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Uncovering Insights into Cancer and Alzheimer's with Marcus Peter, PhD

For decades, Marcus Peter, PhD, has drilled into an area of research focused on cell death and the roles of toxic and protective short RNAs, with the goal of developing a novel form of cancer treatment. Now, this same line of research has led Peter’s team to uncover new insights into the cause of Alzheimer's disease. In this episode, Peter explains his pioneering work in investigating RNA interference in diseases and explains how his lab’s latest novel discovery may have relevance to an array of neurodegenerative diseases beyond Alzheimer’s.


“In Alzheimer’s, indeed, late-stage Alzheimer’s patients get much less cancer. Funny enough, late-stage cancer patients don't get dementia that much. So there is this inverse correlation. And once we did the literature search, we found the same connection to less cancer for Parkinson’s, for ALS, for all these diseases. That's why we got interested in Alzheimer's disease.” Marcus Peter, PhD 

Episode Notes 

What started off as a phenomena in his lab has expanded Peter's career as a cancer investigator towards new possibilities for treating not only cancer but Alzheimer's and other neurodegenerative diseases. 

  • A longtime scientist of cancer and cell death, Peter made a discovery 14 years ago involving a short RNA and cell death that doesn’t impact normal cells.  
  • Recently, a mechanism Peter calls "death induced by survival gene elimination" or "DISE" was discovered. This anticancer mechanism is based on a theory of microRNAs targeting mRNAs that code for critical survivor genes. In his studies, DISE kills cancer cells but leaves normal tissues unharmed, by targeting essential survival genes. 
  • Peter pivoted from cancer research to Alzheimer’s research when he and his wife and colleague, Andrea Murmann, PhD, began searching for scenarios in which DISE was overactive, leading to an understanding of the relationship between DISE and neurodegeneration, such as Huntington’s and Alzheimer’s disease. 
  • In multiple studies, Peter found that chemotherapy, to some extent, unleashes a wave of toxic short RNAs that kill cancer cells through this same mechanism.  
  • In their most recent study, published in Nature Communications, Peter and his team developed a tool to analyze the ratio of toxic and non-toxic RNAs in this context. They then applied these methods to mouse models that mimic Alzheimer’s and found a higher ratio of toxic RNAs present.  
  • Among the study's more dramatic findings was the discovery of a higher ratio of toxic RNAs in older mice versus younger mice. This suggests that with aging comes a loss of protective microRNAs. Similar results were found when Peter and his team examined brains from subjects in Northwestern’s SuperAgers project. SuperAgers are adults over age 80 who have the memory capacity of individuals who are at least three decades younger.  
  • These findings could eventually lead to new treatment methods for Alzheimer’s based on either inhibiting toxic RNAs or increasing the number of protective microRNAs to enhance resilience. 
  • There are also significant implications for neurodegenerative diseases broadly based on these findings, and with sufficient funding. Peter hopes to begin testing in animal models beyond Alzheimer’s. Peter has started a company, NUAgo Therapeutics, to advance this research. 

Additional Reading 

Continuing Medical Education Credit

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Target Audience

Academic/Research, Multiple specialties

Learning Objectives

At the conclusion of this activity, participants will be able to:

  1. Identify the research interests and initiatives of Feinberg faculty.
  2. Discuss new updates in clinical and translational research.

Accreditation Statement

The Northwestern University Feinberg School of Medicine is accredited by the Accreditation Council for Continuing Medical Education (ACCME) to provide continuing medical education for physicians.

Credit Designation Statement

The Northwestern University Feinberg School of Medicine designates this Enduring Material for a maximum of 0.25 AMA PRA Category 1 Credit(s)™. Physicians should claim only the credit commensurate with the extent of their participation in the activity.

American Board of Surgery Continuous Certification Program

Successful completion of this CME activity enables the learner to earn credit toward the CME requirement(s) of the American Board of Surgery’s Continuous Certification program. It is the CME activity provider's responsibility to submit learner completion information to ACCME for the purpose of granting ABS credit.

Disclosure Statement

Marcus Peter, PhD, has nothing to disclose. Course director, Robert Rosa, MD, has nothing to disclose. Planning committee member, Erin Spain, has nothing to disclose. FSM’s CME Leadership, Review Committee, and Staff have no relevant financial relationships with ineligible companies to disclose.

All the relevant financial relationships for these individuals have been mitigated.

