Parker Wilson has taken a sometimes-unpredictable path to obtain his MD and PhD degrees and establish his physician scientist career, but he’s been quick to adopt and apply the molecular genetic pathology tools that are changing his field. Join us to hear about his exciting work where he uses digital PCR and NGS methods to identify and quantify rare mutations associated with kidney disease.
Same may think of the pathologist’s toolbox as only the microscope and their eyes, but in reality today’s pathologists are using more and more molecular methods like NGS and PCR in additional to their traditional tools.
Meet Parker Wilson, MD, PhD. Parker is a faculty member Perelman School of Medicine at the University of Pennsylvania, focused on using modern molecular tools to investigate chronic kidney disease. He explains his work phenomenally, both from the general aspects, all the way down to the molecular methods, which include digital PCR. We learn about chronic kidney disease and the interesting genetic mutations associated with it, which Parker and his team are finding, include chromosomal loss. For this application, we hear how dPCR is adept at quantifying chromosome ratios within tissues, and is able to help them spot variations of only a single percent or two.
Our career corner portion uncovers an academic and career path with uncertainty and challenges one might not expect. Parker helps normalize these challenges and underscores the value of mentors in helping navigate them successfully. In the end, you have a phenomenally intelligent physician scientists sharing his exciting work and his insightful career development advice.
Visit the Absolute Gene-ius pageto learn more about the guests, the hosts, and the Applied Biosystems QuantStudio Absolute Q Digital PCR System.
Christina Bouwens 00:00
And I'm Christina Bouwens. And today we have the great prep. Whoa, reading is hard today.
Jordan Ruggieri 00:06
Whoa, blub, blub, blub, blub.
Christina Bouwens 00:08
More turkey dialect.
Jordan Ruggieri 00:12
That's my next costume. Turkey.
Jordan Ruggieri 00:26
Welcome to Absolute Gene-ius, a podcast series from Thermo Fisher Scientific. I'm Jordan Ruggieri.
Christina Bouwens 00:32
And I'm Christina Bowens. And today we have the great pleasure of learning from Dr. Parker Wilson about some fascinating digital PCR applications.
Jordan Ruggieri 00:39
Parker earned his MD PhD from the Medical University of South Carolina in 2013 and has spent the past 10 plus years pursuing a mix of research and clinical work. He is now an assistant professor of pathology and laboratory medicine at the University of Pennsylvania School of Medicine, where he leads a lab developing therapies for chronic kidney disease, we hope you enjoy our conversation.
Christina Bouwens 01:02
This is my regular talking voice. And if I got really loud and might get over here.
Jordan Ruggieri 01:07
I mean, do you really need your speakers out loud when I'm on a phone call?
Christina Bouwens 01:10
No. Not really.
Jordan Ruggieri 01:11
Your children can probably hear me in the other room.
Jordan Ruggieri 01:19
Parker, thank you so much for joining us today on Absolute Gene-ius. We are absolutely thrilled to have you here and we'd love to just start off with will you give us just a background about your research, or your current research and what you're, what you're interested in.
Parker Wilson, MD PhD 01:35
Yeah, thanks so much for having me. I am a renal pathologist. I do renal pathology practice and I also focus heavily on research. And the areas that we're most interested in are single cell genomics, and digital PCR, which is what we're going to focus on today. From a 10,000-foot view, you can think of what are the factors that lead to kidney function decline. And this entity called chronic kidney disease affects lots and lots of people both within the United States and globally and there are some very common causes of chronic kidney disease. But we really don't understand what leads people to develop worse kidney function over time. Are there ways we can intervene to help them improve their kidney function? And more importantly, what is happening on the molecular level that might drive kidney function decline? I am a pathologist. So although I focus on kidney pathology, and non-neoplastic, or non-tumor tissues. I am surrounded all the time by people who are mostly focused on cancer research. And a lot of my training has really focused on how to characterize tumors. And one thing that we really know a lot about in tumors is that they develop mutations. And these mutations can be very small, as small as a single base pair, or they can be really, really big, involving entire chromosomes. So we've always had this in the back of our minds and a question that's emerging is this concept of somatic mosaicism. And this is a really fancy word for as you age, all of your cells in your body accumulate mutations over time. And the kidney certainly has this going on as you age or as you develop chronic kidney disease, you have a higher risk for cancer. But what happens in that intermediate period? The vast majority of people with chronic kidney disease do not develop cancer, although they do have increased risk. And we know that certain cell types in the kidney are predisposed to developing tumors. And these cell types that are most likely to become tumors are the same ones that line the inside of these nephrons of these tubes. So what we wanted to know is, can you interrogate a single cell in a kidney and ask whether or not it has accumulated