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Hamish McLachlan: Why Professor Miles Prince wants to get rid of chemotherapy

PROFESSOR Miles Prince has devoted his life to battling blood cancer. His great hope: getting rid of chemotherapy. Hamish McLachlan spoke to him about his work and former patient, Maddie Riewoldt.

Dr Miles Prince. Picture: Tony Gough
Dr Miles Prince. Picture: Tony Gough

NEED a new hero in your life? New role model? Some inspiration? I’ve got a suggestion for you — Professor Miles Prince.

Regal name, cool man, humble and seriously clever.

I met Miles through the Snowdome Foundation which raises funds to fight blood cancers.

Among other things, Miles is the Director of Cancer Immunology at Epworth and Director of the Centre for Blood Cell Therapies at the Peter MacCallum Cancer Centre.

He has dedicated most of his life to saving the lives of others and curing blood cancer.

He is a remarkable man doing groundbreaking work that he hopes will end the need for chemotherapy.

HM: You are one of the world’s leading blood cancer experts. What did you want to be growing up?

MP: When I was seven, I really didn’t have much of an idea. My dad was a businessman and we emigrated. I was born in India, and then we came to Australia. Then from Melbourne we moved to Geelong, and I started going to school there. I went to St Joey’s, so we were totally football obsessed. There was one kid in the class who barracked for Richmond, and he got the strap.

HM: For barracking for Richmond?

MP: Yes! Brother Whitten wouldn’t let you NOT barrack for Geelong! We were stuck in Geelong in the 1970s, and Dad was in shoe manufacturing. He was a very smart guy; he could sell manure to Werribee, so I thought I’d be good at selling stuff. I was at school when I worked out I wasn’t bad at science, and I became absolutely obsessed with it.

HM: When did you fall in love with medicine?

MP: My first project on blood was in grade 6. I loved that industrial-type stuff, about how things work. Eventually I became passionate about the human body in form 1, and that developed into doing medicine. I always wanted to be a surgeon. I was going to be the best orthopedic surgeon in Melbourne.

HM: What happened?

MP: I went to India on my elective, thinking that I was going to do surgery. Then I ended up doing a medical job, and discovering all of these horrible medical diseases. I found that medicine, as opposed to surgery, was about trying to work out how drugs worked. I found out that trying to work out why you were sick and working on ways to avoid becoming ill, was more interesting to me than diagnosing what you had.

HM: Prevention rather than diagnosis?

MP: Yeah — people move from just being a doctor into doing more research because they start to think about why the person is sick. From there, the research is all about finding ways of treating them better, or cure what they have. It’s about trying to find something that’s better, and trying to do stuff that is cutting edge. That’s ultimately what I try to do day to day. I try to look at what is a better treatment than what I’m doing now.

HM: It’s a “grown up” job — it’s life changing, and hopefully life saving.

MP: Part of giving people hope in medicine is the recognition that you are working on something, and there is going to be something better, or something else when the current treatment runs out … you need to be able to provide hope that there are going to be more options, and that we aren’t at the end of the road. You want to be in a situation where you’re treating patients and you can cure them.

HM: Sometimes you can’t?

MP: It’s really interesting. Some of my colleagues are palliative care doctors. They’re looking after people who are dying — that is the start of their relationship with the patient — they know the outcome. They are in a different part of the doctor-patient journey, but they still love what they’re doing.

HM: The outcome for the patient is a fait accompli.

MP: It is. I had a patient who I’ll never forget. All he wanted to do was sit in a special room down the coast, on the Peninsula, in the house that his daughter had designed and built. All he wanted to do was get out of bed, and look at the view. I remember getting a letter back from his daughter, who was a well-known architect, saying “Dad got there”. That was my first experience with looking after someone who was dying. It was incredibly rewarding, but it wasn’t something that I want to do every day. Some of my friends do that, but what I wanted to do was have a balance. When I was in registrar training in the 1980s, (with) a lot of cancers such as advanced lung cancer, bowel cancer, or ovarian cancer, there wasn’t much that you could do if you didn’t get there early enough. You could improve their lives a little, but they weren’t diseases that were generally curable. Blood cancers are. With acute leukaemia, and lymphomas, you’re treating people with life-threatening, challenging treatments, but often you can cure them.

Dr Miles Prince has had an interest in blood since he was in year 6. Picture: Tony Gough
Dr Miles Prince has had an interest in blood since he was in year 6. Picture: Tony Gough

HM: Why did you choose to specialise in blood cancers?

