[00:00:15] Speaker A: Welcome to a new episode of few and far between. I'm your host, Chris O'Brien. Today's guest figured out from an early age that big advances in science are often made in a succession of very small steps. Professor Justin Stebbing is the editor in chief of Oncogene, one of the world's leading cancer journals and one of the most productive people I know.
[00:00:33] Speaker B: Justin was the UK's first national institutes for Health Research professor of oncology and has published nearly 700 papers in some of the world's most prestigious journals.
[00:00:42] Speaker A: Justin has continued to make it his mission to help improve both the quality and quantity of life for every patient, one step at a time. And his goals have been actualized through his important contributions to HIV immunology and COVID-19. In this episode, Justin and I had a chance to talk about his early use of AI in finding a critical treatment for COVID pneumonia. The multitude of benefits gained from sharing knowledge and research, and realizing at times that the stupidest cancer cell can still be cleverer than the smartest oncologist. We also touch on some advice for a younger generation of STEM students, including the importance of intelligence, which he defines as both IQ and EQ, and two dimensions called CQ and PQ. It was an amazing experience to have Justin on few and far between, and I hope you enjoy episode. Okay, let's start the podcast.
[00:01:38] Speaker B: Professor Justin Stebbing, welcome to few and far between.
[00:01:41] Speaker C: Thanks so much for having me, Chris. Great to be here.
[00:01:43] Speaker B: Yeah, it's a delight. I've really been looking forward to it. Justin. So let's start a little bit with kind of your career. What inspired you to pursue a career in oncology and, you know, maybe talk a little bit about your educational experiences and how you got to this interesting place.
[00:01:56] Speaker C: That's a great question, Chris. I was originally a student in Oxford for six years under the very beautiful dreaming spires and really developed a love of linking the laboratory to the clinic and the clinic to the lab, where we could take findings at the bench site and translate them to helping patients quality and quantity of life. Because I only ever wanted to do medicine to help people. It sounds corny, but it's true.
[00:02:22] Speaker B: I think it sounds lovely, actually.
[00:02:23] Speaker C: That's sweet. And then after that, I went to a little hospital on the east coast of America called Johns Hopkins for a few years, and that was a culture shock. My typical patient in Oxford was a little old lady with blood clots and pneumonia. My typical patient in Baltimore was not that individual, but in all seriousness, I realized I liked dealing with serious illnesses that affected men and women of all ages, where you could develop a relationship with the patient, but also one that was very humbling. I learned very early on that the stupidest cancer cell was clever than the cleverest oncologist. And combining that with research naturally led me wanting to deal with serious things into oncology. And when I look back on my career, then 2030 years ago, seeing how we've developed precision drugs now, treating the right person at the right time, with the right medicines for the right tumour, it's really staggering to see those advances which have led to improvements in quality of life, but massive improvements in quantity of life as well. When I was a junior doctor, we'd walk around the wards and see patients writhing in agony from bone metastases, bone secondaries from cancer. We rarely, rarely see that now, whether it's due to better painkilling drugs or radiotherapy, or better still, better drugs to treat those diseases, things are so very, very different now. We truly, even if we can't cure people, we can truly often turn it into a chronic disease that people live with, as opposed to dying from. Not always, but often.
[00:04:01] Speaker B: This is such an extraordinary thing about the moment we're living in. But if you go back to that young Oxfordian who comes to the United States, did you think you saw coming the cancer revolution that we've experienced over the course of your career, or did you expect that things would stay the way that they were and it was still going to be a meaningful career because you're going to be working with desperately ill people?
