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Hi, everyone! It’s Dr. Trish Murray – physician, bestselling author, and the Health Catalyst Speaker. I am so excited to be talking with Dr. Robert Nagourney today on the topic of – listen to this – functional profiling for the selection of cancer treatment. Folks, obviously we all don’t want to get that c-word, cancer. When you do, you want to make sure that you’re getting the best treatment to try and eradicate these cells that are over producing, they’re over re-producing, and they’re causing these problems for you and we want to be able to eradicate it properly.
Let me tell you a little bit about Dr. Robert Nagourney’s background and read his bio for you, and then we’re going to get right into this because you need to hear this information. It could save your life!
Dr. Robert Nagourney is an internationally recognized pioneer in cancer research and personalized cancer treatment. With more than 20 years of experience in human tumor primary culture analyses, Dr. Nagourney has authored more than 100 manuscripts, book chapters, and abstracts including publications in the Journal of Clinical Oncology, Gynecologic Oncology, and the Journal of the National Cancer Institute.
Over the past 20+ years, Dr. Nagourney and his team at the Nagourney Cancer Institute have developed a laboratory technique, called functional profiling, that measures how cancer cells respond when they are exposed to a wide variety of drugs and drug combinations.
By using this approach, Dr. Nagourney’s team can determine the best drugs for each patient before they receive them. This reduces the guesswork in selecting the right drug treatment for you and is why our analysis is more powerful than any of the genomic testing that’s offered by most centers.
So, wow! Dr. Nagourney, I am really excited to hear more about this from you! The first question I always like to ask all my guests, so people get a better understanding of you and what’s brought you to where you are is how have you come to being of service the way you are today?
Well first of all, Trish, thank you for having me. I’m happy to be here. I guess when you ask me how I’ve got to where I am, I always knew I wanted to be doctor. From the time I was a kid. There’s this friend that says that doctors aren’t made, they’re born. I came from a tradition of physicians. My son is a medical student so that’s four generations.
So, I knew I wanted to be a doctor. I went on my college degree, I took chemistry, from Boston University. I finished medical school at McGill in Montreal. During the course of my medical studies, I never really thought I wanted to be in cancer research. Somehow it had the feel of…I guess when we were kids people used to say, “Well, my son’s a doctor. He’s a brain surgeon.” I felt like, well my son’s a doctor; he’s a cancer researcher. I felt like that seems so cliché, and I’m not going to do that.
But I found myself in a laboratory doing basic cancer research, and I published a couple of papers in cancer research, and I was launched. As I came through my training and I did my fellowship at Georgetown University and my second fellowship at Scripps Institute, all the while I was very disappointed by the fact that people didn’t seem to be getting better. I just felt this sense of great dismay that we were using what at the time were really poisonous chemotherapies. We didn’t have the supportive care. There was no Neupogen®, there were none of the modern day antiemetics. Cancer therapy was horrific. I thought, there’s got to be a better way to do this.
I met a colleague who had come out of the National Cancer Institute and he was here on faculty where I trained at UC Irvine. He was working on tissue culture techniques to predict response. I worked with him, and the first technique we used was called the clonogenic assay, that may be before many of the audience’s time, but the clonogenic assay was predicated on the idea that cancer cells will propagate, grow, into colonies and the colonies were clones. If you could stop the colonies, you could stop the cancer. At least they thought so.
In the 70s and 80s, a little before my time, people were studying how to grow cancer cells and then stop them from growing. It didn’t work. I mean, it really didn’t work. It worked so badly that everybody didn’t just say, “It didn’t work.” They said, “I’ll never do this again, and I hate anyone who talks about it.” The degree of disappointment is directly proportional to the degree of expectation. When people thought, Eureka! We can all take up cigarettes again because I can cure your cancer with this cool new technique, and it didn’t work they were furious. That was just about the time I got involved.
We looked at it differently, and we said, “Well, instead of growing cells and forming colonies and doing all this hard work, what if you just killed it? What if you just entered into the tissue culture environment with drugs in combination that just cause cell death? Okay!” We did it, and we did it with little kids’ leukemias. It worked! So, then we did it with adult leukemia, and it worked! Then we did it with lung cancer, breast cancer, colon cancer, and it worked. It was really effective.