MP: I think when I discovered that I liked continually seeing people. Part of a surgeon’s life is moving on. Meet, operate, fix, move on. I like a longer relationship; I like to get to know my patients. When I have students who are junior doctors who say, “I’m still deciding what I want to specialise in”, the first thing I say to them is, “Do you want to ‘speed date’ your patients, or have a long-term relationship with them?” An orthopedic surgeon will have a very short interaction with that patient, whereas if you are a physician, you can have an interaction with a patient for years. You see their kids grow up. You see them change. They see you. I’ve got patients who have watched my kids grow up, and they have an interest in that, so there is a relationship. That’s always the challenge. It’s about getting to know them. Some of my friends ask me if I get worried about knowing my cancer patients “too well”. I got over that years ago. I just thought, if you want to be in this game, you’ve got to let your guard down. You’ve got to let people in, and you can’t put barriers up.

HM: Is your day spent researching blood cancers and how to cure them, or dealing with patients?

MP: The vast majority is dealing with patients.

HM: They’ll come to you, you’ll diagnose them as having blood cancer, and then your role is to try and eliminate the cancer or manage it?

MP: Yeah. Eliminate and manage it, and try to find and develop the new drugs if those that we have aren’t working.

HM: You are one of the world’s leading doctors in “gene therapy”... which is?

MP: Essentially the introduction of normal genes into cells in place of missing or defective ones in order to correct genetic disorders. I finished my training in Sydney, and at that time, the big focus was around bone marrow transplants. I went to Canada in the ’90s to do bone marrow transplants, and when I got to Canada, I discovered bone marrow transplants but also the immune system and gene therapy. That’s what I’ve spent a lot of time on since — researching how gene therapy can help blood cancer sufferers. We have established some remarkable things in the last 30 years around the immune system.

HM: Like?

MP: How the immune system fights cancer. In the 1800s, people had the idea that the immune system must be important to fighting cancer. The body’s capacity to fight bacteria can be the same at fighting cancer, but it’s only been really in the last 20 years that we’ve been able to prove it. We have proven it, and that means so many things are possible!

HM: We’ve proven that the body’s immune system does try and fight cancer?

MP: Absolutely, but people have only started to be believers of that in the last 20 years. It was like climate change. It was a religious argument in the 1980s, you either believed it or you didn’t.

HM: And now scientific evidence says what about the immune system?

MP: That the moment the cancer starts, the immune system starts to try and fight it, and similarly, it starts to fight back. It’s only been because we’ve had the technology to be able to isolate cells, and watch the battle take place, both in the lab and in the body, that we have proven it.

HM: A lot of these discoveries have been happening at the Peter MacCallum Cancer Centre here in Melbourne. Are we world leaders?

MP: Yes, we are, for sure. One of the big areas that Peter Mac is strongest at, is researching the cancer-immune system battle. When I got back from Canada, I was passionate about gene therapy. We built the labs at Peter Mac, the first ever, and there were only about six in the world. The CEO at the time was a thoughtful sort of person. They were tearing down some operating suites, and he said, “That’s the area you should use — build it there”, so we built it in there. I couldn’t believe it; we just couldn’t have got it done now. We built these laboratories, and the guy who is now head of research at Peter Mac, Joe Trapani, came to me and said, “We’ve got this idea about these things called CAR T-Cells”, which stands for Chimeric Antigen Receptor T-Cells. T-Cells can be grown outside your body, and when you put a gene into them, that gene will allow the cells to attack the tumour directly. The reason it works is that the cancer cells sets up a sort of “force field” that pushes the body’s normal immune system away, which sets up a whole lot of defence mechanisms against the immune system attacking it. One of them is to not allow the immune cells to dock onto the cancer cells — just like a Sputnik space craft docking onto a space station. Literally that’s what happens, at what is called the immune synapse. With the gene therapy, there’s this sort of kiss of death between the immune T-Cell and the cancer target cell.

HM: Which allows it to bind?

MP: It docks directly onto it. Our lab’s shown that. We wrote a paper called “Serial Killers” because what they do is they latch on, they bind, they kill it, and then it moves on to the next one. It kills thousands of cells within a few minutes.

HM: Like Pac-Man?

MP: It’s exactly the same!

HM: And that was discovered at Peter Mac?

