May 31, 2023 • 16 mins
Disease-relevant molecules that cannot be pharmacologically targeted are sometimes referred to as undruggable, and in cancer, a number of proteins fall into this category. With innovation and new technologies, researchers make breakthroughs that turn evasive targets into druggable ones. Recent successes in establishing therapeutics against mutant oncoproteins, such as KRAS, transform the treatment landscape for patients and clinicians. A scientist who takes a unique approach to clinical trial design demonstrates how targeted small molecules are shifting drug discovery paradigms in oncology to better treat pancreatic cancer.
In this episode, Deanna MacNeil from The Scientist’s Creative Services Team spoke with David Hong, the Dougie Johnson Endowed Professor and clinical medical director of the clinical trial research unit at MD Anderson Cancer Center, to learn more.
The Scientist Speaks is a podcast produced by The Scientist’s Creative Services Team. Our podcast is by scientists and for scientists. Once a month, we bring you the stories behind news-worthy molecular biology research. This month's episode is sponsored by NanoTemper.
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Episode Transcript
Available transcripts are automatically generated. Complete accuracy is not guaranteed.
Niki (00:10):
Welcome to the scientists speaks a podcast produced by the scientists creative services team. Our podcast is by scientists and for scientists. Once a month we bring you the stories behind newsworthy molecular biology research. This episode is brought to you by nano temper. Nano temper technologies creates biophysical tools for drug discovery and development scientists who need to tackle challenging characterizations. For researchers facing challenges with affinity screening, molecular interactions or protein stability, Dino temper is ready to talk. To handle challenging drugs and other drug targets like protects intrinsically disordered proteins and fragment libraries, researchers turned to nano temper scientists instrument learn more on Nano temper tech.com disease relevant molecules that cannot be pharmacologically targeted are sometimes referred to as undruggable. And in cancer, a number of proteins fall into this category. With innovation and new technologies, researchers are making breakthroughs that turn evasive targets into druggable ones. recent success in establishing therapeutics that gets mutant oncoproteins, such as K RAS transformed the treatment landscape for patients and clinicians alike. A scientist who takes a unique approach to clinical trial design demonstrates how targeted small molecules are shifting drug discovery paradigms in oncology to better treat pancreatic cancer. In this episode, Deanna McNeil from the scientists creative services team spoke with David Hogg Dougie Johnson Endowed Professor and clinical medical director of the clinical trial Research Unit at MD Anderson Cancer Center to learn more.
Deanna (01:50):
One of the most fundamental challenges in cancer biology is understanding how normal cells transform into malignant ones. Several decades ago, researchers discovered oncoproteins, which are molecules that hijack normal regulatory pathways involved in cellular functions, such as growth, differentiation and metabolism. Despite their known involvement in disease, it's been difficult for scientists to establish treatments that specifically target many of these oncoproteins in the clinic. Through a combination of basic science research and clinical trials. Researchers today are uncovering a new generation of therapeutic molecules that improve patient outcomes. per day, David hyung, and unexpected path towards Clinical Oncology Research connected him with like minded scientists who aim to fundamentally shift the approach to clinical trial design and help more patients with cancer driven by conventionally undruggable targets.
Unknown (02:40):
How I got into research was really kind of a long story of I didn't know if I even wanted to go to medical school, I promised my parents that I would apply my last year of college not knowing whether or not I'd get in. I took a year off I went to Korea to kind of find myself and reconnect with when I was born. I went back there really just to see what direction in life I was going, came back. I had been waitlisted at pretty much every single medical school I got a phone call from Albert Einstein School of Medicine, as that I got into the class in 1998. I was there for five years because actually took a year off at did a Howard Hughes fellowship in a lab of Dr. Mehdi Scharf, who was really known for immunology. I spent a year in the lab and I was out of my element, I was contaminating every petri dish, but I enjoyed the actual experience of research. I decided the lab was not my thing, though, and went on to residency at Thomas Jefferson in Philadelphia.
Deanna (03:49):
During Internal Medicine rotations, homeless faced with the decision between continuing to pursue general internal medicine or picking a subspecialty he turned to his program director for guidance, and after sharing that he enjoyed research, Hong's director steered him toward oncology. At that time, the treatments available for patients with many types of cancer were few and far between, and there was a pressing need for therapeutics with improved efficacy. Early in his medical training, hyung diagnosed a patient who had chronic myeloid leukemia, or CML. This particular experience played a key role in his commitment to clinical cancer research.