I spent my time in my Georgetown year of research working on it. I went to Scripps and developed a technique and actually developed a treatment that cured hairy cell leukemia. The disease hairy cell was cured based on a discovery we made at Scripps while I was there. I actually made that discovery. Anyway, it was evident to me that this worked, but the trouble was that the medical community was so poisoned on the constant that they just didn’t want to hear about it. We repeatedly published and reported and did trials and studies and retrospective and prospective. We finally come to the point where we just had to say, “Well, they’re not going to like what we do. It works, and we’re going to do it.”
That’s my story. I do this because it saves lives.
But how do you isolate to the appropriate cells that are the ones that need to be targeted and not kill healthy cells?
Actually, cancer cells in tissue culture usually that you get are these aggregates. We call them microspheroids or spheroids. These microaggregates contain stromal elements, vascular elements, and inflammatory cells but the majority of most of these tumors, particularly adenocarcinomas and squamous cell, most of the cells in there are cancer cells. If it is a mixed bag of cells, we can do a scoring, an actual visual scoring the same way that a hematologist would do a differential. You can actually look at what cells are dying. That’s a really interesting question because what we like to do sometimes is to see whether a drug seems to selectively kill the tumor cell or may be more damaging to lymphocytes or may occasionally be damaging to other benign elements. That’s a kind of interesting study.
Very often the samples we get, particularly leukemias, lymphomas, and many adenocarcinomas, very often, particularly ovarian cancers, the tumor population is relatively pure. And so, you get a rather good quality sample (70-80% tumor) and you can use a variety of endpoints, but we’re very careful to ensure that we’re killing cancer when we report our results.
Right. So, you’re referring to the analysis of…is it a biopsy? You get tissue from the cancer itself.
You obviously put it in a culture and then you’re identifying which medicines are going to actually kill and eradicate that particular tumor type, correct?
Exactly. We work in what’s known as primary culture. Primary culture means right from the patient to me. We don’t grow it; we don’t expand it; we don’t amplify it; we don’t subculture it. Cancer is not a cell, but a community. The community consists of cells talking to each other, talking to their vasculature, talking to their fibroblastoma, talking to their macrophages and their T cells and their B cells. This big mesh constitutes the aggregate, the ecology, of cancer. If you want to cure cancer you have to cure it where it lives, not in some artificial monoculture propagated franken-tumor. You need the tissue from the patient, and that’s what we use.
For people to understand, basically any organ in our body is really a collection of cells that are living and producing the structure and the function of that particular part of us.
And it’s unique. Then a tumor (cancer) starts to…possibly not supposed to be there…and abnormally reproduce and produce and create its own community, correct?
Cancer is highly contextual. An adenocarcinoma, a glandular tumor arising in the lung, the epithelium of the lung, and an adenocarcinoma glandular cancer arising in the epithelium of the breast reflects as much the community it grew up in as the cell itself.
Right. So people understand, what causes it then to be a cancer and to be something we need to eradicate? If it comes from, like you say, the community in which it grew up?
Well, if you’ve ever encountered a criminal or a juvenile delinquent you know that they may have grown up next to you, but they still have a gun at you raised. You do have to respond. You do have to respond, but it raises a very interesting question, Trish. That question is what is actually the driving feature of a malignant transformation? What causes a cancer cell to become a cancer cell?
Now, if I were to ask you, I mean you’re not a cancer doctor, so if I were to ask you what happens that makes a cancer turn into a cancer? Most people would say that cancer is driven by a mutation. Gene aberrancy, duplication, amplification, translocations, splice variant. There’s a whole lexicon of how cancers come to be. We have come to believe that cancer is nothing more than a broken gene that gives rise to a broken cell and the broken cell gives rise to a cancer for pretty much the last 150 years of research. That’s proven to be wrong, completely wrong.
Like so many things.
It turns out that really, really what cancer is is a cell within some context, within some microenvironment which during the normal process of life and death is born into this community, thrives for some period of time, and then reaches a state of senescence and death. That’s the ebb and flow of life. All cells are given a kind of period of time. They get a shelf life.