[00:04:20] Speaker C: The great thing about science is that it's very humbling. You learn every day from the patients, from the diseases, but also from the research. And every year and every day, almost, I'm learning. And really, it's a gradual progression. Everyone likes the most exciting and the next newest and the sexiest, coolest kid on the block. But the reality is, advances in science, with exceptions, are made in very, very small steps. One thing I did start to see, though, was that the effect of an individual was going to be less with time, that going forwards, whether it was in research or in medicine, you needed collaborations and teams that were around you and that could expand nationally and also internationally. Clearly, the world is a small place now. I only started using email when I was a resident at Johns Hopkins. Right, but what the days of an individual physician or a lab scientist with a pipette by the bedside or the bench, respectively, making a large difference, is very limited. Clearly, you can influence people, but when I work with drug companies, now, in large teams of people, although there's always a danger of groupthink, we always encourage people not to have that groupthink. And sometimes scrappy thought, as long as it's ordered, can be very, very constructive.
[00:05:46] Speaker B: Yeah, it's fascinating. I think there's still a romantic image of the lone scientist curing some horrible disease, but less and less. Right. Do you think that's changed? The level of collaboration has changed over your career as modern communication tools become available, modern online journals, all of these things. Has that gotten easier or harder?
[00:06:04] Speaker C: I think it's gone so much easier with time. There have been specific instances such as the COVID pandemic, moving everyone online, obviously, and that's facilitated telehealth and seeing patients online, although that existed beforehand. But I think over time it's gotten easier. Sometimes I end up collaborating with people in the states, and I don't collaborate with people in the office next door. That's not for any particular design. It's just because they're the best people in that area to collaborate with. And whenever you're doing research, you always think what you're doing is the most profound and meaningful thing ever. But the reality is it's probably a very, very small part of a jigsaw.
[00:06:40] Speaker B: I want to talk for a second now about oncogene. You're editor in chief of oncogene. You also, I guess what I would call you, do scientific writing or medical writing that is aimed at an educated layperson, that's not. Not aimed at a doctor. And then you do lots of high end research. Will you talk a little bit about how you think about those two tasks or, you know, roles that you play?
[00:07:00] Speaker C: I don't think of them separately. I think of them all together as sharing knowledge. There's something to be lost by sharing knowledge and research, people can steal your ideas and do things differently and criticize you. But there's so much more to gain. The gains are enormous, and particularly if you have a long dated vision and can avoid some of the noise. Whether it's scientific writing or being editor of Oncogene, the basic premise of that is to further knowledge, questioning discovery, whether it's hypothesis generating, which means asking the question, or whether it's finding the answer to the question. They're both different ends, if you like, of a spectrum of research which at the end of the day is aimed to make humanity better. A lot of this research are the fundamental building blocks, if you like the foundations looking at what turns genes on and off. I'll give you one example. There's 3 billion letters of DNA that make up your eye, your nose, your mouth, your skin cells or your lung cells. What determines if a cell becomes a lung cell or a lung cancer cell or a lung stem cell or a lung cancer stem cell, which, like a queen bee if you get rid of the cancer, can repopulate the nest many, many years later. What's underlying that, for example, are the way the genes are turned on and off. We call that gene regulation. Now, over the last few years, we've understood a class of molecules related to rna, which is the step between DNA and protein controls that via various interactions. It's beautiful, it's fascinating, but understanding that better can really lead us to control disease. If you control disease, you understand science better, but at the other extreme, you can improve patients outcomes in the clinic. And that, to me, is very meaningful. But the reality is, when you work in the lab and when you work in the clinic, sometimes things don't work and you're just trying your best. We're humans, after all. Despite large language models and all the fantastic discoveries out there and the great new drugs, we're very, very fallible. We make mistakes, we get it wrong, and sometimes we just don't know.
[00:09:17] Speaker B: Will you talk a little bit about translational research and the importance of this bridge between the lab and the clinic? What brought you there? And, yeah, why that matters so much.