mutations over time? And does this define a cell that is more sick or less able to function? And what mutations can we look for? And at the same time, there has been another field that's been developing in parallel. And this is the field of hematology or hematopathology. And this is the study of blood disorders and blood diseases. And one of the precursors of one of the things that happens to some people, often long before, as you age and it is considered sort of a risk factor, is this concept of mosaic chromosomal alterations. This is just another fancy word for somatic mosaicism. And I like to think of it as abnormalities in copy number. Does a cell have an extra chromosome or does it not have enough chromosomes? Can you find these? And strangely enough, if you look back in the literature 50 years ago, maybe even longer, people had known for a long time that as men age, some of their cells in the blood will lose the Y chromosome. This is totally bizarre and counterintuitive and for the longest time in the literature, people have always thought that this was just a function of normal aging, as you get older as a man some of your cells will lose the Y chromosome, but you don't need to worry about this. There is a growing body of evidence that loss of Y chromosome is probably not a good thing. As you accumulate these cells and age in the blood, they probably have adverse effects on other organs. And there is a big paper that came out in the past couple of years, showing that if you remove the Y chromosome from blood cells, these blood cells can then traffic to other tissues like the heart, or the kidney, where they promote fibrosis. And this was some of the most early mechanistic evidence that things like loss of Y chromosome, or these mosaic chromosomal alterations, somatic mosaicism, all these different names for the same thing, have bad effects. So you can find these in the blood and people have developed some PCR assays to do this not that long ago. And the easiest way to do this is with qPCR. But people quickly found out that this is very difficult to do.
Christina Bouwens 06:23
Well, this sounds like a great method for dPCR.
Parker Wilson, MD PhD 06:26
Yeah, so is this great for digital PCR and some digital PCR approaches came out in the last couple of years. And people have published on this to look at loss of Y chromosome in blood. And conceptually, this is very easy to think of, you just design primers and probes for different chromosome targets. The nice thing about the assays that we use is you can use a multiplex reaction, you can design multiple primer probe combinations, to estimate a ratio of the relative number of chromosomes within the tissue. So what we did, for this paper we published back in January, is we designed a digital PCR assay where we have one primer probe set is targeting the Y chromosome, another targeting the X chromosome. And then we estimate the ratio between the quantity of X and Y chromosomes in the tissue.
Christina Bouwens 07:27
This is interesting, because you were saying that you're using this because your whole story of kind of going back to single cell and being able to look at individual single cells. But this sounds like almost like you're using this as a precursor tool to identify those cells that you're going to want to look at, which is so clever, and such a really unique take on it.
Parker Wilson, MD PhD 07:44
Yeah, thank you. And this is this is sort of the way we're starting to use it now. And I came into this, in the reverse fashion, we started off with single cell sequencing and what we noticed was that some cells by single cell sequencing, whether you're measuring RNA, or ATAC, which is sort of a form of DNA sequencing, a proportion of cells is missing transcripts or DNA fragments that map to the Y chromosome. And single cell sequencing is really sparse. So you don't know, maybe “Did we not sequence deep enough? Are we looking at the wrong thing or thinking the wrong way about this?” But we saw these patterns, and we saw that some cells have a much higher proportion of loss of Y chromosome. So if you're only looking at gene expression, maybe that's due to downregulation of Y chromosome, but we were using a technology called multiome sequencing, where we can look at both RNA and ATAC simultaneously in the same cell. And we saw a pattern that was consistent between the two modalities. We looked at this in a variety of other datasets, but we thought, “How do we validate this? Is anybody going to believe us if we try and publish single cell sequencing data alone?” I think you could always argue that it's too sparse and maybe your reads are not mapping very well to the Y chromosome. The Y chromosome has a lot of heterochromatin. It's highly repetitive. It's very hard to map to. People tend to ignore it and GWAS for this reason. And we looked at digital PCR to develop an assay to do this. And we took the same samples that we did single cell sequencing and then we looked at them by digital PCR to quantify a ratio between the X and the Y chromosome. And we saw the same patterns. There was a positive correlation between the single cell estimate for loss of Y and a bulk estimate, which is what we're doing here by digital PCR, of loss of Y. It is convenient that the cell type we're interested in or that gets injured happens to be the majority of the kidney. But you could conceivably sort cells. We have done this in cell culture assays, and we've also developed similar models or similar assays for digital PCR in animal models of kidney disease.