A cancer cell sitting around one day says, “Gee, I don’t have enough estrogen or testosterone or epidermal growth factor or glutamine or something, oxygen, blood supply.” You name it. Something that makes it happy. It’s suddenly unhappy. Now, most cells when they get unhappy, if they can’t find their estrogen or testosterone or epidermal growth factor or whatever, most cells say, “Well, I guess I’ve run to the end of my course, and I’m going to die.” That’s programmed cell death. It’s built in, hard-wired.
Well, that’s only one form of it.
Oh, really? Okay.
Apoptosis is one of many forms of cell death.
And so, one of the things people have to realize is apotopic cell death is one of a dozen things that cells can do. But what they all do when they die is die. So, how they got there – all roads lead to Rome. What we became interested in is if a cell is going to die, what can you do to make it die?
Now, to go back to the original point I was making, the cancer cell is a cell that wants to stay alive. It isn’t a gene driving a cell, but a cell driving a gene. You see, we’re going to have to reverse engineer our thinking about cancer biology if we’re really going to cure this because as long as we allow the molecular biologist to tell us that cancer’s a genetic disorder, we’ll continue to spend billions of dollars on molecular biological studies that are not getting us anyway. We have had the entire human genome sequenced since 2003. Now, I didn’t read the LA Times today, but did we cure cancer?
Alright. There must be more to this than just the genes. It turns out that cancer cells, as it were, arise in the state of deprivation. They’re looking for a way out, and they grab a hold of something that keeps them alive. Imagine if your ship went down and you needed to grab one of those little rings floating around the water to stay afloat. Well, that ring might say KRAS on it or it might say P53 or it might be a piece of a side of wood that you float around on called phosphoinositide kinase or whatever. It might be an amplification of the estrogen receptor. It might be something. What it is is a lifesaver in a sea of death. While all normal cells are regressing, the cancer finds a trick. From then on it uses that trick. It isn’t a gene that drives the cell but a cell that drives the gene. Very often the genes that cells are using are normal genes! Right?
You’ve probably seen patients who’ve had a gene profile and they have no mutations. Oh! Does that mean they don’t have cancer? Why are they dying? They’re dying of cancer that’s using normal genes abnormally. We need to be smarter, more global, more broad in our thinking. When we think of cancer biology we have to think of cellular biology. Not genes, not DNA, not transcriptomes, not RNA, not even protein. Cells. Cells interacting with one another. Cells interacting with their stroma. Cells talking to the world around. Then pry into those cellular behaviors, what it is that they’re using to stay alive.
I was just going to interrupt and say it’s sounding, the more I listen to you, that you’re discussing, you know, the concept of epigenetics and the idea that the concept for so many years we take family histories. You’re going to get your genetics and they’re going to run you down a particular journey in life, you know? The idea that people have been led to believe, in the past, that their genetics determine your historical health. We know now for decades, like you’re talking about, that your genetics is not necessarily your destination. Yes, you want to know it. Yes, you want to know what you’re at risk for, but your epigenetics – the environment you live in, your relationships, your stress, your toxicity, all of these things, your community, again relationships and how you interact – is really more important of what negative genetics get turned on or positive genetics get kept turned on. When you refer to the cell, again, we are a collection and a community of cells. The idea here would be what I hear you saying, if I’m taking it correctly, is we need to stop looking at the genetics as all the answer. We need to look at the cells themselves, the people themselves, and what is their environment in which they’re living in and what’s signaling this and what’s signaling that. What’s the root cause of the problem? Would that be on the right track?
Oh, absolutely. What you are speaking of is what we call genotype to phenotype.
I am a phenotype biologist.
For the audience who doesn’t know the terms. Genotype is your genetic makeup, and phenotype is how you use that genetic makeup as a starting point to be the person you are. If we use an analogy, image that all of the runners in the Boston Marathon line up at the same starting line. When the gun goes off, that’s your genotype. Two hours and twenty minutes later, somebody wins. That’s your phenotype. All the ways you ran and what you did and when you stopped for water and all the stuff you do makes you…starting from the same genes as everyone else got, we all got the same genes, but you use them differently. That’s why we believe the secrets of life have to be explored at the cellular level. We have to get away from the informatives of biology and look at the phenomenon of biology. That’s what I do. I’m a tumor phenomenologist.