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Read the Full Transcript

[00:00:00] Erin Spain, MS: This is Breakthroughs, a podcast from Northwestern University Feinberg School of Medicine. I'm Erin Spain, host of the show. For more than 30 years, Dr. Marcus Peter has immersed himself in cancer research. Most recently at the Robert H. Lurie Comprehensive Cancer Center of Northwestern University, pioneering studies in the field of cell death research and developing strategies to selectively kill cancer cells. He is now using the same trailblazing methods he has uncovered in cancer research to lay the foundation for a new avenue of treating Alzheimer's disease and potentially other neurodegenerative diseases. He is the Tom D. Spies professor of cancer metabolism, and a professor of medicine and the division of hematology and oncology here at Feinberg and joins me today to discuss his research. Welcome to the show. 

[00:01:05] Marcus Peter, PhD: Thanks Erin, and thanks so much for having me. 

[00:01:07] Erin Spain, MS: So let's start off by talking about cell death research. As I mentioned, this is something you've been doing for about 30 years. Explain this research to me. 

[00:01:16] Marcus Peter, PhD: So how can we make cells die? Obviously, there's one particular type of cell that we'd like to kill. The cancer cells. So for the last 30 years, basically it's all been about cancer research and how we can tackle this. How can we overcome resistance to therapy? How can we eliminate cancer cells without affecting normal cells? And it started out with one particular form of cell death that's called apoptosis. It's one of those regulated forms of cell death, and we studied that and we deciphered how it works, and I learned a lot about what makes cells die. However, more recently, last 10 years or so, I realized is that as a biologist, if I was mother nature, why would I put all my money on one form of cell death only if I wanted to eliminate cancer cells, which is critical for survival, right? And in the early two thousands pretty much all cancer centers worldwide had one mission or was to cure all cancers by 2015. That's nine years ago. So out of that frustration a little bit arose a driving force: the desire to start over and think about what could it be that has made us survive as multicellular organisms the last 2 billion years, basically. And then about 14 years ago we stumbled over something that allowed us to kill all cancer cells in a way they could never become resistant to this day. And we now know when we do this, when we trigger this mechanism that we are gonna talk about today, then we also don't have any measurable effect on normal tissues yet. That's not to say if it ever gets into patients, we won't have side effects, but so far we don't see anything in animals. So that's how it started. So initially it has nothing to do with neurodegenerative diseases such as Alzheimer's disease, but it was this mechanism and so we started diving into how does this work? It is based on short RNAs. 

[00:03:05] Erin Spain, MS: And you have found that these short RNAs, in particular noncoding RNAs play an important role in regulating gene expression and could have implications for cellular functions, survival and potential therapeutic strategies. Tell me more about this. 

[00:03:21] Marcus Peter, PhD: Gladly. So we have a number of large molecules in cells we call macromolecules, and they are these different classes and pretty much everybody knows about DNA. And then there's protein. Proteins basically are what makes all cells function properly. And in between are certain types of RNA, that code for those proteins. So the DNA is converted into these long RNAs. The RNAs give rise to the proteins that make the cells function and survive. It's important, this context. But then there are short RNAs and they don't code for protein. So we call them non-coding RNAs, and they have multiple functions. And a class of those short RNAs, they're only 20 nucleotides long. These are the building blocks of DNA and RNA. These short ones, they actually negatively regulate gene expression. So basically they target the long RNAs. The moment the short RNA, which is a piece, sometimes a piece of the long RNA, targets the long RNA, the long RNA gets eliminated. The protein can no longer be made. They will have effects on cells. We can induce this process. It's called RNA interference or RNAi, but nature of course invented it and does it much better. And there are professional short RNAs that do this, and they're called microRNAs. And microRNAs do target dozens, sometimes hundreds of these genes in networks. And they do maintain differentiation. They do a lot of different functions. 

[00:04:44] Erin Spain, MS: Thank you for that explanation. Can you tell me more about what makes some of these short RNAs toxic? 