Jordan Ruggieri 10:03
So, Parker, quick question for you, I want to take a couple steps back just for some quick hitting questions for our listeners. These mutations, and some of the mosaicism that you're seeing, is this due simply to the fact that they're epithelial cells and they're constantly shedding and regrowing and shedding and regrowing so that the chance of accumulating mutations over time is higher?
Parker Wilson, MD PhD 10:27
Yeah. This is a this is a great question and I think I don't have any answers to this question, but I do have some ideas. We know that since you see loss of Y chromosome in the blood and you see it in certain cell types in the kidney, and potentially some other tissues as well, that, especially in the blood, this might be related to high turnover rates, which is what you're getting at. So the blood, you need to replace your blood cells every couple of months and the kidney, the lining of these nephrons, is always getting turned over and replaced, and you're losing cells. So some of our thinking is that the number of times that a cell has divided in its lifetime is associated with acquisition of things like loss of Y chromosome. Every time a cell divides, there is a small chance that one of the chromosomes will get missorted or you know, end up in the wrong place after cell division. One potential way this could happen is that, as you divide, one cell might end up with, say, two Y chromosomes, the other cell ends up with two X chromosomes. And then the cell that has two Y chromosomes undergoes apoptosis. And there's probably an element of selection here, where certain cell types or certain genotypes within cells, and this might even be specific to certain tissues, are more well tolerated than others. So absence of Y chromosome is relatively well tolerated, but absence of X chromosome is not. And you see these selection processes over time.
Christina Bouwens 12:14
I have lots of different avenues I could go on, but one of them that I was going to ask you about was actually when we were talking about the use of qPCR as a screener tool for CNVs in the blood. And that kind of got me thinking because right now, you know, qPCR, dPCR are used for a lot of different applications, synergistically, but are there some other applications where we're looking for CNVs that you think, particularly in your expertise area as a pathologist that I'm you know that dPCR could really be useful in the short term and where it could bring benefits?
Parker Wilson, MD PhD 12:45
The two that come to mind are these two genetic syndromes called Turner Syndrome and Kleinfelter syndrome. The unique thing about these individuals is that they have different numbers of sex chromosomes. A Turner Syndrome individual will have monosomy X and they are phenotypically female and almost all of their cells, or depending on the tissue this is where it gets interesting, will have a single copy of the X chromosome. And along the same lines, men with Kleinfelter syndrome, almost all of their cells will have an XXY genotype. So the interesting thing about Turner or Kleinfelter's is that you do not need to be universally monosomy X or XXY. You can have some proportion of your cells or some proportion of your cells in a specific tissue that have this genotype. There are examples of kidney disorders where the mutation will happen only within the kidney. So if you look in the blood for this mutation you might not find it. And even if you look in the kidney for this mutation you might not find it because it might be only in a unique cell type. One way you might be able to use digital PCR is to try and identify rare events or copy number alterations in tissues. Now, that could be the kidney, it could be some other tissue, with the idea that you're looking for something you might not easily find elsewhere. Now, obviously with a kidney it's always hard to get a biopsy and to assay the tissue itself. But you can imagine how some of these assays can be used to screen for particular mutations or copy number variant events to help us better understand how genotype might be affecting tissue function at the tissue level not just whatever you started with, which might be your germline.
Christina Bouwens 14:48
Yeah. That's amazing. And just kind of diving into like the actual functional design of your dPCR assays. I know you kind of talked about it a little bit. So right now you're using digital PCR to look at these copy number events. What does the design of your actual assay, not like the specific probe design, but are you using multiple targets? Are you using just one target? What does the design of your assay look like so that you get the resolution that you need to actually be confident that you're, you know, detecting those structural variants with certainty?