How does functional profiling work? So that everybody understands. What is functional profiling for cancer? How does it differ from the other cancer centers out there and what they’re doing? How do you personalize this approach?
Well, just as the word functional would suggest, we’re looking at cellular function. We’re not interested in your blueprint. Blueprints must be read by contractors and built into homes. We want to take a walk around. We want to look at the three-dimensional experience called your home. Now, there are circumstances where a good blueprint can be read badly and there are circumstances where a rather bad design can be put on a beautiful space and still be a great outcome. What we’re interested in is not the beginning but the end result. The end result is phenotype.
Functional profiling is a technology that we developed to look at cell behavior, not information, not DNA, not roadmaps, not satellite maps, not blueprints, but functional biological three-dimensional existence. We do that by isolating cancer cells from patients. We actually do a biopsy, a surgical biopsy or needle biopsy or aspiration of fluid. We isolate these aggregates, these biological little experiments in a test tube environment, and we introduce into that environment the drugs and combinations and targeted agents and metabolic inhibitors that constitute therapy. When and if we see injury to the cells, then those cells will undergo the process of programmed cell death.
Programmed cell death, one form which is apoptosis, is the process whereby an injured cell falls on its sword and kills itself in the service of the organism of a whole. We are made up of trillions of cells. One of the most dangerous things a cell can do in the body is if it’s injured, if it’s damaged, if it isn’t functioning, if it isn’t going to do its job…one of the most dangerous things that cell can do it stay alive and have offspring and carry on. That’s cancer in the making. The cancer cells escape the signal, the process, the elimination, the street cleaner who is supposed to get rid of them. They say, “No, I’m not going to die. I’m going to stay alive.” What happens there is that cancer becomes a disease of cell survival, not growth, not proliferation, but cell survival. Cancers win because they outlive their normal counterparts. I wrote a book called Outliving Cancer. The title was chosen because I wanted people to understand your cancers are trying to outlive you. Your job is to outlive them.
Functional profiling is a measure of how cells respond to injury and if they die in the test tube then they are more than twice as likely to die in your body. That’s called clinical response and cure.
What are the different types of agents that you’re exposing them to? Are they typically like a chemotherapy type agent, or are they other types of agents? Is there sort of different categories of things you’re exposing them to? Like the oxygen we were talking about or the estrogen or the testosterone. How do you choose and what types of agents are you exposing your samples to?
We’re agnostic. We will test anything! You had asked earlier in your prior question about how we’re different from other technologies. At most universities today, if you go and say you want personalized care, they’ll run your genes. They’ll take a look at your blueprint. They’ll take a look at your satellite map, but what they don’t do is your Google map. They don’t really know if the road being there is being used or is passable or is a good way to go.
So, quite different from what most centers do, in fact, all centers, we’re not interested in your blueprint. We’re interested in the building. We’re interested in your function. From a standpoint of what drugs do they test? I don’t care. As long as it kills cancer cells, and it doesn’t kill you I’m all for it. I don’t have a dog in this fight. I don’t really care what I use. We test cytotoxic drugs, 5-fluorouracil, gemcitabine, cisplatin, cytoxin. We test targeted agents, erlotinib or bevacizumab or drugs that target specific agents. We test novel, newly developed compounds like Wnt/beta-catenin inhibitors and drugs that will target things that we don’t even have drugs for yet! These are experimental.
Then finally and most excitingly and, I think, most productively we’re testing metabolic inhibitors, agents that down-regulate the very fundamental biology of human energy production and cellular metabolism. That’s really the future.
Right. Yes, the metabolism of the cell and the idea that what fuels that cell? Because if you can figure that out then you can deplete it of that fuel and then it’s going to die.
That’s exactly what we’re doing right now.
And what are some of the agents you’re finding to be most successful?
Well, you might imagine that on most chemotherapy development, most medical developments are driven by certain ways of thinking. So, you get a kind of herd mentality in as much as cancer biologists were taught, told, instructed to view cancer as a disease of cells that grow too much. I mean that’s what most people think. Most drugs were designed to stop cells from growing. That’s what they did
So, if you look at the chemotherapy drugs of today, they have actions that block DNA synthesis. They have action that stop mitosis. They have actions that stop the reading and use of DNA. So, we have an entire generation of medical oncologists who are extremely good at stopping cancer cells from growing and dividing. It’s just that they’re not very good at curing cancer.