[00:09:27] Speaker C: Everyone has their own niche and research. Some people like recruiting lots of patients in big late stage clinical trials. Other people just like working with understanding an aspect of basic science. The area I like bridging is the bridge between the laboratory and the clinic, and we call that translational research. But what translational research really means is different to different people. What it means to me is using patient samples to provide answers that are useful to those patients. But the answers from those patients also informs your lab work. So it forms a virtuous circle, if you like. And that, to me, I find particularly interesting. But without having those other individuals at the other end, one dealing with basic science and one on the clinical trial side, I'd be very, very lost and alone. So it's part of a big family, if you like. And you know what? As we learned during the COVID pandemic, it worked. It actually worked. It actually achieved an outcome. We developed a vaccine within a year of discovering and sequencing the virus, and that was only because of advances in sequencing technology. Just by way of one example of many that I could name, let's talk.
[00:10:35] Speaker B: A little bit about COVID-19 most oncologists weren't perhaps not directly involved with the COVID-19 pandemic, except as patients. Your work with AI led to an FDA approval. How did you get interested in that and tell that story, if you would?
[00:10:49] Speaker C: I was always really interested in viruses, mainly viruses as a cause of cancer. I did a lot of work during the HIV pandemic, particularly with people like Brian Gazzad and Francis Gotch at the Chelsea in Westminster Hospital. We worked in a very large London cohort where we observed that patients with HIV developed a lot of cancers, lymphoma, kaposysarcoma, other tumors. But if you reconstituted their immune systems, the cancers went away.
[00:11:14] Speaker B: Amazing.
[00:11:15] Speaker C: That was really amazing. When I was at Johns Hopkins, patients with HIV and AIDS would die of cancers and opportunistic infections by the two thousands. That was a thing of the past. It was really, really quite incredible. Fast forward. I then did my PhD on a cancer causing virus, something called human herpesvirus eight causes kaposi sarcoma. But the same applies that typically in immunocompromised people occurs just like in the film Philadelphia with Tom Hanks. Those were the lesions on his face. I developed a large network in virology because of that. But at the start of the COVID pandemic in January 2020, I sat down with the clever computer engineers and scientists at a little London based company run by the CEO Joanna Shields little team. And we asked the AI program, is there an existing drug out there that would have antiviral effects against this pathogen that we were seeing from China, but that I thought was going to come to our shores?
[00:12:14] Speaker B: So this is before the big lockdowns?
[00:12:17] Speaker C: Well before the lockdowns. This was in January 2020.
[00:12:20] Speaker B: Fascinating.
[00:12:20] Speaker C: And it gave us one drug in particular, a drug called baricitinib, made by Eli Lilly, now the world's largest drug company, because the GLP ones in obesity, obviously nothing to do with this, but it gave us one drug, baricitinib, which was approved as a tablet once a day in rheumatoid arthritis. Now, it wouldn't be a surprise to anyone that a rheumatoid arthritis drug could be useful against a drug that could cause an inflammatory cytokine release syndrome. But what was very surprising and what a human couldn't predicted was that the higher order correlations in the artificial intelligence predicted that it would have antiviral effects. And we published a couple of pieces in the Lancet, who kind enough to publish the very first paper on that within 24 hours of submitting it there. And no one believed us.
[00:13:11] Speaker B: Justin, when is that? In time. Where are we now? In time?
[00:13:13] Speaker C: This is now the beginning of February 2020.
[00:13:16] Speaker B: So still before, certainly before lockdown in the US?
[00:13:18] Speaker C: Yeah, well, before. And we called out Lilly with the results. They didn't believe us or didn't want to believe us. They didn't really believe in artificial intelligence. But then collaborators I've built in the virology world were calling me, particularly from places like Italy, Sweden, France, as the virus was hitting them, saying, I don't know what to do. Shall we use baricitinib? And I really had no idea. We started performing laboratory studies, and we were very surprised that in the lab, it validated the computer program better than we could have imagined. But the reality is we needed to perform a clinical trial. So with the help of Lilly, the NIAID, which the National Institute of Allergy and Infectious Disease, based around the NIH, and Bethesda, Maryland, who organized these big trials, we started some big trials in America. It was eventually incorporated into UK recovery studies. And I didn't think the trials would work. In fact, I wrote a book in the COVID pandemic. And when I called witness to COVID describing the breakneck speed of drug discovery, and I cringe when I look at it. On February 6, 2020, I wrote, I think the worst of it is over. I didn't think the trials would work, but they worked beautifully. Well, this is a drug for hospitalized patients with COVID pneumonia, not like, say, paxlovid or the antibodies, which is for use pre hospital. This was for patients with COVID pneumonia, and it wasn't preventative. It was. The data were remarkable, particularly the data for saving lives, the hazard ratio for mortality, for death. It really was an impressive, much lower probability if you were on the drug. The FDA approved it under an emergency use authorization in November 2020. It then developed a full authorization for use by itself and so on. But it was cheap. When used for a short time, it was one pill a day rate. Few drug to drug interactions had dosing flexibility. You could use it in patients with impaired kidneys, and it had very, very few side effects.
