EXCLUSIVE: Dr. Patrick Soon-Shiong on the Cancer Surge in Young People & a Potential Cure I EP 740

Okay, Sean. Let me unpack that. Again, we have to be very careful. What he's been talking about, and the evidence does support that, is the spike protein.

So, the COVID virus carries on its surface this protein called spike. That's how it enters the cells. It uses this protein spike, quite literally, to enter through this thing called ACE2 receptor into your body. So, this spike protein, whether it's carried by a booster, whether it's carried by a vaccine, or it's carried by an infection, I don't think I can get into that because I don't know in these patients where the spike protein comes from. But let's talk about the science around the spike protein. And that's very real now and very concerning. There's now umpteen very well-studied peer-reviewed papers out there that speak to the increased incidence of cancer as a result, we believe, of inflammation and immunosuppression from the spike protein.

Yes, and it seems to be saying not just if you had COVID, but you've had spike protein that resides in your body. Now, you do know that the vaccines were made based on the spike protein. We do know that when you get infection, the virus infection comes in because of the spike protein. The most important question, let me unpack that. Once you get infected, or even vaccinated, but let's just talk about the infection so we don't have the controversial issues about the vaccinations. I want to talk about the science around the spike protein. Now, there's a magnificent paper by the group from UC San Francisco, Tim Henrich, who's shown now, pre-COVID and post-COVID, that he's done incredible science where he's looked at the persistence of the spike protein in the tissue of the colon, in tissue of the brain, in tissue of the parotids, and it lasts for up to 2 years, double-stranded RNA spike protein. That's really very concerning because the hallmarks of a virus that can increase the risk of cancer — one is its persistence. There's clear scientific fundamental evidence that it now persists, meaning the spike protein. Two, does it cause inflammation? And three, does it cause what we call immunosuppression of your cells, the T cells, that help protect you from cancer. Well, it appears to do all three. It persists, it causes inflammation, and that's why we can explain a lot of the long COVID, and then there's now very strong evidence of immunosuppression. One of the most strong evidence just got published this year, this month actually, by the University of Virginia and at Cedars-Sinai in a paper in Cell. In this paper, what they've shown is that not only are the viruses there, but it actually suppresses the immune system to the point that it increases risk of lung cancer. So now we have increased colon cancer, increased lung cancer, and this paper shows a mechanistic way in which it does that. The scientists showed that when you have this virus, you stimulate a cell called a neutrophil that completely suppresses the immune system and increases lung cancer. And now the third paper that has come out, from Spain, and what is very disturbing there in colorectal and anal cancer, they were able to biopsy the cancer tissue itself, and inside that cancer tissue was spike protein and this virus. So we have three independent, very well-respected articles in peer-reviewed journals that show that if you have a viral infection like COVID, the chances and risk of getting cancer is higher.

Well, that's the issue, I think, that's going to face us as scientists, as researchers, as drug developers, for the next decade. I was always fearful that if we did not develop a treatment or vaccine or therapy that did not clear the virus, meaning clear the virus itself from your body, you would end up in this state. So, the treatment is to find ways to clear the virus. And the only things that clear the virus from your body are certain cells in your body that I suppose best way to say it, chomp up the bad cells, and they are called macrophages, natural killer cells, and T cells. And if you can find a way to activate those cells in response to these cells that are contaminated with the virus, you have a shot.

No, these unfortunately — what they're showing now, these aren't good T cells. These are sometimes exhausted T cells. That's the problem. A T cell can be a good T cell that kills, or a T cell could be the opposite cell that actually suppresses. And a T cell could be an exhausted T cell. Sadly, it appears that when you have COVID and long COVID and persistent virus, you end up in the exhausted phase or the phase of the cell that is suppressed. It puts your body in a defenseless position and a pro-tumor position, meaning sadly, this could explain why we're seeing this increased risk and increase rise in cancer and more importantly in young people.