MP: It was discovered in a few places. A lot of people were working on it around the world. Currently our aim is to work against blood cancers and solid tumours like lung cancers. Being a blood doctor meant I did some work on acute leukaemia. We did that work about 10 years ago and published it about five years ago. We’ve been working in that space a long time. At the same time, in the US at the University of Pennsylvania, they’ve been working on Acute Lymphoblastic Leukaemia. They did a trial on that which was a huge success, and they cured these children with Acute Lymphoblastic Leukaemia. Like everything, what happens is that the companies focus on their line to approval, so a lot of their work has focused on Acute Lymphoblastic Leukaemia. We did these trials in that leukaemia at Peter Mac last year, but at the same time we’ve been working on our own CAR T-Cells. CAR T-Cells is the methodology that can potentially be applied to a whole lot of cancers. At the moment we’ve got a trial running in lung cancer. Our hope is that if it goes well, we will be able to treat lung cancer with the same gene therapy.

HM: So with the gene therapy, and with this process, is there any cancer that can’t be dealt with?

MP: We just don’t know.

HM: What does nirvana look like? When you’re 80, what would you love to be able to say has occurred?

MP: That we’ve got rid of chemotherapy. That it’s no longer required.

HM: And that’s realistic?

MP: Yep. I’ve got patients now who I don’t use chemotherapy on. It’s been replaced with other more targeted drugs. The biggest explosion in drugs has been since 2000. The last 17 years have greatly reduced the need for chemo.

Hamish McLachlan, Joe Reiwoldt and Miles Prince.
Hamish McLachlan, Joe Reiwoldt and Miles Prince.

HM: Chemo is a poison?

MP: It is exactly what it is. It’s there to poison the cells. The different chemo varies in the way it poisons. It’s like cyanide versus arsenic. It’s just different types, and poisons can be different. A lot of them are based around plant and animal toxins, around ways that plants and animals kill each other. That’s why the side effects can be tough, and that’s why they are generally not specific. There’s three big aspects that will determine whether we are going to beat cancer. One is around getting more targeted approaches. It’s about using drugs that affect the way that the cells processes work. It’s about trying to use biological agents that are “short circuiting” the normal communication within the cell, which makes it strangle and die, with the end result killing the cell. The second is to use the immune system, because the immune system has got the biggest potential to kill cells. It doesn’t matter whether it’s lung cancer or bowel cancer, if we can get the immune system to work, we can kill them. The third is about getting a better profile of the cancer, to get the barcode of that tumour. If you look at melanoma, for example, the treatment that Jarryd Roughead just had was an immune therapy. It was unlocking the immune system to specifically kill his melanoma. The treatment that Ron Walker had was a treatment that specifically targeted against the mutation of melanoma.

HM: So slightly different.

MP: Slightly different, but achieving the same goals. One was the Achilles heel of the melanoma. It is a mutation that, if we get the right drug, would switch it off. The other is killing it with the immune system. Both of those treatments are now approved for melanoma, and they didn’t exist ten years ago.

HM: Mates have a child who suffers from Diamond Blackfan Anaemia (DBA), a rare bone marrow failure disorder that requires him to visit hospital multiple times each month for blood work and lifesaving blood transfusions — for the rest of his life! Very few people in the world have got it, so it isn’t being researched very hard because it can’t be profited from. Is that common?

MP: Sadly. If they can’t profit, they initially look in areas where they can.

HM: They?

MP: The pharmaceutical companies.


HM: How underfunded are we in medical research? If we had $100 billion, would that be enough to …

MP: … it’s an endless “if”. What you want to avoid more than anything is duplication. What we lack money in is making the fundamental differences. It’s about making some fundamental discoveries. As a society, we don’t spend enough money on science. We don’t encourage science. I think it lacks priority. There has to be an R&D, and that R&D is a proportion to what your budget is.

HM: There are three types of blood cancers: myeloma, leukaemia and lymphoma. How closely related are they?

MP: Very similar. The problem is when you’re trying to explain them, there’s lots of subgroups within each of those. Fundamentally, they’re screwed up white cells. In the bone marrow is where all of those cells are produced.

HM: Hence the relationship with Maddie Riewoldt’s Vision, which is researching to try and solve bone marrow failure?

MP: Correct. Ultimately, if you’ve got screwed up bone marrow, you either have too many bad cells, which can be crowding it out, or you haven’t got enough. In the bone marrow failure syndromes it is where they haven’t got enough. Often the treatment is the same for bone marrow failure and blood cancer.