[00:15:15] Speaker B: And we obviously knew the safety and side effect because it was an approved drug already.
[00:15:19] Speaker C: The worry was, though, was that even though it was approved, there was a slight signal for blood clots. And you remember that COVID caused blood clots.
[00:15:27] Speaker B: Yes.
[00:15:28] Speaker C: We actually showed no blood clots in any of our studies. What was interesting is imagine a lung cell. What the virus was doing is it was infecting the lung cell but causing release of a lot of inflammatory mediators. Think of a drawbridge, like the receptor that the virus binds to. When the inflammatory mediators were released, the drawbridge would come down and the virus would hop onto it, get into the cell. This drug was stopping all of that, and it's still used today. We sent charitable shipments to India during the delta pandemic a few months later. Lilly did well from it. It really was the first time we used AI to rapidly develop and validate a drug at breakneck speed. One paper I published in Science Advances in January 2021 had 53 authors from 14 countries and 33 institutions. Now, normally, getting those individuals together would be like herding cats. Everyone wanted to work together. No one was competitive. It was super collaborative, and it brought down walls between industry, academia. No one cared about any of that stuff. All people wanted to do was make sick people better, and hopefully that we did.
[00:16:40] Speaker B: Justin. So some of that was about the urgency of the crisis, of course. Do you think enduring implications or changes for how we conduct research as a result of the experience that we had with this and with other drugs and.
[00:16:53] Speaker C: Trials during COVID I mean, there's lots and lots of examples I can give you, such as seeing patients in clinic and telehealth and decentralization of clinical trials. You know, Chris, more about that than anyone, because you lead a global CRO with the true picks and shovels of the pharma industry, recruiting patients in clinical trials. Great company that you lead. But just to name one example, the messenger RNA technology that was used for the best vaccines made by Moderna and BioNTech, is now used for other vaccines. We get that, but it's also used remarkably. And you remember I was talking about rna before as the software between DNA, which is the hardware, and proteins, which are, if you like, the things that do things, the programs, if you want, if you like. But messenger RNA vaccines are now being trialed for cancer patients to elicit an immune response. And. And only last week, we saw a paper in nature where the messenger RNA makes a protein that doesn't elicit an immune response, but replaces a lost protein in a very rare kidneys disease called propionic acidemia. So that's a lesson from the technology used in the pandemic, able to cross diseases into rare diseases and cancer. We've already seen amazing results in melanoma, so there's actually specific technological examples that had we not had the pandemic, we wouldn't have today. Now, obviously, everyone wants to work together and collaborate. I get all of that, but it did instill a sense of urgency. One thing I'll mention that you'll be very familiar with is it also encouraged clinical trials to ensure they recruited diverse groups of patients, not just the types of patients I referred to that I used to see in Oxford.
[00:18:46] Speaker B: Hi, this is Chris O'Brien, host of few and far between. We'll be right back with this episode in a moment. I personally want to thank you for listening to our podcast. Now in our fourth season, it continues to be an amazing opportunity to speak.
[00:18:57] Speaker A: With some of the top thought leaders.