I think we're already seeing that, Sean. That's what's worrying me. I think if you speak to most oncologists in the nation and the world and you see all these papers, they're actually saying — if I may read from this paper — and this is from very reputable institutions: University of Pittsburgh School of Medicine, University of Virginia, Cedars-Sinai, Mayo Clinic Jacksonville. These are all the authors of this actual paper that just came out this month. It says, "Here we show that patients previously hospitalized with severe COVID-19 have an increased risk of subsequent lung cancer." So I'm referring to a paper published in Cell, a very highly respected peer-reviewed journal. I don't want to sound the alarm just for the sake of alarm, but oncologists, clinical practitioners, are now not only seeing a high instance of cancer, they're seeing high instance of people that were in remission and then post-COVID now get recurrences. Dr. DeChabert here at UCLA did that analysis and just presented that at ASCO — patients with breast cancer that were in complete remission or had complete pathological complete responses, once they had post-COVID or an ALC level low, they got recurrences. I've never seen in my personal career, and I've seen a lot of patients with metastatic pancreatic cancer — a 12-year-old boy with metastatic pancreatic cancer that we were able to treat and unfortunately weren't able to save. I worry about this now constantly. This is something that the world should come together to try and address.

I can't answer that question. Shortness of breath. It's very hard for me to answer any questions about what the government does or doesn't do. But I can tell you this is a real issue. I can tell you that the call to action is really, really important. Maybe the United Nations or somebody at the government level, a larger body, has to address this. But maybe us in the private sector, we are trying to address this. And if you don't address this, this is what we call a health crisis. We call this a non-infectious pandemic. And that's what the World Health Organization has raised that alarm about. One of the most fearful things, especially in continents like Africa, where the next wave is this non-infectious pandemic of cancer.

Well, that's exactly — I think now we've come full circle. It is not yet fully proven that COVID is what we call oncogenic. Let me describe what I mean by oncogenic. Viral infections can somehow in your body induce the causation or increased risk of cancer. Example: human papillomavirus, HPV. Patients with HPV have an increased risk of cervical cancer, head and neck cancer. Hepatitis — you have hepatitis, you increase risk of liver cancer, and so on. If, and I say this as an if until we fully prove it, but the evidence is now growing — COVID is an oncogenic virus, then we are in real trouble because we then have to address this and seeing this increased incidence of cancer, and because we're seeing this in young people. It says that this virus is immunosuppressing even a young body's immune system.

Well, the evidence of oncogenic viruses will take time because what you're going to need is — as you begin to see now, the study that came out of UC San Francisco shows you double-stranded DNA going for 2 years and longer at the site of infection. You're seeing now a patient from Spain where they biopsy the tumor cell itself in the colon and see the COVID virus. So the question is: is it an actor or is it just a bystander? In order for it to be an actor, meaning participating in the causation of cancer, you need to then say does it also block a thing called P53? Does it block the genes in your body that protect you from cancer? I think that evidence has been developed. I know actually that evidence is being developed. I think until it gets published in a peer-reviewed journal and validated by multiple centers, when that comes through, and we can call it an oncogenic virus by everybody agreeing to that fact, then I think we can call it that. I say if now because while the evidence may be growing, I think we need a little bit more evidence and more time. But I'm worried now because we're already seeing — I don't think there's any question just as you gave this quotation of the numbers — that the number of cancer patients both young and relapsed is increasing dramatically.

I'm not sure we really fully understand it, but you're completely right. I'm seeing now, for example, very high incidence of breast cancer in very young women. I'm seeing now in our clinic patients who were in remission and now all of a sudden rapid recurrence. I'm seeing instances of thyroid cancer and breast cancer, whether it's hormonally related or whether in fact, for example, in prostate cancer, which is another hormonally driven tumor, there's a gene associated with the prostate called the TMPRSS2 gene that allowed a higher penetration of the COVID spike protein. Now, whether that exists also in breast and in thyroid, I think remains to be explored. But yes, there's a molecular dynamic that happens in some of these tissues, and I really believe it's part of the spike protein problem.

Well, think about this now. I have never seen in the history of my career metastatic pancreatic cancer in 11-year-old, 12-year-old. We now have reports, and I've spoken to the doctors who are now seeing colorectal cancer in 10-year-olds. Think about it — 10 and 11-year-olds. There has to be some relationship because we had never seen that before. There's a syndrome called Lynch syndrome, L-Y-N-C-H syndrome, that affects maybe close to 2 million Americans that don't realize they have it. They have an 80% higher risk of colon cancer. Now, if you have both a combination of Lynch syndrome and an immunosuppressed environment from COVID, would you get a high instance of cancer? If you have inflammation in the colon like ulcerative colitis or Crohn's disease, so this is where all this happens. And then finally, the ACE2 receptor that is the harbor receptor for the spike protein has high levels in the colon and the rectum. So there's enough circumstantial evidence that says it's all about the spike protein here.