[00:04:51] Marcus Peter, PhD: To understand why certain short RNAs can be toxic, we need to understand that we have about 20,000 genes in our genome, roughly and about, again, roughly 10% of those genes are required for survival of all cells. Of those 20,000 genes, many of them can be eliminated. You may have some effects, some response by the cells, but it's not critical. And then there is a subset of about 10%, about 2000 of those genes, and they're defined by taking one of them out in a cell and every cell would die. And we call those essential survivor genes. Now think about it. If there's a long RNA that codes for one of those critical survivor genes, what would happen if we eliminated or target that long RNA, the cells would die? So that means that over the last 800 million years, at least, that's how old microsRNAs are, all the way from little worms to us, that there must have been an evolution to prevent microRNA from ever targeting, attacking the mRNAs that code for those critical survivor genes. So, and that is exactly what we found. And since the way the short RNA targets the RNAs is only worth a minimum of six nucleotides, it's a very short region that we call the seed sequence. So if that seed sequence has a certain nuclear tech composition. We have four nucleotides in all of nature. And if there has a certain G richness as we say, but only in the short stretch, what we call the seed, and we put that in any, any short RNA and it does its thing and targeting the long RNAs, every cell would die. So that's why not a single highly expressed microns we have in every cell, or almost all cells in our bodies carries this code. We call the kill code 'cause every cell will die. Now if you really believe in our hypothesis, if you buy into that, that it is that old, and that could be a mechanism, that would be of course a fantastic way for nature, not only to protect us, but also kill cells that are unwanted. So in fact, this would be the ideal anti-cancer mechanism if you could control it, because obviously it is very dangerous. It's very powerful and needs to be controlled tightly. And coming back to what I said initially, it does activate multiple, multiple cell death pathways. We have about 20, 30 of 'em today, not just one or two or three as a few decades ago. So now you have it. You can activate all those in parallel. And you can imagine once you're attacking dozens or hundreds of genes in these targeted sites, in these genes there are even more. How can a cancer cell ever become resistant to that? It would have to mutate. Basically all these genes eliminate all these sites. So that is the mechanism that we believe we discovered. We call "death induced by survival gene elimination,”  in short, "DISE." 

[00:07:46] Erin Spain, MS: Tell me how you discovered that these toxic RNAs allow cancer cells to die, but not normal cells. 

[00:07:52] Marcus Peter, PhD: When we realized that we have certain types of short RNAs that are toxic to pretty much all cells and were super toxic in killing cancer cells, we then started delivering those constructs to mice, to rodents in cancer models. And yes, we had all expectations that those mice would drop dead after the injection, but they didn't. They're perfectly fine to this day. So it turns out that, at least from what we can tell, every tissue we'd looked at, the liver being the most important one in this case, is unaffected. Which raises the question, since those survivor genes you would think would be expressed in all cells, like all of us have a heart and a liver, why would normal cells be spared? And then it hit us. It was basically the fact that microRNAs are expressed in all cells and microRNAs are required to maintain differentiation and maintain all of what we are. And when you look into what cancers do, they're the opposite. They are de-differentiated. Cancer, for the most part, is not really killing people. It's metastasis. 90% of our deaths occur through metastasizing cancers. Metastasizing cancer are the opposite of a differentiated tissue. So then if you believe that microRNAs maintain differentiation, then in order to become a really good mobile highly killing cancer cell, you need to get rid of those microRNAs. And that's exactly what we found. It's also been published by others before as a global downregulation of all microRNA in all human cancers and some of the cancers they studied in rodents as well. And that kind of opens up the machinery in the cell that mediates RNAi in a simplified way. And then the other aspect is that those survival genes, they're not only good for survival of normal cells. Cancer cells are under a lot of stress. In order to resist that, to become a resilient, guess what? They do upregulate all those survival genes that we are targeting with our therapy. So there you have it. You have a complex of proteins that mediates RNAi that is open because the protective micron is no longer there and you have more of the targets that we're targeting and that allows the cancer cells to die, in normal cells, not. And that was exactly the question, what would happen if normal cells would lose their protection? Again, known for many years. There is a downregulation of microRNAs in many tissues in mammals, including humans with age. So there is an aging connection. 

[00:10:21] Erin Spain, MS: So, why does this mechanism exist? And why are normal cells protected? 