[00:18:58] Speaker B: In the clinical trials industry. If you're enjoying this episode, please leave us a review on Apple Podcasts. It really helps people discover the podcast. And don't forget to subscribe to few and far between so that you never miss an episode. One last request. Know someone with a great story. You'd like to hear me interview? Reach out to us at few and far
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[00:19:15] Speaker A: Dot thank you.
[00:19:16] Speaker B: And now back to the podcast.
Yeah, one of the most, I think, enduring things that we see is that I think the pause that the FDA put on those large COVID trials caused everyone across the industry to focus on this. And now there are new guidelines, of course, pushing for that. You mentioned making this drug available in India. That leads me to my next question for you, which is about biosimilars global health and kind of healthcare equity and access, particularly in cancer. I know this is another topic that's important to you. So you were directly involved with the development of, I think you led the development of a biosimilar herceptin. Can you tell us a little bit about that and how you think about the inequities in access to care?
[00:20:00] Speaker C: So herceptin and other antibodies used in cancer and other diseases are seriously expensive drugs. Cancer drugs typically cost ten thousand dollars to twenty thousand dollars a month in the states, and it's not too dissimilar in Europe. And before their patents expired, we wanted to develop cheaper versions of those. Think of it like a generic. But when generics come along to a simple white pill like an antidepressant, you get hundreds flooding the market, and the price changes from $100 a month to a dollar a month. These drugs are difficult to develop. You still need to perform clinical trials with them. You need to ensure that they're safe, they're expensive to manufacture, they still require R and D. So when you develop a biosimilar, although it's going to be cheaper in maybe say, 50% of the cost of the branded product, and to me, I think healthcare, and I've always thought that without meaning to sound too idealistic, because I'm not that idealistic, is a fundamental right. There's no healthcare system that's perfect.
Every healthcare system is abused. Whether you want to say that America spends 19% or whatever it is, of its gdp on healthcare and the UK spend 9%. And why is that? And the different models. It's interesting. Very few countries try to copy any other country's healthcare systems.
[00:21:17] Speaker B: That's a great point.
[00:21:18] Speaker C: And if you focus on trying to make the individual better, I think that's a very laudable aim. Whether it's via running clinical trials like you do, whether you're recruiting patients or providing patients for them, or trying to be involved in the drug development aspect or translational science like I've been involved with, I think these are just parts of a jigsaw and you're just trying your best, really, not more than that, because none of us have perfect answers to the healthcare system comment that I just made.
[00:21:48] Speaker B: But do you think that maybe this is an unfair question, but are we doing enough in terms of trying to develop biosimilar alternatives in oncology?
[00:21:55] Speaker C: Yeah, it's interesting, isn't it? Because at first, biosimilars were made by biosimilar companies. Now, what's interesting is that Amgen, Pfizer and even AstraZeneca, for example, have their own biosimilar programs, as if they're saying, this is important. We understand the need, we'd like to generate revenues on our own drugs when they come off patent, but actually it's about continuing the brand and helping sick people get better. Excuse me being repetitive.
[00:22:22] Speaker B: Yep. I think that makes perfect sense. We spoke a minute ago, you mentioned diversity in clinical research and trials. Do you see broad awareness for that in your world now? And do you see solutions in place that are driving different sorts of people into clinical research?
[00:22:37] Speaker C: For the first time? I'm seeing real solutions for that. Previously, clinical trials would be very limited to certain demographics of patients one would see in teaching hospitals. Now we're seeing patients recruited from community hospitals, companies looking for those individuals to recruit them for clinical trials, with an emphasis, as per the FDA guidelines, on not just diversity, but looking at real world evidence. Because we understand that clinical trials avoid things like comorbidities. Patients need to be really healthy otherwise. And it's not just just about diversity, it's about actually, does this drug actually work and help people in the real world setting, not just in the clinical trial setting, because there'd be numerous instances in oncology with various regimens, such as the IfI regimen in colorectal cancer, which worked really well in the clinical trial published in the New England Journal of Medicine, but in the real world setting was unbelievably toxic. And so now we're understanding those dynamics so much better. And it's helped if you go to the FDA website and look at diversity, there's huge sections, as there are for real world evidence or real world data, whatever you want to call it. And Chris at Biosi, you will be intimately familiar with all of that, probably far more than I am.