Well, early detection is key to everything with regard to cancer. I believe that if we can detect cancer before, at the point of either biopsy or detection, or even prevent it — I know that sounds nuts that you think you could prevent cancer. What's exciting to me, we have a clinical trial sponsored by the National Cancer Institute as we speak, and we've fully accrued that trial, in which we are attempting to prevent cancer with patients with Lynch syndrome that have a high incidence of 80% of colon cancer, breast cancer, ovarian cancer, endometrial cancer, in which the patient is receiving IL-15 together with an adenovirus against the tumor markers of the cancer. That's one opportunity, but it's in research. The other opportunity, frankly, is this early detection mode and then therapeutically capturing that cancer early on and then treating and putting the patient into what I call durable remission. My dream is that one day cancer's not a disease you die from. My dream is that one day cancer becomes a chronic disease where you've treated it just like HIV — you can live and show that you are free of that disease and not die from that cancer. And I think the science and the technology that we are now building is bringing us closer and closer to that dream.

How interesting you say that because literally tomorrow I'm meeting with a group, an organization that's built a machine — a PET MRI and a SPECT machine — that can now molecularly detect micro metastases at the cellular level. So we can get what we call a PET MRI as well as the normal screening tests like a sigmoidoscopy, the biopsies, the stool analysis, looking at your lungs. The technology now has been developed that we can screen patients very safely with a PET MRI and reduce the risk of radiation and then treat the patient. This science is now called theranostics, and by that it means the diagnosis early on — the ostic part — and a therapeutic. The whole concept of theranostics is about to break through, and you tie that to AI, tie it to these machines — you can not only capture it early but you can find the treatment early.

Well, you sort of pre-announcing my next adventure. I wasn't intending to say that on your show but we're going to do it. So for the last decade I've been working on supercomputing, AI, artificial intelligence — with Dr. Jim Kim who was at the World Bank and president of Dartmouth many years ago — we presented that concept to President Obama, believe it or not, that artificial intelligence is coming to medicine. So going from natural killer cells, as you know I've spent my time talking about it, is this next evolution. And the next evolution is antibodies. But not the antibodies that you and I are making, but antibodies that camels and sharks make. With AI today, now soon we'll be able to find the way to target every area in your body that either has cancer or autoimmune disease or metabolic disease and target those systems with these next generation antibodies generated through AI. That's the next chapter. That chapter is so real that the first antibody is about to go into the United Kingdom, into Marsden, Christie's — the largest cancer centers in the United Kingdom — first in man. And these AI-driven antibodies is this next revolution. Through AI-developed antibodies of this next generation called heavy chain nanobodies, we can do 100 targets in 100 days. And what we plan to do is launch first in cancer but also in autoimmune disease and metabolic diseases. And all is this AI-driven what I call nanobodies. For many, many years I ask a question: why don't sharks get cancer? Why do whales not get cancer? Why do camels have no incidence of cancer? And the answer, believe it or not, they make an antibody completely different from us. And for 50 million years of evolution, this antibody — if we can generate it through AI, which we have — the opportunity then to transform how we target diseases in the body, whether it be cancer, infectious diseases, autoimmune disease, is a real possibility. And I'm really excited to say — I've said it again, Sean, on your show — this is our next adventure.

Yes, because guess what? Many years ago I couldn't figure it out, so I took shark cartilage and tried to extract it. There must be some magic in there. Well, it turns out 15 million years ago the evolution of mankind — sharks and camels and whales developed an antibody which is the shape of a watermelon. Whereas our humans develop antibodies shaped like a Y. Now, that may sound like what's the difference? With the shape of a watermelon, those antibodies called heavy chain antibodies would then go into a tumor and act like a porcupine. So think of a pincushion of porcupine needles. Now, you have a tumor surrounded by all these porcupine needles, and guess what goes on top of those needles? Your NK cells and your macrophages. So it quite literally devours the cancer or the abnormal cell instantaneously. And that was the secret. So this is the beauty of evolution. The NK cells, 450 million years, then these nanobodies, 50 million years, and finally these human beings walking around in two legs and two arms with an antibody that's different from the rest. So if we go back and look at all the elements that protect us through evolution — from the natural killer cell to the T cell, and now to these what I call nanobodies — we have a shot of understanding how to treat diseases.