Unknown (04:23):
Everybody is motivated by certain stories that I remember as an intern, we emitted a patient who had some left upper quadrant pain and it turned out he actually had splenomegaly looked like he had CML, chronic CML. And in 2000, we referred them to hematology and that time, the only kind of approved therapy was interferon based therapy.
Deanna (04:51):
interferons are cytokines the plant integral role in the immune response and the introduction of interferon alpha and CML treatment in the 1980s was initially considered a break through therapy for this disease, however, it can cause significant side effects and leads to a cure for only a minority of patients. Unfortunately while Hung's patient received the standard of care therapy at the time, they passed away shortly after diagnosis. This patient's experience and the timing of their diagnosis is a devastating example of the need for swift progress and clinical trial research. Today, such progress contributes to better therapeutics, including one of the first targeted small molecule therapies Imatinib, which inhibits and oncoprotein responsible for leukemia. This drug and others targeted small molecule therapies have dramatically changed the outlook for patients with cancer, including those with CML.
Unknown (05:39):
This disease is now almost like diabetes, right? It's a chronic disease, that if you can treat it a catch it early, particularly in this chronic stage, and with the new targeted agents beyond just the matt nib, you can put this disease into remission, people can live almost normal lives. And so I think that for me is really been kind of a sticking point. And I did my rotations and fellowship, was able to translate some of that preclinical data into an actual clinical trial. Later on in my fellowship, which led to a young investigator award and eventually a trial that I ran here at MD Anderson.
Deanna (06:22):
Around the time that hung joined MD Anderson as a professor, a new generation of targeted therapeutics was emerging, which prompted a paradigm shifting approach to clinical trials at his institution. The late professor of medicine, American Cancer Society professor and Samsung distinguished university chair in cancer medicine, Dr. Huang ki hyung, spearheaded a new department to oversee clinical trials for novel therapeutics. At that
Unknown (06:45):
time, Manipur had just been approved, vast in and some of these other drugs were starting to emerge as standard of care. And he could see that there was this beginning explosion in targeted therapy, new therapies and possibly immunotherapy kind of nimble department to run these clinical trials was needed. So he commissioned Dr. Result Kurzrock to create this working group.
Deanna (07:11):
In the world of oncology, major academic cancer centers are typically divided by tumor type. The vision of this new department was to be cancer type agnostic. Instead of focusing on one type of treatment for one type of cancer, they created a department based around classes of drugs, with the goal of identifying the molecular underpinnings of different cancers to better match patients to appropriate targeted therapies. This approach was so new to the field at that time, that some people doubted its feasibility.
Unknown (07:38):
I remember getting advice from some my other mentors, and they all told me Don't Don't take this job. You're never going to be known. You're never going to have a career in academic oncology, unless you have a tumor title. I remember sitting down with result Kurzrock. And she said something to me, which was prescient, but eventually became true. She said, David, at some point, in oncology, we're not going to just get approvals based upon individual tumors, it's going to be based upon molecular phenotype, not tumor phenotype. And she said this in 2005.
Deanna (08:20):
Almost a decade later, this foresight from Dr. result, Kurzrock has proven correct. In 2017, the FDA approved Pember lism AB, which was the first cancer treatment approved based on a biomarker rather than a tumor type. This therapeutic agent blocks a pathway that depends on the PD one biomarker, and has led to clinical responses in patients with multiple different types of cancer, including specific types of melanoma, lung cancer, kidney cancer and lymphoma. Since its inception, Hyung has helped build up this trailblazing department at MD Anderson, which has grown to be one of the largest academic phase one clinical trial units in the world. Recently, Hyung has turned his research attention to an important protein called K RAS. As a member of the wrasse family of proteins. K RAS relays signals from outside the cell to the cell's nucleus, instructing the cell to grow and divide or take on specialized functions through differentiation. However, mutations affect K RAS is normal function, creating an uncle protein that drives several types of cancer, including lung, colon and pancreatic cancers. Although researchers discovered the role of K RAs and oncogenesis, in the early 1980s, it has been largely undruggable. Until recently,
Unknown (09:27):
we knew that it was important particularly in lots of cancers like pancreatic cancer, but it's been very, very difficult to target. And we've tried different things. In fact, one of my first studies was a drug called tipifarnib. And that drug inhibited this enzyme called for Nestle transferase. And we know that wrasse needs to be foreign escalated to bind to the cell membrane, and so tipifarnib was initially developed to inhibit that The process we tried but found out very quickly that it did not work. It's not as easy as just oh yeah, this is important. We know this is important in oncogenesis in cell and animal models, but it was very difficult to try to translate that into human beings for a number of reasons. It was really difficult to develop direct inhibitors mutant K RAS is a protein, it's got a very smooth surface. It's got relatively limited binding sites, and it has incredibly high affinity for GTP, which is kind of the driving engine of the Charis protein.