And that’s because cancer doesn’t grow too much, it dies too much. Our job isn’t to make cells stop growing because every cell in your body is growing, your hair follicles and your bone marrow and the inside of your mouth and your reproductive system. All of those cells are growing. Life is growth. To stop cells from growing is to burn the house down, to heat it. It’s nuts, and we’ve made a great mistake. We’ve poisoned our patients indiscriminately, and it’s extremely distressing and it’s how I got into this field because I couldn’t believe how crude this whole thing was.
So, we said well if we’re going to get patients to get better, we have to make their cells die. It turned out that some drugs can make cells die really easy. I mean there are drugs like dexamethasone. The first paper I ever published was on a study of pediatric leukemia. We said, “Why do children live or die when they get leukemia?” And we reasoned that the leukemia children had cells, blasts, that didn’t want to die. Normally, when a bone marrow produces a cell that’s the earliest primordial cells called a blast. The blast grows up into its teenage years. It finally becomes an adult.
It goes out into the circulation and beats up viruses, and then it dies. The blasts in leukemia don’t want to die. They’re having too good a time. So, we reason, “What if you expose these cells to one of the drugs that causes them to die?” And that’s a drug called dexamethasone which is a steroid. It’s a corticosteroid.
So, we said, “Well, everybody with leukemia gets corticosteroids. Let’s see if the corticosteroids, if these drugs, will cause the cells to die.” And we took children, we took 49 children, we studied them with this one drug, just one drug, and we said, “Okay, do these kids’ cells remember how to die?” We didn’t poison them with a bunch of chemotherapies and stuff. We just used a corticosteroid very commonly used in this disease and we found that the kids whose cells died with the corticosteroid were by the fourth day, after we’d met these children and gotten their bone marrow aspirations, by the fourth day we knew who was going to be alive twenty years later. We published that and at the time I published that I thought, Eureka, everyone’s going to take this seriously. We’re really good at what they do. They didn’t care because everyone was so dead set against this concept that they wouldn’t listen.
So, the point being that drugs don’t have to be poisonous, they don’t have to be toxic, they just have to be effective. What a novel idea! We’re gauging efficacy of any drug. I have published experiences in patients getting drugs that no one would ever have thought of. I published a paper a few years ago on a young woman from southern Brazil with a rare cancer, adrenal cortical carcinoma. She flew from the southernmost regions of Brazil, from Parana, Brazil, and she had adrenal cortical carcinoma and she was failing therapy and she was dying. I looked at her and I said, “Well I have no idea what to do for you.” And I happened to be experimenting on a drug from a Japanese group, and that drug worked metabolically. I thought, Well, this is such a metabolically active tumor. Maybe I could look at something metabolic for this patient. So, I added a drug into the mix called phenformin, which is the parent compound of metformin which is the diabetes drug, and it killed her cells completely. I turned to her doctor in Sao Paulo, Brazil and I said, “Would you be willing to give this young woman, who was obviously dying at twenty-six years of age who has already had all the chemotherapy, surgery, and everything I could do for her, would you be willing to get her metformin?” And she did, and she went into complete remission.
A similar case with another patient who had a very, very rare breast cancer and we gave her a drug that’s used for kidney and liver disease, liver gases. In her case it went to a complete mission we published it. Those are published experiences. So, what you have to realize is that…I joke about it but it’s a truism, drugs don’t know what cancers they were invented for so it’s silly for us to imagine that we know better than the tumor. You’ve got to ask the tumor; you’ve got to interrogate the tumor.
Absolutely! So that folks understand because you’re an oncologist talking the way you are. There have been so many studies out there actually that have shown that chemotherapy doesn’t really save people’s lives, you know. What does it face, a five-year life expectancy or survival? And what is it a two or four percent improvement in life expectancy and life survival with chemotherapy over studies essentially? Is that about the statistic?