Well, the best way for me to respond to that is I've spent my life trying to really address exactly what you said. I don't think we're going to win this war through incremental changes. Having said what you just said, that was an important breakthrough through the KRAS, and I developed a vaccine in the first line. We need to capture patients early so that we can get to the curative word. And the way I'm now going to approach this is go globally. My opportunity now is to go to places where there's no treatment available for them. Do you know that the survival rate for children in the United States with cancers is 80 to 90%? The survival rate for children in Africa is 20%. That's so morally wrong. But the opportunity for us to go into Africa and make a change for that entire continent and leapfrog the world is something I'm really excited about. And soon you'll have an announcement about how I'm going to go about that on a global basis. I will need somebody to help me maneuver through that opportunity where we go globally and change the world on that basis. But you're right.

Yeah, well that is a call to action and a job announcement for anybody who wants to go to any part of the world who wants to actually change the course of cancer.

Well, I think you and I understand that probably more intimately than anybody else since you and I were the basis of a warning letter. But—

Well, hopefully that is not the end game. The answer is, yeah, I do want to help, and I'm first and foremost an American. Just so you know, I love this country. I couldn't do what I'm doing now, Sean. As you said, I was — I'm Chinese, born in Africa, so I'm Asian-African, and I'm American. So I'm a triple A — an Asian-African-American. And I'm an American first, but having said that, I'm a doctor. I think you need to look upon me as somebody who wants to really make an impact in medicine. And the opportunity for me to do this in this country was what I really hoped to do, I still hope to do. But the opportunity to help a lot of people very quickly, very fast, change the course of their lives — they don't have time. I always said cancer is a war against time. Whether I go to Africa, whether they go to China, whether they go to Turkey, whether they go to Greece, Brazil, the UK. And by the way, this nanobody is now being funded by the Cancer Research of UK, called CRUK. And this is the first-in-human, first-in-kind of a nanobody in first-line head and neck cancer patients that have never seen any other treatment. I doubt that any such trial could be done in this country. So yes, there are countries that recognize the opportunity and grab it. As you know, Saudi Arabia as a country grabbed the opportunity to treat patients with lung cancer. So I think there is an opportunity to leapfrog whatever other reasons are preventing this coming into America, around the world. And I think that's going to be a charge, an opportunity for me to pursue. And come July, we'll make some very important announcements of how I'm about to pursue that.

I got to tell you, I spent 10 or 20 years of my life working on very sophisticated genomic sequencing and looking at genomics and proteomics and very exotic tests about how would I predict that you got cancer. Crazy that may sound, it turns out there's a simple test that could say, Sean, let me see how strong your immune system is. And if your immune system is strong, God gave you that immune system to protect yourself. So you would ask me, well, how do I know if my immune system is strong? Well, there's a simple test called the absolute lymphocyte count. It's about a $4 test that if you measure the ALC and it's more than 1,500, you're in good shape.

You just go to your regular Quest. It's a CBC. It's like how do you measure anemia? That's a test. The same test that measures—

Correct. The absolute lymphocyte count. Now, let me tell you something disturbing. There's a paper that just got published in JAMA. For the United States, there's another paper published by the Copenhagen Group that says if your ALC is low, meaning less than 1,500, you have a 1.2 to 1.3 increased incidence of dying earlier from any cause. If it's less than 1,000, it's like a 200% increase of dying early. Now, from any cause, whether it be cancer, diabetes, any cause. Which means that your immune system is the basis of your longevity. So the flip side of dying early, I suppose, is living longer. And the craziness is there's now very high reputable papers out there. So forget cancer — for any cause from aging, because the T cells come from a thing called the thymus. That's why it's called T cells. Thymus is T. And as you age, your thymus becomes fat. It stops making the T cells and your T cells drop. And your ALC drops. So there's now one in five Americans with an ALC less than 1,500.

Yep. So your ALC is affected by all these things. It's affected by infection, just a regular infection. It's affected by chemotherapy. It's affected by radiation, but it's also affected by a lack of sleep and lack of sunlight and lack of exercise. It's also affected by your microbiome. So all the things that you do to keep yourself healthy is as important because it affects the level and activity and strength of your immune system. And the level of strength of your immune system is a reflection of your natural killer cells and your T cells. And your natural killer cells and T cells are measured by a simple test called ALC. So if you want to look at the monitoring of your immune system to know whether you're in good shape, it's your ALC. Now, a lot of people are taking GLP-1. What we worry about down the line is muscle weakness. That's a different thing, nothing to do with your immune system, but if you don't have activity, you have wasting of muscle mass. And one of the dangers in the elderly are fall and a broken hip, etc. So these are the kinds of things that are common sense. Good sleep, good diet, good activity, less stress, and sunlight, and just measure your ALC.

Well, thanks for having me again, Sean.