Parker Wilson, MD PhD 15:19
I'll tell you that all the primers and probes are published. So there's, there's no secrets out there. And the way we've approached this is, we designed a primer probe combination and we ended up targeting a region near SRY, which is a gene on the Y chromosome, and this is important for determining male sex characteristics. It's in a region called the male-specific region of the Y chromosome. So once you find a region like this, you then need some other reference or target probes. We chose a region on the X chromosome. And just very simplistically, we were going to use a two-color assay where you have, say, for example, green that targets the Y chromosome region, and then you have red that targets the X chromosome region. And then we did our digital PCR assay, and we work with a digital microwell machine, you know, the Absolute Q. And within this machine, you have 20,000 micro wells. And you take a sample of extracted DNA, we're using somewhere between 100 and 200 nanograms per sample. And we take that and you put each of that in each of your individual wells. And for those of you that are not familiar with these plate setups, you have 16 wells in your digital PCR micro well plate and each of those wells then has 20,000 micro wells within it. So you put your sample in there and you put it in with your Y chromosome and your X chromosome probe and then you do an endpoint PCR reaction. We're using 40 cycles. And then you count the number of positive wells that come up for X or Y. Maybe you're trying to achieve roughly 50% positivity for the number of wells. So if you get 10,000 positive wells, you're usually in pretty good shape. Because then you can ask if you have, say, 10,000 wells that are positive for the Y chromosome, but you see 15,000 positive wells for the X chromosome, you might think that there are more X chromosomes than Y chromosomes in the tissue from a male sample. And all the important assumptions here are that, for the tissue that we're looking at, the vast majority of cells are going to have an equal number of X and Y chromosomes, which is certainly true for a non-tumor, kidney sample. So that's the way we do it. And then we're kind of interested in how can you push this to the next level? You know, what are other things that we can incorporate? And I mentioned earlier, what about women? So this is a question that some of my reviewers ask, “You know, you're interested in studying Y chromosome, but women don't have the Y chromosome and they develop kidney disease and they have the same cell types or states that you see in the kidney. What are some of the other events that could be very closely related to loss of Y chromosome?” And the one that we've thought of is loss of X chromosome. And loss of X chromosome has been described in the blood, it seems to happen at a much lower rate than Y chromosome loss. But not that many people have really looked at this. We're interested in developing an assay to develop loss of X chromosome in the kidney or the blood or other tissues and animal models. So if we know that loss of X chromosome happens much less frequently than loss of Y chromosome, are we looking for samples that have 1% or less? Is it possible to find that by digital PCR is a is a question that we're interested in pursuing. We think we can see it by single cell sequencing, but we want to push the boundaries with the digital PCR because then you could use digital PCR as a quick, low cost, very effective assay to screen tissues or disease models, and then you could move on to a more expensive assay if you wanted to really dive deep.
Jordan Ruggieri 19:17
Are you looking to precisely quantify rare targets in your sample? Are you always struggling with standard curves or measuring limits of quantification? If so, Applied Biosystems™ QuantStudio™ Absolute Q™ dPCR System is for you.
Christina Bouwens 19:30
With the Absolute Q, reliable and precise digital PCR can be as simple as preparing your samples, loading onto the plate and running the instrument. This system consistently delivers more than 20,000 micro chambers and provides results in as little as 90 minutes.
Jordan Ruggieri 19:45
That's right Christina. And the Absolute Q utilizes more than 95% of the sample that you input, so you won't have to worry about missing rare targets due to dead volume. You can learn more at www.thermofisher.com/absoluteq or visit the Absolute Gene-ius webpage. The Applied Biosystems™ QuantStudio™ Absolute Q™ dPCR System is for Research Use Only. Not for use in diagnostic procedures.
Christina Bouwens 20:10
Let's go back to our guest.
Jordan Ruggieri 20:15
All right, so hopping into the career corner element of the podcast. Parker, can you tell us a little bit of your background? How did you get to where you are in your career, you know, educational wise, but also, as you graduated and went into practice? Are there important steps that got you to where you are?