[00:23:50] Speaker B: Interesting. Let's jump up to, I don't know, 50,000ft or something. What's most exciting right now in oncology? I mean, we're maybe slightly spoiled for choice here, but what are the areas that you look at and think, here's where I'm yeah, I see the most promise, or the most what are the next few years look like?
[00:24:05] Speaker C: So I think, in general, the future of oncology is we're going to have drugs and the whole future of medicine, despite the GLP ones and obesity, that work on fewer and fewer people. But the effects of those individuals will be greater and greater and greater, and that's what genomics has taught us. But in my career in HIV and in oncology, the biggest advance has been harnessing the immune system. And in oncology, years ago, we learned that not stimulating the immune system, but inhibiting the inhibition of the immune system. Stopping cancer cells, turning off the immune system by blocking the way they do that with molecules such as anti PD one, anti PD L one, or anti CTLA four S, will really prolong survival. You get a very long tail of survivors. Sometimes the tail isn't that large, but it's often very real. And diseases like lung cancer, melanoma, renal cancer, head and neck cancer, bladder cancer, and so on, that used to kill people, often very rapidly. We failed to build on that for the last decade, but now I'm actually seeing next generation anti CTLA four s and next generation immunotherapies, such as botancilumab, to name but one. Where I'm seeing responses in cold tumors, where they're not that antigenic, they don't stimulate the immune system, they're not tumors traditionally known to get better with immunotherapy, things like microsatellite stable metastatic colorectal cancer. That's the common type of colon cancer. That's where I'm really, really excited about, and the ability to combine those treatments with small molecule inhibitors, even with chemotherapy, is what excites me the most. Again, it's part of a jigsaw.
[00:25:50] Speaker B: Very, very exciting. There was some research that came out recently that said, I think it was just the other day saying that many cancer treatments that had been approved by the FDA under EUAs had failed to perform in patients. Did you see that? And if so, what do you think about that? How should we think about our zeal to approve as quickly as possible? Obviously, we have patients advocating, especially with some really terrible conditions for any treatment. There also is a cost to all these treatments, to the healthcare system and to patients, et cetera. So will you talk a little bit about that?
[00:26:22] Speaker C: What you're describing, Chris, very well, is not new news. Just to be clear, this has been discussed for many years, and it's not just an oncology. Recently we saw amlics pull its drug for motor neuron disease, ALS, off the market because their confirmatory study failed. I thought that was very, very decent of them to do that before the FDA said nothing. Just for the record, I think in oncology, sometimes we have rushed a bit too much, we have been too fast, sometimes we've been too slow. It's difficult to strike the right balance. If I look at my life and things that have happened, sometimes I've got it wrong on one side or another. I think we're learning all the time. As I said, the stupidest cancer cells clever than the cleverest oncologist. We often get it wrong. I don't really know. I don't have a perfect solution to it. But what I would say is, is that in areas of unmet need, so where there's very few existing treatments, or the existing treatments are of a particular type, then I think that the bar should be lower. Just to give one example, I mentioned botancilumab and metastatic colorectal cancer. That is clearly not an area of unmet need because we have lots of drugs for that. But you know what? In later stage disease, in the third, fourth and fifth line settings, all those drugs are what we call tyrosine kinase inhibitors. They work in the same way. So to have a new immunotherapy working, there would be completely a different approach, provided that we saw often very, very good outcomes in those patients, because often the only thing we can guarantee is side effects. We can't guarantee that the patient's going to get better. But if the patient's willing to try, they're fully informed and educated, and they want to do that, then it should be a decision between the patient and their treating physician, supported, not hindered by the regulatory authority. Because although the FDA has made a big thing about the cures act and making any drug and clinical trials available to patients, the bureaucracy behind that, as far as I understand it, is completely impossible.