[00:10:25] Marcus Peter, PhD: I think we ask ourselves, oh, it's great that we can treat mice and we can have an effect on tumors in these mice with no effect on normal cells. Why? I mean, there's an evolutionary underpinning, there's a rationale why this exists. If this were a mechanism that would be effective on every single cell hardwired into the cell, it would always be limited to a cell. The selectiveness between a cancer cell and a normal cell would just be at the level of what makes a cancer cell different from a normal cell. It would not explain why a normal cell is resistant to this mechanism. So there had to be something, and I believe we found it, and that is there are endogenous RNAs in the cells that have this coat and they are needed. and these are long RNAs and many of the long RNAs, they're, in fact, the majority of all RNA in the cell are so-called ribosomal RNAs for the aficionados or tRNAs. And they are structural RNAs. That means they're not really regulatory, they're structural, and they have this specific nuclear tech composition. It's known for many years that they can be degraded into small RNAs, and since they are so hugely abundant, they can sneak into this risk complex and they could potentially kill cells, and that's also known that they get degraded and enter this complex and mediate RNAi. So we now believe, that's how nature works, that those microRNAs are not only maintaining differentiation and they're very highly expressed in all differentiated cells, but they're also protect us from any endogenous toxic RNAs. They're not just these microRNAs, they're also the fragments of these usually abundant RNAs said contain the kill code. So that I think is why it evolved this way. And fun fact that's also known for many years that these, again, for the aficionados, tRNAs, are highly increased in Alzheimer patients and when we age. It's all published and you put this all together. I said, wow, that's what we need to protect it for. That's why we now come in from with exhaustion of sources basically put it coming from the outside with the therapeutics. That's why normal cells are still protected because they're still busy protecting themselves from themselves basically. 

[00:12:38] Erin Spain, MS: Are there other folks around the world who are also studying this? This is something that your lab has discovered and now that you're bringing into other diseases, but tell me about around the world. Have other folks started to look into this type of science for cancer treatment? 

[00:12:53] Marcus Peter, PhD: To this day we have published 21 papers on this in multiple diseases, in major journals. And no, to this day, not a single group worldwide has picked this up but one. There's one group in Kentucky that four years after the original discovery traced our steps and did exactly the same that we found and published it in the context of prostate cancer. To this day, to my knowledge, this is the only paper that ever followed our path, but that's fine because we just keep developing it. 

[00:13:21] Erin Spain, MS: Well, that leads me to this next question, which is you're continuing on this journey through cancer research and then there's this pivot to Alzheimer's research. How does that come about? 

[00:13:31] Marcus Peter, PhD: It actually was my wife who's in the group, Andrea Mermann, who figured, well, if you're right and there is this death inducing, anti-cancer mechanism, shouldn't there be a case where this is overactive and shouldn't that result in some sort of disease because of loss of tissue, such as neurodegenerative diseases, for instance, and said, Hey, that's a good idea. Since this is an anti-cancer mechanism, we figured, well then we would postulate that these patients may have a neurodegenerative disease, but they may have less cancer because the anti-cancer mechanism will be active in every cell in the body, right? And so she started searching and the first thing found was a disease called Huntington's disease. Nice thing about Huntington's disease, in contrast to Alzheimer's disease, has a single cause. There has one gene affected Huntington by an amplification of a certain sequence in nucleotides. And there is evidence in the literature that these sequences can act like short RNAs and they're uploaded into the complex that mediates RNAi and regulates genes just like microRNAs. When we realized that, Andi ordered short RNAs and tested whether we can kill cancer cells, and boy could we kill cancer cells. This was 10 to a hundred times more potent than the original ones, the DISE inducing ones. And so we looked into Huntington's disease and indeed Huntington's disease patients, there are multiple studies corrected for age and everything that showed they have 50 to 80% reduced cancers and that's all cancers. Wow, we thought. Maybe we should start looking to that. So that's one of the reagents we're developing, as a new form of cancer therapy, these Huntington derived super toxic RNAs. Well, Huntington patients have decades of symptom free life, and then there is an onset and it kicks in and then it goes downhill from there. And that is also true for pretty much all those neurodegenerative diseases from Parkinson's to ALS, to Alzheimer's disease. And since here at Northwestern, we have this fabulous collaborators, I teamed up with the group, Bob Vasser at the Mesulam Center for Alzheimer's Research here at Northwestern. We started looking into this. And then we tested multiple models, mouse models, neuron derived cell line models treated with the specific toxic proteins that are believed to be the cause of Alzheimer, induced pluripotent stem cells differentiated into neurons and something we're gonna talk about, I guess also later the Super Agers. And we put all this together, we realized indeed these toxic RNAs accumulate in the cells in this complex that mediates RNA, RNAi in Alzheimer's patients. In Alzheimer, indeed, late stage Alzheimer patients get much less cancer. Funny enough, late stage cancer patients don't get dementia that much. So there is this inverse correlation and once we did the literature search, we found the same connection to less cancer for Parkinson, for ALS, for all these diseases. That's why we got interested in Alzheimer's disease. 