Actually, you’re quoting an Australian paper I think which examine the impact of chemotherapy across all diseases and all cancers treated. The data was 2.4% survival advantage. Yeah. I agree, but chemotherapy that works, works. Our job for patients is to make sure they don’t get the wrong drug or that they don’t get treated at all with drugs if they’re not going to work. So, what we say in our work is that there are basically three applications for my work in essence. If you believe that you can make better decisions for each patient and if you believe that these tissue culture techniques can help you then there are three things I do for you:
- A – I cure the curable patients
- B – I treat the treatable patients
- C – I avoid feudal care
If you have a leukemia or a lymphoma or a newly diagnosed breast or ovarian cancer and I can cure you then using this technique twice as often I will cure you. If you have recurrent lung or recurrent breast or ovary and the likelihood of cure is small but good outcomes are possible then I use this test to get you the best outcome at the least toxicity. And if you’ve come to me with a disease like a widely metastatic treated melanoma or a hepatocellular carcinoma or a heavily treated pancreas and you’re at the edge of life and death and I say, “I don’t think these drugs will help you.” That’s a service.
Of course. It’s always a service. I can help you to live or I can also help you to understand that things are not working, and I can help you to die. I mean you know we all we all get that outcome; we just don’t know when. We come in it’s a one-way street. I mean you know what’s going to take us out is something, whether it’s a cancer or a cardiovascular event or a stroke or whatever it might be, or you fall off a cliff. We all are going to have that outcome we all do need to understand that and sometimes as physicians we need to be reminded of that too.
Robert, what does it look like for a patient to work with your institute, you know, as far as people are listening and it’s like, Wow! I like this approach. I understand what they’re saying in the basic concepts, and I think it’s the way I want to go. What does this look like for a patient?
Well, we relish the opportunity to help people with cancer. We know only too well the outcomes from most treatments. The minority of patients who have advanced cancers today get better and a very, very, very small minority get durably better or cured so we need to start reversing those statistics. In order to work with us, the patient needs to sort of take charge of their care and what we recommend is look up our website, Nagourney Cancer Institute. Take a look around. You can read our blogs, you can look at our patient testimonials, you can look through the techniques that we use. Just familiarize yourself with the ideas that we promote, the concept of cancer biology, the concept of drug selection using your tissue your cancer not some textbook or journal article or meeting discussion but you, your own individual biology.
Secondly, if you like the idea of this reach out to our staff. They’re very expert, and they will walk you through the prospects of working with us. Now, let me explain, I can’t fix everybody. My job is to find people who are at a point either newly diagnosed needing treatment or recently relapsed. We cannot treat or test patients who are on chemo, so the first thing is you have to be off treatment for me to help you.
Number two, we’ve got to be able to get out a site of disease. There’s got to be a lymph node or a fluid accumulation in the lung of the abdomen where someone’s going to surgery to remove the tumor or they’ve got to, you know, alleviate an obstruction. There’s some reason or accessible side of disease that we can get at.
We need about a cubic centimeter which is a gram, more or less the size of like an almond or a grape, or for fluid several hundred cc’s which would be like a cup or a few cups of fluid. We get those submitted to us by overnight courier alive and healthy and fresh like you were transporting a kidney for a transplant. It’s a living organ in a test tube, and you’ve got to treat it delicately and get it to me by overnight courier. We ship samples from Bahrain; we ship samples regularly. I’ll be getting a sample from Sao Paulo, Brazil this week. We can ship almost anywhere in the world, but it takes a little lead time. We need enough opportunity so we can coordinate with the doctors.
Once the sample arrives in my test tube environment, we disaggregate it, we look at what we’ve got, and we’ve got a lot of cells that we set up standard chemotherapies. We set up targeted agents, we set up experimental agents, and if we’ve got enough, we set up the metabolic agents. We will also ask if the patient has a particular interest in one area or another or if their physician has a particular type of treatment they’re thinking about, we can set that up and test it.
The report comes back in about a week, takes us seven days. It’s interesting, for as long as it used to take people to grow cancers and all the problems that was fraught with it…it’s not that hard to kill cancer cells. Cancer cells that want to die are dead in three or four days. If the cancer cells are going to commit to programmed cell death, apoptosis necroptosis, ferroptosis, whatever process all roads lead to run, whatever kills the cancer cell in the test tube we can pretty well gauge that within seven to ten days and have the report. Before the patient is ready to start their treatment, we’ll have the results back.