Deanna (10:38):
GTP is an energy source in the cell, and the K Ras protein is a GTPase, which means it transfers energy by converting GTP into a molecule called GDP. In this way, K RAS acts like a switch that is activated by GTP binding and turned off by GDP conversion. When the protein is in its off state, it does not relay signals to the cell's nucleus for cell proliferation and differentiation. But because of how tightly K RAS holds on to GTP, it's difficult to develop drugs that turn K RAS off. This was a challenge for decades, until researchers from the University of California San Francisco showed that there was a way to target K RAS activity without directly competing for GTP binding.
Unknown (11:19):
They were able to develop a molecule that binds allosteric ly, which means near that GTP pocket and pretty much locked it in this inactive form that showed that there could be molecules that could target RAs, and obviously that led to the development of sotar acid, a similar molecule that ultimately got into the clinic which I was involved in.
Deanna (11:46):
Sutter acid is a small molecule that's specifically and irreversibly inhibits a mutated form of K RAS called K RAS g 12. C through allosteric binding. The FDA recently granted accelerated approval of sotar acid and a specific type of lung cancer with this mutation for patients who have had at least one previous systemic therapy. The G 12 C mutation also contributes to pancreatic cancer, which led hyung to investigate whether SOTA rasa would be an effective treatment option for these patients for whom there's a dire need for improved therapies.
Unknown (12:16):
Right now, most pancreatic cancer is usually in the metastatic setting. That means stage four, it's already spread beyond the pancreas and the majority of patients present that way. Unfortunately, and at that point, it is usually incurable and there are a number of different regimens that we can give but usually, a lot of patients depending on how their overall condition is are sent home to hospice and palliative care.
Deanna (12:47):
Sought or acid may one day be an alternative to current standard of care chemo therapies which can contribute some survival benefit, but at the cost of high toxicity. As a first step in that direction. Hyung led a phase one phase two trial of sotar acid treatment for patients with K RAS G 12 C mutated pancreatic cancer, those tumors had previously not responded to chemotherapy,
Unknown (13:07):
sort of acid had a clinically meaningful response rate of about 21%. And significant progression free survival in this population that is being for all by it is a small number of patients. This is not a home run, but clearly shows that K RAS can be a major driver in pancreatic cancer and the targeting it can have some clinical benefit.
Deanna (13:34):
Mutations in the K ras gene are found in about 90% of pancreatic ductal adenocarcinomas, making them the most prevalent mutations in pancreatic cancer. Although the G 12 C mutation, that sort of acid targets is found in only one to 2% of cases. Scientists are also working on therapeutics that target other K RAS mutations in pancreatic cancer, as well as drugs that inhibit K RAS as a whole. Looking into the future. Hyung hopes that this progress in targeting G 12 C will open the floodgates for targeting undruggable proteins, comparing today's drug discovery landscape to the watershed moment in track and field. When Roger Bannister first ran a mile in under four minutes.
Unknown (14:11):
There were all these kinds of pundits and experts who said this is impossible. No human being could break the four minute mile. Right? And that was humanly impossible. Well, he broke that four minute mile, with the help of many of his colleagues and friends is Pacers. It was almost like a psychological barrier that was broken because since then, many people have broken this record. This is kind of the pattern that we see in all innovation, right? All of a sudden somebody breaks through and then people realize, Oh my gosh, we can do that somebody's cracked the code. Now this is possible. I think this is what's happening now. I think we're going to see the additional rapid changes in this field specifically in wrasse. It is an exciting time in drug development. And really for me, my interests will really be Developing those new generation of molecules, but also, how do we best combine them? How do we find out who will best benefit from these trials and these molecules? That's really my next goal. This is such a huge space that this may be like the focus of the rest of my career, and I'm still young, but I could see working on this for a decade or so beyond this, just because there's so much here to dive into.