[00:16:36] Erin Spain, MS: So now we're gonna dive into the current study that we're talking about today, recently published in Nature Communications. Tell me about this study, some of the results and what you were able to publish. 

[00:16:45] Marcus Peter, PhD: Yeah. This study actually was based on a previous study in the context of ovarian cancer where we looked at patient material and mouse models, and we realized not only can we kill cancer cells with these toxic RNAs. But when the cells become resistant to chemotherapy in ovarian cancer, that would be mostly platinum based, the chemotherapy. Then the ratio of the non-toxic to the toxic short RNAs in this protein complex in the cell that mediates RNAi, it's called the risk complex, by the way, changes. So in the resistant ones, you have more of the non-toxic ones, providing a better protection against toxic ones. And in two previous papers including this one, we showed that chemotherapy to some extent unleashes a wave of toxic short RNAs and in part kills cancer cells through this mechanism. So we kind of knew that the ratio of the non-toxic versus the toxic ones in this risk complex that may predict treatment outcome, or in other words, may predict whether any tissue will be susceptible to this or not. And then we had to develop this tool that allows us, in a very standardized fashion, to analyze the contact of this protein complex that mediates RNAi and plot it and quantify it. And so once we had that and validated it, we then started establishing mouse models, different types of mouse models that mimic the human disease, Alzheimer's. We got cell lines that were treated with the toxic proteins that everybody else studies, which are of course on top of this cascade that leads to the neurotoxicity seen in the disease. And we looked in other components, and we got, as I mentioned, cells that arrived from stem cells turned into neurons, and we got those actually from Alzheimer patients and studied them. And in all these cases, we found that in the context of Alzheimer, the amount of the toxic seed containing RNAs in this complex is higher than the non-toxic or the ratio shifts. Similar to the study on the drug resistant ovarian cancer patient. It shifted, so they become more susceptible to DISE, this mechanism we discovered. And when we treated the cells acutely with this toxic protein that we know induces Alzheimer's disease in patients, then that resulted in a very clear dip of the non-toxic, the protective microRNA, that's why we call them protective microRNAs. There's a clear correlation between your ability to deal with the stress and having the protection. 

[00:19:21] Erin Spain, MS: You were able to leverage these findings from your study and apply what you found to the brains of SuperAgers. Now we've done previous episodes about SuperAgers and the SuperAging research program here at Northwestern. It recruits and studies adults over the age of 80, who have memory capacity of individuals who are at least three decades younger. And after they pass away, super-agers donate their brains to the research program to help investigators understand what's going right with aging as opposed to what is going wrong. So tell me what you found when you investigated your theory on their brains of the super-agers. 

[00:19:58] Marcus Peter, PhD: It was a very preliminary study, but we got three brains of these super ages and subjected them to the same type of analysis and compared them to regular folks like us, right? The non-super agers. And it turns out, indeed, as predicted the ratio in those brains of the toxic to non-toxic one was toward the non-toxic. They still have more protective ones. So I think, we postulate, we hypothesize at least that these people for a reason that are unknown, aging more slowly, which of course gets us to where we need to take this whole thing, right? We need to find a way to reduce the loss, to slow down the loss. We'll probably never be able to reduce it, but the slow down the loss of the reproductive microRNAs, a number of tissues selectively, hopefully in the brain, and that should help with basically make us more resilient towards getting any of those neurodegenerative diseases or may even be helping with aging. 

[00:20:50] Erin Spain, MS: But there's also this idea out here that this study could lead to new treatments for Alzheimer's, which is desperately needed. Can you talk about that aspect a little bit and sort of a pathway forward for potential new treatments for Alzheimer's? 