[00:28:29] Speaker B: It's challenging. Yeah, that's for sure. Yeah. Well, you sound kind of american there, as you described that. That sounds like the individual should have the right to make those decisions for him or herself.
[00:28:37] Speaker C: I think so.
[00:28:38] Speaker B: I heartily agree with that. I think we run up against some challenges, especially as we move to poorer countries with tighter, tighter budgets, but I guess we just muddle forward.
[00:28:47] Speaker C: But when you make drugs available on a compassionate use basis, when you're thinking about a world of biosimilars, all you're trying to do is democratize healthcare. You're trying to remove sort of, you're basically removing the financial resources of the individual from that equation, which in an idealistic world, is what you'd want to do.
[00:29:04] Speaker B: So, Justin, you have one of the strangest careers of anybody that we've talked to on the podcast. We like to talk to polymaths. You're an incredible example of that. You're an investor, you're a, you're a practicing scientist, you're involved with a number of companies. You're an editor of scientific journals, and you're, if I can say, sort of a popular science writer as well. What advice would you give to a young person with a stem background who's looking forward to doing something in the sciences in their career? I think about this in part because of some of my kids, but I'm curious for, like, what advice you would give to people as they're sort of thinking about what turns into a meaningful career.
[00:29:40] Speaker C: I would say a few things. Firstly, I think most of it's perspiration, not inspiration. I'm not that smart. People say I'm, I'm not, I know I'm not self and I don't understand simple things, but I work really hard. The second thing is, I always think it's really important to be nice and decent. I have two beautiful boys who are the most remarkable academic underachievers, but they're nice, they have good values. And when I think about people, I think about four things. I think about their IQ. We all know what that is, their Eq. We all know what that is, because everyone says, what about their EQ? I think about their CQ, which is their character, trust, integrity, and I think about their PQ productivity, which basically means the ability to get things done. And at the end of the day, I look at all four of those things and people that I work with, and it's really nice to work with like minded individuals there. And you really don't have to be the smartest person in the room. If you're very good at something, which I never was, run with it. But because I was never very good at anything in particular, I didn't have that opportunity. So I had to do lots of things not very well, as opposed to one thing really well.
[00:30:48] Speaker B: I think you are perhaps being a little bit humble there. But I'll tell you, that framework of Iq, Eq, CQ and PQ is pure magic. So we're certainly going to quote that in the call out for the podcast. Last question. I would be remiss if I didn't ask you, of all people, about artificial intelligence and how you see that changing drug discovery, drug development as we move forward. You know, you've had, of course, direct experience with this. We talked about that during COVID And the chair you have at oncogene, I'm sure gives you insight here how over hyped, under hyped, or appropriately hyped, I guess, is my first question. And how do you see AI changing the way in which we develop drugs as we go forward?
[00:31:25] Speaker C: Well, it was under hyped, then it became massively overhyped, and now no one really notices it. And because of that, I think it's entered the real world and entered our frameworks, and there will be productivity gains, whether it's booking appointments and making notes or helping us diagnose. But I'd say two things about it. First, human plus AI seems better than human or AI with anything.
[00:31:52] Speaker B: Yes, I agree.
[00:31:53] Speaker C: And then the second point is that we have these amazing, amazing things like Alphafold and other programs predicting all of protein space and protein binding. But let's make sure we see the drugs and the products that come because of this before we jump to any conclusions, let's see the results first. Because when we start getting with drugs that work from it, I'll say it's great. And if we don't, I'll say it's not so great. The proof will be in the pudding. I'm results driven. Let's see the results before all the hype first.
[00:32:23] Speaker B: Hear, hear. Well, Justin's Debbie, a complete delight. Thank you so much. Thank you, Chris, for joining us on food and far between today.
[00:32:29] Speaker C: Thank you.
[00:32:34] Speaker B: Thank you for listening to the latest.
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