Dr. Nagourney, how many folks out there, doctors, providers, institutes are using this approach?
Well, as I told you there was a kind of strange experience where it didn’t work, so people decided it couldn’t work. And so, you’re kind of fighting an uphill battle to get the doctors to rethink things. As you might imagine, these are what are known as paradigm shifts and you probably know the term. The concept of a paradigm shift is that something that you thought you knew or understood is now explained by a different principle. The flat earth or the sun going around the earth and all this sort of stuff. These are paradigm shifts, and these were described by Thomas Kuhn who said that it is very hard to get people to relinquish their paradigm!
If you say to a smart guy at Harvard, “Hey, we’ve got this technology out in California that’ll enable us to study tumor biology and examine the stuff,” they’re going to say, “Well, we’re Harvard University, and if we don’t do it then it must not be worth doing.”
You have to kind of explain to the gods on Mount Olympus that there may indeed be little earthlings running around down there doing things like discovering fire and maybe they’ve got something to teach you. It’s a little bit of an uphill battle, but if the patients reach out to us, we communicate with their physicians and we explain what we do and how we do it.
We have an enormous data. I have published, and my colleagues with me, have published over 2,500 peer-reviewed outcomes in the literature. 2,500 patients who got biopsies, got treated, and we correlated. Some of them were retrospective where we went back and looked what we suggested without affecting the treatments, and some of them are prospective where we actually entered into the into the treatment and suggested the very treatment.
In fact, I published a paper in lung cancer several years ago where we took biopsies of patients with lung cancer, we studied the drug combinations and recommended the treatment, actually selected the treatment. This is rare. Most of the time you don’t get the opportunity to do that, but this was a protocol under my own creation. We doubled the response rate. Quite by coincidence yesterday I had a visit from one of my patients who was one of the people on that study, and she presented with metastatic non-small cell lung cancer. She had a seizure with a brain metastasis, and I saw her yesterday. We were discussing celebrating her 13th year of survival.
Based on our drug selection from her biopsy she’s a remarkable…and she’s not even my longest living! I have another patient who we treated not once or twice but three different times based on separate biopsies and he’s now sixteen years!
Folks, you know, if you’re hearing and listening to this and if you’re following the concepts we talked about a paradigm shift earlier in our conversation, Robert, about the idea of genetics versus epigenetics and the idea of shifting. Some people have shifted, most people have, but there’s still certain things in traditional medicine that are still extremely based on the genetic concept, cancer being one of them. The idea that, folks, if you’re hearing what we’re talking about, Dr. Nagourney and the way he looks at it he’s going to take your true tumor tissue, he’s going to put it in a test tube and he’s going to test the different agents to try and find the one or the combination of ones whatever they might be to kill your tumor so that you can survive. I’m signing up if I develop a cancer for sure!
Robert, again, remind people how do they learn more? How do they find you? How do they seek this out because it’s not on every street corner that’s out there in every cancer center that’s around this country today.
Well, very simply if you just put the name “Nagourney” into Google you’ll get pages of my publications. More importantly to use this on a practical level you want to go to the Nagourney Cancer Institute. That website will introduce you to the concept. There’s the list of all our publications, there are patient testimonials, there’s techniques for getting the tissue. You can reach out to my staff and they’re very nice, they’re very accommodating, and they will answer questions. We’re not here to sell people, we’re not trying to sell anything. What we’re saying to patients is we are a resource that you didn’t realize existed. If you have a bad cancer or recurrent cancer or somebody doesn’t know what to do, we may be able to solve your problem. It’s a shame, it’s heartbreaking when a patient who could get better doesn’t get better because they didn’t know what to do and no one helped.
I will tell you an interesting story. This is a personal victory for me. Many years ago, I was contacted by a doctor who said his wife had ovarian cancer, she was failing therapy, and she was actively dying. I said, “Oh dear, I’m so sorry to hear that. What can I do for you?” He said, “Well, she’s re-accumulating fluid four liters, a gallon, of fluid a week.” And he said, “Could I send you some of that fluid?” I said, “Of course,” so they did. We tested her, and we found a treatment. I said, “I think this will work for you,” and they said, “well should we come to California?” I said, “No you don’t have to. I’ll call your doctor.” I called the next day and he said, “Well, thank you very much for calling, but they’re already on their way to California.” I wasn’t expecting that because you don’t have to come here to get treated, Trish! I’m one doctor. I have colleagues, but you want to stay home you want your life to be good and you just want to get the right treatment.