Niki (15:34):
Thank you for listening to the scientists speaks. This episode was produced by the creative services team for the scientist and narrated by Deanna McNeil. Thanks again to nano temper for sponsoring this episode. Please join us again in July as we learn about mitigating infectious diseases with fecal transplants. To keep up to date with this podcast, follow the scientists on Facebook and Twitter and subscribe wherever you get your podcasts.
Welcome to the scientists speaks a podcast produced by the scientists creative services team. Our podcast is by scientists and for scientists. Once a month we bring you the stories behind newsworthy molecular biology research. This episode is brought to you by nano temper. Nano temper technologies creates biophysical tools for drug discovery and development scientists who need to tackle challenging characterizations. For researchers facing challenges with affinity screening, molecular interactions or protein stability, Dino temper is ready to talk. To handle challenging drugs and other drug targets like protects intrinsically disordered proteins and fragment libraries, researchers turned to nano temper scientists instrument learn more on Nano temper tech.com disease relevant molecules that cannot be pharmacologically targeted are sometimes referred to as undruggable. And in cancer, a number of proteins fall into this category. With innovation and new technologies, researchers are making breakthroughs that turn evasive targets into druggable ones. recent success in establishing therapeutics that gets mutant oncoproteins, such as K RAS transformed the treatment landscape for patients and clinicians alike. A scientist who takes a unique approach to clinical trial design demonstrates how targeted small molecules are shifting drug discovery paradigms in oncology to better treat pancreatic cancer. In this episode, Deanna McNeil from the scientists creative services team spoke with David Hogg Dougie Johnson Endowed Professor and clinical medical director of the clinical trial Research Unit at MD Anderson Cancer Center to learn more.
Deanna (01:50):
One of the most fundamental challenges in cancer biology is understanding how normal cells transform into malignant ones. Several decades ago, researchers discovered oncoproteins, which are molecules that hijack normal regulatory pathways involved in cellular functions, such as growth, differentiation and metabolism. Despite their known involvement in disease, it's been difficult for scientists to establish treatments that specifically target many of these oncoproteins in the clinic. Through a combination of basic science research and clinical trials. Researchers today are uncovering a new generation of therapeutic molecules that improve patient outcomes. per day, David hyung, and unexpected path towards Clinical Oncology Research connected him with like minded scientists who aim to fundamentally shift the approach to clinical trial design and help more patients with cancer driven by conventionally undruggable targets.
Unknown (02:40):
How I got into research was really kind of a long story of I didn't know if I even wanted to go to medical school, I promised my parents that I would apply my last year of college not knowing whether or not I'd get in. I took a year off I went to Korea to kind of find myself and reconnect with when I was born. I went back there really just to see what direction in life I was going, came back. I had been waitlisted at pretty much every single medical school I got a phone call from Albert Einstein School of Medicine, as that I got into the class in 1998. I was there for five years because actually took a year off at did a Howard Hughes fellowship in a lab of Dr. Mehdi Scharf, who was really known for immunology. I spent a year in the lab and I was out of my element, I was contaminating every petri dish, but I enjoyed the actual experience of research. I decided the lab was not my thing, though, and went on to residency at Thomas Jefferson in Philadelphia.
Deanna (03:49):
During Internal Medicine rotations, homeless faced with the decision between continuing to pursue general internal medicine or picking a subspecialty he turned to his program director for guidance, and after sharing that he enjoyed research, Hong's director steered him toward oncology. At that time, the treatments available for patients with many types of cancer were few and far between, and there was a pressing need for therapeutics with improved efficacy. Early in his medical training, hyung diagnosed a patient who had chronic myeloid leukemia, or CML. This particular experience played a key role in his commitment to clinical cancer research.
Unknown (04:23):
Everybody is motivated by certain stories that I remember as an intern, we emitted a patient who had some left upper quadrant pain and it turned out he actually had splenomegaly looked like he had CML, chronic CML. And in 2000, we referred them to hematology and that time, the only kind of approved therapy was interferon based therapy.