Parker Wilson, MD PhD 20:34
Sure I can take you through my timeline. I was an undergraduate in biomedical engineering and I went to Johns Hopkins. At the time I was finishing undergraduate, I thought maybe I would apply to a medical scientist training program. And my family had moved from Greater Boston down to South Carolina. So I applied to the Medical University of South Carolina MSTP, which is the medical science training program there, and was admitted. So I thought, you know, “Hey, I should go.” You know, this is a great opportunity. And I moved out of Charleston, and I was there for eight years. And again, I had planned on doing a PhD in bioengineering. But you know, as many things in research, you know, not everything works out the way that you think it should. And I found a much better fit for myself in a lab that was doing molecular biology. So I switched over and I did molecular biology as my PhD, sort of another small change, and had a great mentor who taught me all about signal transduction. And I was doing wet lab work and pipetting and cell culture and animal models and everything, but really nothing with computers. I went back to medical school and did my clinical rotations and found out that I had an interest in probably either internal medicine or pathology and had done some pathology rotations towards the end of my, sort of, medical student career and had really enjoyed it. You know, I liked the diagnostic expertise that was acquired to work as a pathologist and I liked the fact that pathology was so integrated with genomics. And I think there are two big things that are happening in pathology during my career. One is that we're sequencing the heck out of everything and somebody needs to figure out how to analyze that data. I thought, “I could fit in there.” And the other exciting thing is we are starting to image everything. So everyone envisions this pathologist as sitting behind a microscope or working in the lab, but that's really not the reality. I kind of like to think of pathology as the marriage of something that is very, very low tech, which is looking at tissue under microscope and the extreme high tech, which is you know, NGS. So I did this as a pathologist and then decided to go into pathology residency at Yale. And at Yale, you get very early exposure to renal pathology, and I had done some of my PhD work in kidney disease. And due to that early exposure, I ended up doing a fellowship in renal and genitourinary pathology. And what that means is that you learn how to look at kidney biopsies under the microscope and diagnose kidney diseases or evaluate kidney transplants. And you also get trained in genitourinary cancers, which can be prostate cancer, bladder cancer, these kinds of things. After my year of fellowship at Yale, I moved on and did a year of molecular genetic pathology at Washington University in St. Louis. And what that is, is using molecular techniques like PCR, or next generation sequencing was something that I was very interested in, to study kidney disease and they had a panel out there where they're doing, you know, targeted NGS for exome sequencing to look up subjects with kidney disease. And I was interested in learning how to better interpret germline variation in the context of kidney disease and also how these different assays fit into a clinical workflow. So I did that and then, as part of my move out to Wash U, I had met a senior investigator, Benjamin Humphreys, who is a very talented nephrologist physician scientists and joined his lab right after I finished my fellowship. And that was when I really started to get into single cell sequencing. He is a pioneer in the field of single cell sequencing. He started doing it very early on and were able to publish a couple of high impact papers, which was great, and you know, working in that lab environment was always very exciting, and it was something that you know, I really enjoyed. And then it became time to decide whether we were going to stay in St. Louis or whether we were going to move elsewhere. I met my wife when we were in New Haven, when I was in residency at Yale, and her family is still here in New Jersey. And we had always wanted to move closer to family and we thought, you know, if an opportunity presents itself, you know, we should seriously consider it. I had met some of the faculty at the University of Pennsylvania through some editorial responsibilities at the Journal of American Society of Nephrology. And they tuned me in to some different opportunities here. So I ended up relocating my NIH career development award, which was part of this transition, to a another very talented, and you know, senior physician scientist nephrologist at Penn, who was Katalin Susztak. So I have now relocated my career development award to her lab, but was offered an independent position to start my own lab here at Penn. And I think that's all really worked out really well. And I think that this idea of somatic mosaicism is new in the field and might help me to, you know, to achieve greater independence and pursue some new ideas that can help differentiate me from these giants in the field. So I'm pretty optimistic about it.
Jordan Ruggieri 26:12
What an amazing journey. Careers are nonlinear and you will encounter adversity and you will encounter success, and they're not mutually exclusive of each other. And, you know, I think that's important for people to understand is, is, you know, you're going to encounter both. You might get lucky and encounter success early on, but that doesn't mean that you're always going to find success the rest of your career. And you may get lucky or unlucky, depending on how you look at it, and get a lot of adversity early on, right? And, and I think the important, the important thing, and evidenced by your journey is you know, keep pushing forward, keep looking for those opportunities, but also being linked into mentors. And that's something that's been a theme on the podcast. How have mentors kind of shaped your career path, and how important and critical have they been for you?