So, she came to me, and we gave her the treatment both intraperitoneally and systemically. She had already failed not one but two lines of therapy and was considered to be untreatable. She will celebrate twenty-two years this July with an ovarian cancer that was exquisitely sensitive to something no one was thinking about.
A combination that I went on to test through the GOG and publish extensively, but at the time twenty-two years ago no one was using it. So, those stories make you say no one should simply go on chemotherapy, particularly if they have recurrent disease or difficult to treat cancers because their doctors are guessing. I don’t want to be unkind, but their doctors are guessing, and when it comes to life and death you don’t want to guess.
If you think about if you’re going to get diagnosed you talk about mammogram versus thermography versus any type of imaging test, you can’t diagnose any cancer without having tissue and looking at it and testing it and seeing what it is. So, in the same concept, folks, how can you try a treatment unless you are able to test which treatment is going to be the most effective?
Absolutely. Trish, the thing is that when you go to a diagnostic worker, they tell you what you’ve got. I tell you what to do about it.
But then they go to a protocol.
That’s the problem with a lot of traditional medicine today is they go to a protocol and they’re not talking and working with the individual in front of them and their life and what’s led them to where they are today.
Functional medicine is all about that. We start with a timeline and a matrix of your life, the individual. I get to know everything from the time someone was born, and even before that what was their mother’s pregnancy like, to the time they’re born throughout every decade until they are as old as they are at the present time.
Then I put it all in the matrix of the systems of the body looking under every rock, every crevice to try and find out what are the patterns and what are the issues that have been the root causes for this particular person’s issue.
You’re doing a more focused thing, obviously, of a tumor but you are trying to find what is the medicine or combination of chemicals and medicines that is going to destroy this eradicated tissue. Folks, if you understand this flow it makes common sense to me and when common sense makes sense it just is so powerful. Doctors are not just following protocols. Robert, Dr. Nagourney, thank you so much for coming on to the show. I think this is so much what people need to hear and, again, it’s the nagourneycancerinstitute.com. Below our conversation will be all the information and some links and things like that.
Dr. Nagourney, thank you so much for coming on today. I will end with asking you one more question I always like to ask each of my guests – what is your number one secret for living a healthy life?
We are biological entities and ultimately metabolic entities, and our metabolism, our cellular production, and utilization of energy drives all. If you see life through the lens of metabolism, what is your body in need of? What are you doing to support and sponsor it?
I would say that if you think of life as how we make and use energy then you think about food stuff and diet and micronutrition. You think about sleep pattern. You think about lifestyle and exercise. Your machine has to be well oiled, run on good gasoline, you have to change the air filter, and you have to take it out for a spin.
I’m a rower. I’m on the water when COVID isn’t present, and during the year the past year when I couldn’t be on the water, I keep a Concept2 and I’ll row tonight. I eat very carefully but not extraordinary. I mean, I’m not fastidious. If someone offers me something a little off my regular diet…I probably eat a rather low glycemic calorie restricted diet. I do take micronutrients but not excessively. I try to get good night’s sleep. I try to be happy and fulfilled in my life.
Life is not so complicated. It’s like your grandmother’s advice. Your grandparents were very smart! Before we got so sophisticated, we were very smart.
So, my trick to life is probably moderation. Living the life you were designed for, really. Living the life we were designed for and not doing anything crazy. I don’t jump into the frozen baths, I don’t take ice baths, I don’t do crazy stuff. I just do what my body was designed for, and I guess if that’s helped me to stay healthy and alive then that’s my secret. My secret is really just living the life you were designed for.
Thank you, Dr. Nagourney. And, you know, like my mother used to say everything in moderation as she got older. There it is!
Thank you so much for all this information and you know giving people insight into a functional profiling for the selection of cancer treatment. Thank you so much.
Thank you for having me.
All right, everyone! Thank you for listening, and we’ll see you on the next episode of Discover Health Podcast.
Find out more about Dr. Robert Nagourney on his website: Nagourney Cancer Institute
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