Deanna (04:51):
interferons are cytokines the plant integral role in the immune response and the introduction of interferon alpha and CML treatment in the 1980s was initially considered a break through therapy for this disease, however, it can cause significant side effects and leads to a cure for only a minority of patients. Unfortunately while Hung's patient received the standard of care therapy at the time, they passed away shortly after diagnosis. This patient's experience and the timing of their diagnosis is a devastating example of the need for swift progress and clinical trial research. Today, such progress contributes to better therapeutics, including one of the first targeted small molecule therapies Imatinib, which inhibits and oncoprotein responsible for leukemia. This drug and others targeted small molecule therapies have dramatically changed the outlook for patients with cancer, including those with CML.
Unknown (05:39):
This disease is now almost like diabetes, right? It's a chronic disease, that if you can treat it a catch it early, particularly in this chronic stage, and with the new targeted agents beyond just the matt nib, you can put this disease into remission, people can live almost normal lives. And so I think that for me is really been kind of a sticking point. And I did my rotations and fellowship, was able to translate some of that preclinical data into an actual clinical trial. Later on in my fellowship, which led to a young investigator award and eventually a trial that I ran here at MD Anderson.
Deanna (06:22):
Around the time that hung joined MD Anderson as a professor, a new generation of targeted therapeutics was emerging, which prompted a paradigm shifting approach to clinical trials at his institution. The late professor of medicine, American Cancer Society professor and Samsung distinguished university chair in cancer medicine, Dr. Huang ki hyung, spearheaded a new department to oversee clinical trials for novel therapeutics. At that
Unknown (06:45):
time, Manipur had just been approved, vast in and some of these other drugs were starting to emerge as standard of care. And he could see that there was this beginning explosion in targeted therapy, new therapies and possibly immunotherapy kind of nimble department to run these clinical trials was needed. So he commissioned Dr. Result Kurzrock to create this working group.
Deanna (07:11):
In the world of oncology, major academic cancer centers are typically divided by tumor type. The vision of this new department was to be cancer type agnostic. Instead of focusing on one type of treatment for one type of cancer, they created a department based around classes of drugs, with the goal of identifying the molecular underpinnings of different cancers to better match patients to appropriate targeted therapies. This approach was so new to the field at that time, that some people doubted its feasibility.
Unknown (07:38):
I remember getting advice from some my other mentors, and they all told me Don't Don't take this job. You're never going to be known. You're never going to have a career in academic oncology, unless you have a tumor title. I remember sitting down with result Kurzrock. And she said something to me, which was prescient, but eventually became true. She said, David, at some point, in oncology, we're not going to just get approvals based upon individual tumors, it's going to be based upon molecular phenotype, not tumor phenotype. And she said this in 2005.
Deanna (08:20):
Almost a decade later, this foresight from Dr. result, Kurzrock has proven correct. In 2017, the FDA approved Pember lism AB, which was the first cancer treatment approved based on a biomarker rather than a tumor type. This therapeutic agent blocks a pathway that depends on the PD one biomarker, and has led to clinical responses in patients with multiple different types of cancer, including specific types of melanoma, lung cancer, kidney cancer and lymphoma. Since its inception, Hyung has helped build up this trailblazing department at MD Anderson, which has grown to be one of the largest academic phase one clinical trial units in the world. Recently, Hyung has turned his research attention to an important protein called K RAS. As a member of the wrasse family of proteins. K RAS relays signals from outside the cell to the cell's nucleus, instructing the cell to grow and divide or take on specialized functions through differentiation. However, mutations affect K RAS is normal function, creating an uncle protein that drives several types of cancer, including lung, colon and pancreatic cancers. Although researchers discovered the role of K RAs and oncogenesis, in the early 1980s, it has been largely undruggable. Until recently,
Unknown (09:27):
we knew that it was important particularly in lots of cancers like pancreatic cancer, but it's been very, very difficult to target. And we've tried different things. In fact, one of my first studies was a drug called tipifarnib. And that drug inhibited this enzyme called for Nestle transferase. And we know that wrasse needs to be foreign escalated to bind to the cell membrane, and so tipifarnib was initially developed to inhibit that The process we tried but found out very quickly that it did not work. It's not as easy as just oh yeah, this is important. We know this is important in oncogenesis in cell and animal models, but it was very difficult to try to translate that into human beings for a number of reasons. It was really difficult to develop direct inhibitors mutant K RAS is a protein, it's got a very smooth surface. It's got relatively limited binding sites, and it has incredibly high affinity for GTP, which is kind of the driving engine of the Charis protein.