HM: Bone marrow failure seemingly stimulates blood cancers through getting the balance wrong, but it’s not the reason for all blood cancers?

MP: Absolutely not. You could almost see lymphoma, leukaemia, myeloma, and bone marrow failure syndromes as four challenges in terms of how we treat them. The white blood cells are like the military. There’s an army, an air force and a navy, and those white cells can each get cancer. That in some ways describes the difference between myeloma, leukaemia and lymphoma. Lymphoma is a disease of the lymph glands. Those three conditions are about something that’s growing too much and taking over the body. You want to eradicate them. The bone marrow failure syndromes are where you just haven’t got enough of the cells and the bone marrow looks empty, like the Sahara desert. What we don’t know is what makes the marrow empty, and part of that can be the immune system, it can be toxins, and sometimes it’s genetic. That’s what MRV is working on. There’s a lot of similarities between bone marrow failure and blood cancers.

HM: Am I right in saying you initially treated Maddie Riewoldt?

MP: I did. What happens is often at the start of bone marrow failure syndromes, the immune system is taking over. When she was being treated with me, we were using drugs to suppress her immune system. That worked well, for about four years. Then they started to fail, so she needed a bone-marrow transplant. That’s when I handed her over to David Ritchie. He did the bone marrow transplant, but tragically she died of a complication of the transplant.

HM: The Snowdome Foundation, of which you’re a director, and MRV are now working together on a joint project.

MP: We are — it is about trying to improve the bone marrow. It’s a fascinating project in itself. It’s asking some basic biology of how important blood is. As blood gets old, it seems to set up the situation where it can make the rest of the body fail. I won’t go into it, because I don’t think we fully understand it yet. What’s happening in medicine is we’re discovering interactions between the different body systems. There are nerve cells that go from the brain to the bone that make them grow. We didn’t even know that!

HM: Until how long ago?

MP: Eight or nine years ago.

HM: How many patients would you see on a daily basis?

MP: About 40.

Miles travelling in India with his family. Picture: Supplied
Miles travelling in India with his family. Picture: Supplied

HM: How long is the average term you have with a patient? Once you’re with them are you with them for awhile, in some format?

MP: I look after all sorts of blood disorders. Some blood disorders I look at are simple blood disorders like through pregnancy, and I see them every time they’re pregnant, just because they’ve got clotting or bleeding problems. Haematology is a great specialty because you’ve got the chance to also look after patients with non-cancerous conditions. You look after people who bleed too much or clot too much. It takes the pressure off. With blood cancer, often the diagnosis is made years before you actually need to treat them. You go through this relationship where we’ve seen each other every three months or six months, until finally they receive treatment. Then you look after them, and then there’s the post treatment and the monitoring. It can be a lifelong interaction. You don’t realise just how important that interaction is, both for yourself and them. It’s only until you start to see other people around you who are sick that you realise how important a doctor is. You don’t realise that when you go into medicine. I have people who have become some of my closest friends, who started out as patients, because I know them better than anyone, and they can have more trust in me than anyone else. I don’t try and block that relationship. I think my greatest skill, in terms of the relationship with my patients, is being able to fly at the same altitude. Whether the guy is a farmer, sitting there grunting, or someone from Fitzroy who’s a medical student, or a teenager, you’ve got to try and get at the same altitude. A lot of people complain about their doctors because they’re not relatable. The reason I’m in research that often involves treating patients is because I don’t want to give up the clinical bit. I don’t want to give up seeing patients. I don’t want to give up interacting with them and seeing those successes. At the same time, I couldn’t see a patient day after day after day, and just be able to offer them just routine drugs available on the PBS.

HM: You begin a journey together with your patients, and it almost becomes a partnership.

MP: I’ve got a patient and I’m giving a speech at her 60th, because she wasn’t sure she would still be alive when we started her journey with leukaemia. It’s happening in September. She’s just the most beautiful woman. Everybody has their own aims, and she’s been able to tick off the various marriages of her kids, the babies, and now her 60th. You watch people tick these things off, you go through a lot of it together. You get very close, you get to know all about them and their family. I rarely go to a funeral, just because I find it so difficult, but I have spoken at people’s funerals, just because we’ve had some really close relationships.

HM: When you get so close and then you lose a patient, how do you compartmentalise and rationalise it? Is losing a patient any different to losing a friend?