Parker Wilson, MD PhD 27:08
I have had a number of really great mentors and a couple of really terrible mentors over time. And I think, you know, people will always talk about the really excellent mentors, but what you need to remember is that if you find yourself in a situation, which might be a lab or a mentor relationship that's not the right fit for you, you could always move on. And I think that's sort of the element of an adversity. This is more common than you might think, is you'll find yourself in a position where you need to find new mentorship. And I have had a number of really excellent mentors over time, and they helped to develop you and help find career opportunities for you. So you really need to actively seek these people out. The first mentor that I'll mention was my PhD mentor. He was really very excellent at not micromanaging. And I found that that was probably the most important, you know, feature of his, you know, besides the fact that he was a brilliant scientist and developed a good project for me, he was able to let me work independently. And this was definitely not true of some other labs that I had tried out before. So I found out that that was a really important thing that I needed in the mentor relationship. And then he was able to push me to, you know, compete for independent funding at the fellowship level and knew, as a physician scientist, what are some of the milestones you need to check off. Another thing that comes up a lot when you're talking about mentors is you, there is no such thing as having one mentor for your whole career. Not, there is no one person that can do everything. And you need to have different interactions or relationships with mentors who can provide different elements to your career. My PhD mentor had a very different relationship with me than my clinical residency mentor. And then ultimately, I moved on, I think I mentioned before to Ben Humphreys lab in Wash U. And he's kind of a, you know, a superstar physician scientist who's able to coach me on how you start a career and pursue a career as an independent PI. Which is again, yet a totally different thing from being a graduate student. This is a different thing from being a resident or doing clinical training. He's not a pathologist, so he can't teach me about pathology. But what he can do is help identify opportunities for what that means to become a physician scientist that's focused on kidney disease. As I've moved here to Penn, I've started to find more people who are along the physician scientist line and I'm quickly finding out that, as junior faculty, you need people within your faculty department that are going to be able to help you navigate the politics and what are the expectations within the department. Who are the people that are going to be able to help find your research opportunities? Who are the people that are really well connected within the university that help make you make other connections with other people who might have similar interests? You know, all of these things are elements that you're going to need.
Jordan Ruggieri 30:11
Awesome. I have one question with two parts left. We asked this of everybody who comes on the podcast. In your entire journey, what would be your most embarrassing lab moment? And then on the other side, what would be your proudest moment?
Parker Wilson, MD PhD 30:28
My most embarrassing lab moment? Oh, this is, yeah.
Jordan Ruggieri 30:32
We have we have stories of things blowing up and crazy lab stories. I don't know if you want to share anything blowing up, but…
Parker Wilson, MD PhD 30:40
Yeah. Yeah. No, I'm happy to share this. And so I think I mentioned earlier on that I had planned on pursuing a PhD in bioengineering and had done some rotations through a lab and was making modest progress. And one day woke up to an email from my then mentor who had fired me from the lab. And I had to go and explain this to my MD PhD program director, who did not know that I had been fired from the lab, which I think was embarrassing from his part, and then had to get relocated to a new lab. So you know, looking, looking at this from my perspective, is that this was probably the best thing that I could have had happen, is you move from a bad mentoring relationship to a good mentoring relationship. Not every lab is a good fit for every person and changing labs or switching your research directions is more common than you might think. I think my proudest moment was my mentor, Ben Humphreys, at Wash U. As I was finishing kind of at Wash U, they have this award series called the American Society of Clinical Investigation, Young Physician Scientist Award. So ASCI is a national organization of physician scientists. He nominated me for that award, kind of as I was leaving Wash U and coming to Penn. And I ended up getting the award with roughly 40 or 50 other people who are also young physician scientists and then got to go out to the meeting, and you meet other people that are a lot like you, which is great, because, you know, you can be pretty lonely here in research and you often feel as a junior faculty that, you know, where are the other physician scientists who are doing this. A lot of the people that I finished with that, that trained with me are no longer pursuing these kinds of careers. I think, you know, they might be in academic medicine doing more of a clinical focus or they might be in private practice. But there is a very leaky pipeline, as the NIH is happy to point out, that the number of people who start the physician scientist pathway and then ultimately end up running a lab is actually quite small.
Jordan Ruggieri 33:03
Excellent. I have no further questions. Christina, anything on your end?
Christina Bouwens 33:07
No, this is an amazing conversation. Thank you so much for joining us today. I really enjoyed you. This is a great episode.
Parker Wilson, MD PhD 33:14
Well, thanks for having me. And, you know, I'm, I'm pretty excited about the potential.
Jordan Ruggieri 33:21
That was Dr. Parker Wilson, Assistant Professor of Pathology and Laboratory Medicine at the University of Pennsylvania School of Medicine. This episode of Absolute Gene-ius was produced by Sarah Briganti, Matt Ferris, and Matthew Stock. Until next time, stay curious as we've got more fascinating conversations around the corner in future episodes.
Christina Bouwens 33:41
Jordan, I have a joke for you.
Jordan Ruggieri 33:43
Oh, I'm always down for a joke.
Christina Bouwens 33:45
Why do you never see elephants hiding in trees?
Jordan Ruggieri 33:48
Why don't you see elephants hiding in trees?
Christina Bouwens 33:52
Because they're so good at it.