sound a lot, but if you think of a human being that would be nine or ten feet tall rather than five or six feet tall, then you can see what a dramatic effect it had.
Interviewer: That's in a mouse ‑ was there an analog gene in the human?
Prof. Hilton: There is an analog gene in the human, almost exactly the same as the gene in the mouse, so that's an indication that this is an important process that is conserved across evolution. Naturally we haven't deleted it in humans to see if we can generate giant humans, but nor is there any link yet with disease in the humans.
Interviewer: So coming back to some of the current projects you've got in that busy lab outside there, why don't you get us excited about some of the things you're doing at the moment.
Prof. Hilton: One of the most exciting things that's happened in the last five years is that there has been sequencing of genomes and people must have heard about that, about the human genome project. That was an international consortia that aimed to find the sequence of every bit of the DNA that makes up a human. Well, that's only one part of the exciting genome projects, because there've been mouse genome projects and genome projects in lots of other model organisms. The DNA sequence of the genome of probably 100 or more organisms has been solved. That provides us with a really rich resource, because what my group outside the office is interested in doing is understanding how proteins form pathways. We've already talked about hormones and receptors and transcription factors, they're parts of pathways. Really my interest is in how we find the pathways that regulates different cell processes.
Interviewer: So tell us about some of the signature projects you're currently working on?
Prof. Hilton: Within my division, I'll tell you about a project that has been carried out by a new lab head in my division, a guy called Ben Kyle, in collaboration with another lab at the Hall Institute led by David Wang. What Ben and David were able to find was the genes that controlled, and the pathways that controlled, how long platelets last in the blood. Now red cells last about three months. White cells can last, some of them, for the entire life of the person, and that gives you your immunological memory. Platelets are a bit different ‑ they only last five days in the mouse and 10 days in the human. And that presents some real problems, because they need to be replaced. That's not just a problem for the body. It's a problem for organisations like the Red Cross blood bank, because platelets only last a few days in the blood bank, so they have to be replaced constantly, and that's a real logistical challenge. For 50 years there's been a puzzle about why these platelets, which are tiny little fragments of cells, last such a short time in the circulation. And using some very nice genetics and a bit of detective work, Ben and David were able to fine the proteins that regulated the lifespan, and showed in fact that platelets undergo cell death. And nobody had thought previously that cells without a nucleus undergo cell death.
Interviewer: So platelets are anuclear ‑ they're like red blood cells, they don't have a nucleus?
Prof. Hilton: They're even more different than red blood cells in the sense that they're tiny fragments of cells. Red blood cells are like whole cells from which the nucleus has been lost. Platelets are like a disintegrated cell. They're a tiny fragment of a cell, yet their lifespan is regulated in the same way all of the other cells in the body are regulated.
Interviewer: Yes, if you look at it under a microscope, they just look like dead bits of cell, as you say.
Prof. Hilton: Yes, little bits of dust.
Interviewer: That's right. Now how can something that's got ‑ what, has it got a mitochondria in there, a power house?
Prof. Hilton: There is some mitochondria in there, yes.
Interviewer: Is that what keeps it going?
Prof. Hilton: In part, absolutely, and the process of cell death is very much tied up with disregulation of mitochondria. The nice thing that Ben and David found was that if they delete the gene that is important for the survival of the platelet, the survival goes down, and it can be regulated over fivefold. So we have now mice in which the platelets last only one day instead of five days. But if they delete the proteins that are required for the cell death, then they can extend the life of the platelets.
Interviewer: Dare I ask you the name of these proteins that are responsible for cell death?
Prof. Hilton: They are called BCL‑2 family proteins. And they're the proteins that are disregulated in some cancers. So, for example, in certain types of leukaemia, the BCL‑2 protein is turned on and those cells now last much longer than they would normally. And that's an important step in the cancer process. So the same genes and processes that are used to regulate lifespan of cells in cancer are also used to regulate the normal lifespan of platelets, and that's pretty neat. That's exciting.
Interviewer: It also shows that they're probably very ancient genes?
Prof. Hilton: Very ancient genes shared all the way back to worms.
Interviewer: So of fundamental importance in growth and regulation?
Prof. Hilton: Absolutely. But more excitingly, I think, is not only does that discovery shed light on a really fundamental piece of biology, but it also opens up the possibility for now of manipulating the lifespan of platelets therapeutically. So what Ben and David are now doing, now that they understand this pathway, they can begin to find small molecules that block the cell death of platelets and they might be used down the track in patients or in blood bank storage.
Interviewer: That's a good segue into your links with industry. Why don't you tell us about that?