MP: No — it’s not, you feel it like it was a close friend, and you always question how you could have done things differently. The thing that really rocks me is when I look at somebody who has died two or three years earlier, and you wish they were still here today, because now, with all the advancements, you think “I could have fixed that if it was now!’’. If I have one recurring agitation, it’s that. Two months ago, that happened. I was brushing my teeth and I thought, you know what, if Marie was still here, and if we had the treatment that we have now, she wouldn’t have died.

HM: You deal with a lot of sadness, from diagnosis to the inevitable. Have you got better at dealing with it?

MP: That’s a very good question. I don’t know if I can answer it immediately, and I actually don’t know if I’m that good at it to be honest, or if I am getting better at it.

HM: Do you get affected?

MP: Yeah. It’s interesting. The other day I had a patient come in to see me, and I’d been chasing up some results, but I couldn’t quite remember whether we’d got something through. She sat down. I was looking at my computer and I was just thinking, and searching for the result, and my face must have looked worried. She said, “You are scaring me!” I told her that everything was OK, because normally when a patient comes in I try to let them know immediately. She said, “I am still worried!”. I knew that the pause in answering her was just a fifth of a second too long. There’s no book on how to break bad news, and it is very delicate. People are desperate to hear the news, good or bad, quickly. No grey. And sometimes it is grey.

HM: You are the only guy who can tell them what they want to hear — and they are hoping you will tell them good things.

MP: Yeah, but I can’t read everybody really well, and my weakness is probably sometimes not being blunt enough.

HM: It’d be very tricky.

MP: Very. You can’t rob the hope from people, but at the same time you can’t let them plan for things that aren’t possible. As you get older you realise that people want simple things, and if you tell them that they can go on a holiday in a few months but deep down you really don’t think that’s the case, then they’ll complain that you didn’t tell them earlier. I have got better. You get better with everything as you get older.

HM: Hope’s a big word.

MP: When you ask people about what they want to hear when they first meet you, the word they want to hear is “cure”. You can’t sit them down and just blurt out and say, “You’ve got myeloma, it’s incurable”. You have to be gentle.

HM: You’re dealing in a space where you’re hoping and praying, but the pharmaceutical research and development teams aren’t pedalling fast enough. You’re dealing in your time with patients who are getting closer to death, and you’re just hoping the timing will be right.

MP: One of the big saviours for myeloma is this new drug. It’s an antibody treatment. It’s an immune therapy. There’s these antibodies that directly latch on to the cell, but right now there isn’t one for myeloma. The only access we can get it is usually through a clinical trial. This guy I’ve been looking after is a typical example of someone who I’m close to. I know everything that his family does, I know the problems he’s had with his work and with his sons, and how they’ve been causing problems. Just all of these stories that come out over the years.

I’ve looked after him, and he’s basically run out of options. The thing we need to do is to get these clinical trials open, which is a lot of work. You’ve got to trial for him, to see if we could go on to this drug. He had a 50/50 chance of getting this new antibody, which is brand new. It’s not approved in the US, but we did all the tests. The tests took all week. He had scans, bone marrows, which we had all done in time to try and get the drug. Everything is set to start on Monday. Friday night, St. Kilda plays GWS. St. Kilda are winning, he stands up, screams out at home, and gives himself a hernia. He has to go for an urgent operation over the weekend. It took him two weeks to get over that operation, which meant he wasn’t eligible for the trial. He had to start all over again. He’s gone onto the trial, with a 50/50 chance of getting the active drug, because it was a standard treatment, plus this new drug. Eventually, he got the new drug, and it’s working. His disease is now in its eighth remission! That stuff takes up a lot of time, and that’s how you spend your time on the way home.

Professor Prince was involved in Maddie Riewoldt’s care before she passed away.
Professor Prince was involved in Maddie Riewoldt’s care before she passed away.

HM: It was a good win by the Saints, but a hernia?

MP: (laughs) It was. He was embarrassed to tell me. That’s the reality of where the research, the new drugs and the treatment interface with the patient’s journey. It’s very satisfying. You don’t kick yourself over the mistakes, you just kick yourself about things not happening fast enough.

HM: Is blood cancer curable? Or just manageable and treatable?

MP: A lot are curable, but some of them are not. You can say lymphoma is curable, or acute leukaemia is curable, but it just depends on the percentage. Part of the difficulty is the predictability. I’ve still got patients who relapse. If that happens, I go back and look at all of their stuff and determine why they have relapsed. They’re in the 10 per cent bracket.

HM: How do you tell someone that you’re out of options and that there’s only weeks left?