[00:21:02] Marcus Peter, PhD: Absolutely. That of course, is exactly the flip side of our cancer approach. In cancer, of course, we're trying to design the most toxic short RNAs that have the highest selectivity for cancer cells are not affecting normal cells. Now, Alzheimer’s is exactly the opposite. Here we want to either prevent the toxic RNAs if they have a major contribution to the disease to do their thing. Or we would like to increase the amount of the protective ones to make it more resilient and maybe push the onset of Alzheimer's from, you know, your early eighties to your early nineties, and then it may not be that much of a problem anymore. And this is, I think, could be feasible, but requires a lot of basic science work. Because what we need to study now, and there are some ideas and some data out there, is what are the mechanisms that regulate this? What is the mechanism that regulates the ratio between the toxic and a non-toxic one? What's the specific about the non-toxic ones and how could you elevate that in cells? And that is a biological mechanism that has not been discovered. But there are some ideas, and we have some ideas of screenings that we could set up, design certain screens to screen for small molecules that could do that. There's actually an antibiotic called anoxycin that has been shown in mice, not with Alzheimer, but with a ALS, a model for ALS, to alleviate pretty much all symptoms in two different models. And this thing is known to stabilize microRNA, in our book, protective microRNAs. So there is already a drug out there which was never screened for, it was never designed to do that. And I'm sure we can do better once we know what'll we looking for, to design specific screens, to get small molecules that increase the number of protective ones. I think that would be my favorite approach because I think that may have the least side effects rather than, you know, playing with the toxic ones. And that's the whole thing. Treatment is one issue. Prevention's another. Obviously, the safety profile for anything that you want to use for prevention is very different because you want people to take this for decades, so you better have no side effects whatsoever. But if you're in an acute situation, like somebody has advanced cancer or advanced Alzheimer's, you can have a beneficial effect with something it just has a less favorable safety profile. And so these are two different avenues which hopefully will be explored. And we can't do this alone. We are a small group. We need the help of the community to buy into this, start looking into that. And some people that are way smarter than us coming up with ideas to make this happen. 

[00:23:32] Erin Spain, MS: So if you could wrap this up for me today, what would you like people to know about your lab and what's next? 

[00:23:38] Marcus Peter, PhD: What's next in the cancer arena is that even though this is, by design, a pan-cancer mechanism, that's not to say that there may not be toxic RNA that are particularly active in one or another cancer. So we need to get the full landscape of what are the endogenous short RNAs. As a basic scientist, I would like to continue to make discoveries in this area and figure out how it's regulated. That's the next big step and how it works to be able to use it in a better way to treat diseases. And of course, again, all depending on funding. And opportunities. We have no issue in venturing out into other diseases. We did have a paper last year in Journal of Virology on the first evidence of how viruses, in this case, HIV one kills infected cells using the DISE mechanism because if it's a billion years old, it has to be everywhere. And so obviously we are a single, very small lab. We cannot study everything, so we have to focus. 

[00:24:38] Erin Spain, MS: I understand. You've also started a company to help move this forward into the translational science field. 

[00:24:45] Marcus Peter, PhD: the name of a company says it all, NUAgo, which is "NU" for Northwest University or 'new' if you want. And Ago is of course for Chicago or for the key proteins. They're called the AGO proteins that are part of this complex that mediates RNA interference. There you have it. NUAgo is not specifically, it's in the name, a cancer fighting company only, but we'll see what happens. We will be able to sponsor some of the research, at least initially in my lab here at Northwestern through the company that should start hopefully this year. And then obviously, who knows where this will take us. 

 [00:25:22] Erin Spain, MS: And I just have one more question. What advice would you give to younger investigators who are listening to this and they're realizing, wow, you had to forge your own path and take a lot of risk and maybe do things that weren't the popular thing to study or do. What advice do you have for folks who that may sound a little intimidating to them, and what advice would you give to a younger person just starting off on this journey? 

[00:25:45] Marcus Peter, PhD: All depends on your level of risk tolerance, right? So you have to develop something that is grounded on what others are doing because you always, as we say, standing on the shoulders of giants and you have to take off from there, from their shoulders. Then you really need to make sure that you make a name, you carve out a niche, and you make a career in order to get a grant, a federal grant, which is the only thing that counts at institution like ours. Don't find what proves your hypothesis. Always try to disprove your own hypothesis. This thing started out by phenomena we couldn't explain. And when I realized what it is, I challenged everybody in the lab. Disprove me. Show me that it is not true. And every time we dove into further. we found another mosaic piece that fit into something that turned into this whole concept, I think that's the advice for young people. Go your own way, but initially have your bread and butter project. Play safe. Make a name. Get the funding, but then, don't care about anybody. 

[00:26:45] Erin Spain, MS: Thank you Dr. Peter for coming on the show. You have some very exciting things in the pipeline. We'll continue to follow along, so thank you. 

[00:26:53] Marcus Peter, PhD: Thank you so much for having me. This was fun. 

[00:26:55] Erin Spain, MS: Thanks for listening, and be sure to subscribe to this show on Apple Podcasts or wherever you listen to podcasts. And rate and review us also for medical professionals. This episode of Breakthroughs is available for CME Credit. Go to our website, feinberg northwestern edu, and search CME.