Prof. Hilton: Okay. So I grew up scientifically with Don Metcalf and Nick Nicola, and Don has a very firm view that at the Walter and Eliza Hall Institute we are a medical research institute, we're not a basic biology institute. And he very much likes the idea of basic research, but if you're working at a medical research institute, you have an obligation, if you discover something that could be useful, to work with people to try and allow patients to benefit. I think that's one of the reasons why medical research is well thought of among the public. So when we come to an election and people are asked about what's important, health and medical research rank quite high. And I think there's a good reason for that. So I've grown up in that environment. And I absolutely agree with that. We're in a very privileged position that as scientists we can pursue what we're academically interested in, we can pursue where our curiosity leads us, but I think we have a mutual obligation, for want of a better word, that when we stumble across something that looks very exciting we work with other people ask take it upon ourselves to have those discoveries translated into the clinic. The problem for basic scientists is to go from a discovery until your lab to a drug in a bottle benefiting a patient in a hospital takes many hundreds of millions of dollars. And that is ‑‑
Interviewer: Over a billion dollars these days?
Prof. Hilton: Indeed. And that is an amount of money that is beyond the reach of governments and there are probably a dozen or so pharmaceutical companies around the world that are capable of developing drugs. Now one very exciting part of working in Melbourne is we're beginning in Australia now to have a pharmaceutical industry, and CSL really are the leaders there. For example, they've been working with Gardasil, which is the papilloma virus vaccine. That's very exciting.
So we have people around Melbourne that are now capable of working with us to develop drugs. So we've seen that as being very important. And what we've done over a long period of time is to find the appropriate partners in the commercial world, not just to handball them the work at an early stage, but to work very collaboratively with them to bring our expertise and their expertise together into the mix, to try and push forward development of new therapeutics. And that's a very long process. So, for example, for a protein that I discovered with colleagues here 10 years ago, one of the receptors that we talked about, we thought this receptor was important in the development of asthma ‑ we found a way of blocking the receptor. Now, 10 years later, we're just about at the point where we're going into clinical trials.
Interviewer: This is phase 1?
Prof. Hilton: Phase 1 clinical trials that we hope will start in the next three months. That's been in collaboration with an Australian biotech company called Amrad, that translated into Zenith, and that was then bought by CSL, and an American multinational pharmaceutic company called Merck. So that's exciting, but it's taken 10 years.
Interviewer: And it's not an uncommon story at all.
Prof. Hilton: Absolutely.
Interviewer: Always in the background you've got the patent ticking ‑ a 17‑year lifespan of a patent, and it's 10 years into phase 1, it's always a challenge, isn't it?
Prof. Hilton: It's a race.
Interviewer: I think the message out of this is you're continuing to run an extremely large research group, highly productive research group, and yet you're also capitalising when you can on this translation either into the clinic or into the clinic via a pharmaceutical company development?
Prof. Hilton: Absolutely. I find it extremely exciting.
Interviewer: It's almost like a moral obligation, isn't it?
Prof. Hilton: I think it is a moral obligation. The taxpayers are not putting money into medical research because they get excited when I publish a high impact paper in an academic journal. They're putting money into medical research because they want their children to benefit from the discoveries. So we have to help drive the benefit. I find that also excites the younger people in my division. If you walked round the lab as you came in you'll notice it's pretty young. I'm 43 and I think I'm the oldest person in my lab by five years.
Interviewer: How do you inspire young people to take up careers in science, technology and medical research?
Prof. Hilton: Look, I think when you go to the universities there is a lot of really talented, passionate young people out there. So what I've tried to do is to give students an opportunity to taste the excitement of research much earlier, at a point where they haven't decided what they want to do. So, for example, I started a program 10 years ago, a program that I saw in Boston when I was a post doc at MIT that was called UROP ‑ undergraduate research opportunity program. What I saw in Boston was 18‑year‑olds in their first year of science at MIT coming into the labs and doing their own research projects ‑ not washing glassware, not making solutions, but working with a senior PhD student or a post doctoral scientist on their own research projects.
Interviewer: How long would they do that? Was it like a summer project?
Prof. Hilton: No. The best thing about this project is it wasn't a summer project ‑ I think there's a great place for some projects. It was to work a day a week all the way through the year and then full time over summer and the holidays, but it could last for the rest of their undergraduate life. We've had students through, for example, doing double degrees that have ended up working in the lab for four years before they've started their PhD.
Interviewer: So you're running that program here?
Prof. Hilton: So we're running that program ‑ we started that program here. There's probably 20 students at the Hall Institute. But now that program has been expanded to eight or 10 institutions in Melbourne and across four states. So it's happening in Western Australia, New South Wales, Queensland, South Australia ‑ there's probably 200 or 300 undergraduates at any one time in the country that are getting a taste of what research is like. For some of those that will really galvanise them and they'll say, 'Research is for me. I want to go ahead and do an honours degree and a PhD and I want to be a researcher.' But equally, some of them might say, 'I thought research was for me, but now I've had this experience, I realise that I'd much prefer to do teaching or work in patent law.' That's a great outcome as well. What we want to do is allow talented people to make informed decisions.