MP: I did that yesterday. I’m still pretty bad at it. You just have to tell them how it is.

HM: “I don’t have anything else I can do for you, and I think you’ve got a month or so to live?”

MP: Yep. You hold their hand, you sit on the end of their bed and you tell them that you’re going to try and do your best. It could be a few weeks, it could be a couple of months, or you’ll be lucky to get to Christmas.

HM: Terribly tough. What gives you the greatest satisfaction?

MP: At home, it is sharing in my daughters’ achievements with them. My daughter got her first job the other day. That was a moment. She’s got there!

HM: And the greatest satisfaction at work?

MP: The “punch the air moments” come when you save a life that looked unlikely, or you get a really good grant funding, or, selfishly, when you realise people recognise what you’re doing. If you get that email that says a paper has been accepted in the journal we wanted it to be, that’s another big moment. But like all of those great victories, somehow they just progressively get diluted. It never happens in one big moment.

HM: There’s no final siren, where you’re all together hugging in the middle of the MCG?

MP: No. That’s a good point, because you just move on. You don’t spend enough time celebrating those achievements. You always go on to the next bit of worry. Mark Dawson, who you’ve met, is a clinician-scientist at Peter Mac. Whenever they get a good research publication that comes out of their laboratory, he takes the guys down to the pub and they have a beer. They’ve been known to have beers at breakfast. He goes out of his way to make sure they are celebrating those achievements. I think it’s a stupid thing to say, but sometimes for me it is also about those small reliefs that you get rather than the victories. If there’s a patient that you’re really worried about, and the results come back good, it’s almost like the anxiety is being released.

HM: It’s relief more than joy?

MP: Yeah. The research successes are far more tangible than the clinical ones. My biggest anxiety, long term, is sticking in the wrong environment. It’s interesting — I was reading a book about a stockbroker and he was talking about investing. When you’re a stockbroker, it’s really easy to realise when you’ve made the mistakes in terms of what you’re investing in, because you lose money. You lose money for your clients, and for yourself. I did administration at Peter Mac for a year and I hated it. I was falling asleep at meetings, and everyone was talking about “low-hanging fruit”, and all of these public service things which I just hated. I think subconsciously I moved out of that and took another job. I moved into another area, because subliminally I realised I wasn’t in the right spot. I think I’ve been lucky in that I’ve moved out of positions when I’ve realised I’ve got as much out of them as possible, and I think that in the same way, if you’re looking at a life change, that’s a subliminal pulling out of that investment. You’re no longer going to invest in that commodity. There’s another commodity. There’s nothing wrong with that. We don’t do that in our lives as much as we should. We don’t reassess and think about where we should be investing our time and energy. With research, you’ve got to be quite swift. For example, we’ve done some fascinating drug trials over the years and a number have now been approved for patients with lymphoma. On average though, it takes quite a lot of time. When I’m talking to young research people who are coming through, I tell them, you’re 30, you’ve just finished your medical degree. You’re going to go out there and start doing some clinical research. You’re probably going to retire at 60ish. That means you’ve got 30 good years of doing some work. The average time between starting a drug trial and getting it published is going to be about six to 10 years each, so be selective on “what horse you are going to back”.

HM: You’ve got to pick the right ones.

MP: You do; you need to think about it. You have to be constantly strategic about how you’re doing things, and I think that’s where I’ve been lucky. I’m a bit unusual in that aspect of maintaining my clinical research, and my patient contact. Often you lose one or the other.

HM: You spoke about Professor Mark Dawson. I heard you speak recently. Were you sincere when you said that you thought he might win a Nobel Peace Prize?

MP: He is the right calibre, no question.

HM: And he’s in Melbourne working?

MP: He is. The way he thinks is very different to other researchers. He was so successful so early, in so many fundamental things. The way to win a Nobel prize is to have something that’s a total paradigm shift. He has made some discoveries that link concepts that we wouldn’t otherwise have linked, and he’s definitively proven them. He’s just shown how the immune system links in to some of the genetic processes.

HM: It’s been humbling speaking to you. You’re a hero to many. I hope your nirvana, a world without chemo, happens soon.

MP: So do I. Thank you very much.

snowdome.org.au/donate/ or mrv.org.au/donations

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Original URL: https://www.heraldsun.com.au/news/hamish-mclachlan-why-professor-miles-prince-wants-to-get-rid-of-chemotherapy/news-story/27dee44ef255d7fbcaf21f22de85483c