Deanna (10:38):
GTP is an energy source in the cell, and the K Ras protein is a GTPase, which means it transfers energy by converting GTP into a molecule called GDP. In this way, K RAS acts like a switch that is activated by GTP binding and turned off by GDP conversion. When the protein is in its off state, it does not relay signals to the cell's nucleus for cell proliferation and differentiation. But because of how tightly K RAS holds on to GTP, it's difficult to develop drugs that turn K RAS off. This was a challenge for decades, until researchers from the University of California San Francisco showed that there was a way to target K RAS activity without directly competing for GTP binding.
Unknown (11:19):
They were able to develop a molecule that binds allosteric ly, which means near that GTP pocket and pretty much locked it in this inactive form that showed that there could be molecules that could target RAs, and obviously that led to the development of sotar acid, a similar molecule that ultimately got into the clinic which I was involved in.
Deanna (11:46):
Sutter acid is a small molecule that's specifically and irreversibly inhibits a mutated form of K RAS called K RAS g 12. C through allosteric binding. The FDA recently granted accelerated approval of sotar acid and a specific type of lung cancer with this mutation for patients who have had at least one previous systemic therapy. The G 12 C mutation also contributes to pancreatic cancer, which led hyung to investigate whether SOTA rasa would be an effective treatment option for these patients for whom there's a dire need for improved therapies.
Unknown (12:16):
Right now, most pancreatic cancer is usually in the metastatic setting. That means stage four, it's already spread beyond the pancreas and the majority of patients present that way. Unfortunately, and at that point, it is usually incurable and there are a number of different regimens that we can give but usually, a lot of patients depending on how their overall condition is are sent home to hospice and palliative care.
Deanna (12:47):
Sought or acid may one day be an alternative to current standard of care chemo therapies which can contribute some survival benefit, but at the cost of high toxicity. As a first step in that direction. Hyung led a phase one phase two trial of sotar acid treatment for patients with K RAS G 12 C mutated pancreatic cancer, those tumors had previously not responded to chemotherapy,
Unknown (13:07):
sort of acid had a clinically meaningful response rate of about 21%. And significant progression free survival in this population that is being for all by it is a small number of patients. This is not a home run, but clearly shows that K RAS can be a major driver in pancreatic cancer and the targeting it can have some clinical benefit.
Deanna (13:34):
Mutations in the K ras gene are found in about 90% of pancreatic ductal adenocarcinomas, making them the most prevalent mutations in pancreatic cancer. Although the G 12 C mutation, that sort of acid targets is found in only one to 2% of cases. Scientists are also working on therapeutics that target other K RAS mutations in pancreatic cancer, as well as drugs that inhibit K RAS as a whole. Looking into the future. Hyung hopes that this progress in targeting G 12 C will open the floodgates for targeting undruggable proteins, comparing today's drug discovery landscape to the watershed moment in track and field. When Roger Bannister first ran a mile in under four minutes.
Unknown (14:11):
There were all these kinds of pundits and experts who said this is impossible. No human being could break the four minute mile. Right? And that was humanly impossible. Well, he broke that four minute mile, with the help of many of his colleagues and friends is Pacers. It was almost like a psychological barrier that was broken because since then, many people have broken this record. This is kind of the pattern that we see in all innovation, right? All of a sudden somebody breaks through and then people realize, Oh my gosh, we can do that somebody's cracked the code. Now this is possible. I think this is what's happening now. I think we're going to see the additional rapid changes in this field specifically in wrasse. It is an exciting time in drug development. And really for me, my interests will really be Developing those new generation of molecules, but also, how do we best combine them? How do we find out who will best benefit from these trials and these molecules? That's really my next goal. This is such a huge space that this may be like the focus of the rest of my career, and I'm still young, but I could see working on this for a decade or so beyond this, just because there's so much here to dive into.
Niki (15:34):
Thank you for listening to the scientists speaks. This episode was produced by the creative services team for the scientist and narrated by Deanna McNeil. Thanks again to nano temper for sponsoring this episode. Please join us again in July as we learn about mitigating infectious diseases with fecal transplants. To keep up to date with this podcast, follow the scientists on Facebook and Twitter and subscribe wherever you get your podcasts.
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