Interviewer: What inspired you to follow a path as a research scientist?
Prof. Hilton: That's kind of a difficult question. I was pretty good at science early in high school, so for the first four or five years in high school, but then kind of went off the road academically for a couple of years. I think sport and girls and parties and things like that, lots of different reasons. I think reasons that a lot of young people would sympathise with. So until about second year of uni I hadn't really thought about what I wanted to do. I kind of drifted into a science degree. But I was accepted into a summer project at John Curtin and went to a lab, and although it wasn't a very productive three months, I really enjoyed the environment and I enjoyed the idea that you could follow your curiosity. And I had a wonderful biology teacher in Year 12, Libby Holland ‑ hello, Libby. She was fabulous. I think the reason she was fabulous was that she, rather than presenting biology as something where all the answers were there, she presented it as a subject for which there were many unknowns, and that really made it come alive for me.
Interviewer: That was pretty unique back in those days?
Prof. Hilton: It was. You know, she got me interested in genetics. She was pretty flexible in allowing me to pursue bits of the curricula that I was interested in ‑ probably not a very good idea in the sense that I concentrated on those and didn't study hard in other areas, but in terms of passion it really lit a spark. That experience and the experience at John Curtin really galvanised me to do science, and the realisation that there were a lot of scientists having fun. They went to the pub, they played sport, they were in bands, they were not kind of geeks in ivory towers, they were just normal people, and that was really important.
Interviewer: I think it's being in that collective environment, as you say, over a summer can make a big impact as you start to see the way people interact and the discussions that go on and so on and so forth.
Prof. Hilton: It's fun. I mean, that was the thing that I realised, that science was fun. And in having young people come to the lab, I hope they realise that while it's a serious business and we want to make important discoveries, unless it's fun you don't want to come to work every day. That's the real key.
Interviewer: The National Health and Medical Research Council has obviously played a big role in helping to develop your career.
Prof. Hilton: Absolutely.
Interviewer: Do you want to tell us a bit about how that has helped you get through the various stages.
Prof. Hilton: So the NHMRC plays a really central role in Australian medical research life. I think it does so on a number of levels, but there are two that I think are particularly important. The first is that through the NHMRC grants are awarded to particular groups for doing work, and the NHMRC has a wonderful system of peer review in place that makes sure that the money goes to people that are going to use it productively. And I've benefited from that as a junior scientist, because my supervisors and mentors were able to attract money that enabled me to do the experiments and in turn I've been reasonably successful in attracting funds that allowed my staff to do the experiments that they're very passionate about. So on one hand it is the NHMRC being the mechanism by which the taxpayers' funds are distributed, but the other side of it is ‑ and this is probably more important ‑ that the NHMRC provides the taxpayer with assurance that the money is well spent. So it's really the guardian of the common good ‑‑
Interviewer: The purse.
Prof. Hilton: ‑‑ the purse in medical research. And that cannot be underestimated. The public have enormous confidence in the NHMRC and they have confidence because they're a very carefully considered group of people that are managing the purse.
Interviewer: And have you had roles in sort of contributing to executive review and things like that?
Prof. Hilton: Absolutely. Over the years I've had roles on committees that have set the policy for funding, for example how we're going to try to fund teams of researchers. Often tackling the big problems that we've talked about today requires big teams. That's a trend that we've seen in modern science. And that requires a different approach to funding than the classical funding of an individual scientist. I've been involved in that and, like most people in medical research, involved in the peer review process ‑ that is, the assessment of research projects and ensuring that the best research projects get the funding.
Interviewer: And it's important ‑ we were talking on Judith Whitworth on one of these conversations recently, and she was emphasising how important it is for scientists when they reach certain levels to start giving back to the discipline in which they've received so much.
Prof. Hilton: Absolutely. So being part of a scientific community also has obligations, and I think that involves helping administration, helping policy development, and then eventually retiring and making space for the next generation.
Interviewer: So where do you see the future being for you, Doug?
Prof. Hilton: Look, I really enjoy building teams of scientists. I enjoy the cut and thrust of the experimental side of science. I don't do many experiments myself. I still do a few. But I enjoy my staff bringing me exciting results. But I think in the longer term I'm interested in science administration and science policy and perhaps taking a broader role in directing departments or institutes or divisions or however or whatever group it is. But I really enjoy bringing teams of people together, especially young people, and giving them a shot at trying to do what they're passionate about.
Interviewer: Medical science in the future in Australia is in good hands with people like you who want to take on those leadership roles. Doug, thank you very much for your time and the comments that you made today.
Prof. Hilton: Pleasure.
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