In this presentation Dr. Dino Prato, founder of Invita Medical Centers, discusses a recent Spanish preclinical study in which pancreatic cancer tumors were eliminated in mice using a "triple‑lock" multi‑target approach. The study simultaneously inhibited the KRAS driver mutation, an EGFR bypass pathway, and the STAT3 stress‑signaling backup, resulting in complete tumor regression, no resistance development, and extended survival. Dr. Prato frames this as a validation of precision oncology, arguing that successful cancer treatment requires mapping each patient’s unique DNA mutations, RNA‑driven escape routes, and immune microenvironment to design custom multi‑drug regimens—often combining on‑label, off‑label, and repurposed agents—plus immunotherapy for durable remission. He critiques the one‑size‑fits‑all model of standard NCCN‑based protocols, emphasizing the need for adaptive monitoring (circulating tumor DNA, circulating tumor cells, methylation scores) to detect early recurrence. The talk concludes with practical advice for patients on questions to ask their doctors to ensure a precision‑targeted strategy is being employed, and a call to support the channel’s mission to spread this approach.
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A Spanish research team just made pancreatic cancer tumors disappear in mice. You may have seen this in the news, and they didn't do it with one magic drug. They did it by locking the cancer down in multiple escape routes at the same time. That's why tumors didn't come back, and that's why resistance didn't develop. And here's the most important part. This study didn't just test drugs. It tested a design strategy, a strategy that is the exact same strategies we use in precision oncology. I'm Dr. Dino Prato, founder of Invita Medical Centers. For the last 25 years, my team and I have treated thousands of patients who failed some of the top cancer hospitals in the United States, and we did it with precision targeting, immunotherapy, and looking at targets like this. In fact, more than 3 targets, many targets depending on each patient's unique tumor. There's nothing else we can do is often what patients will hear, or the treatment wasn't done correctly and the cancer returns. But we don't guess, and that's what this researcher did and his team. We don't guess. We don't use a one-size-fits-all model. Typically, patients will use the NCCN guideline, National Comprehensive Cancer Cancer Network guidelines for their cancer. And sure, that may work for some, but it's really a one-size-fits model. It may use a tumor marker, a biopsy, and essentially imaging to direct care. And if you're lucky, a few biomarkers and DNA. This is not enough. What we need to do is map out the entire cancer, build a custom strategy for each patient. And that's what I'm going to show you today. The Spanish pancreatic cancer study is so important, and why it validates everything about precision oncology is so important to cover today, because that's what people need to understand, is that precision and targeting makes makes a difference. Don't change anything unless you are working with a doctor. Here we go. Pancreatic cancer is one of the hardest cancers to treat. After 5 years, survival rate is around 13%. So why is that? Because pancreatic tumors are wrapped in dense scar barriers. We call them stromal barriers. And if you try to do IV chemotherapy, let's say less than even 1% gets to the tumor. So the chemotherapy may not actually get there, it may not do its work. Secondly, most patients are diagnosed late. The complexity of the cancer is already there— mutations, growth rates. Third, this is one of the biggest problems. Pancreatic cancer adapts and it blocks the one pathway they try to give you with chemotherapy, and it finds another way to survive. It's called resistance. So this is why this Spanish study was important. It used what I call a triple lock strategy. The Spanish research team asked a smart question: what if instead of blocking cancer in one place— gee, pretty novel question— we would block it in 3 critical places? Or I would say, in precision oncology, everywhere it needs to be blocked. When we're looking at DNA, RNA, immune spatial biology, and immune profiling, we can look at 1,000+ markers and block it on multiple fronts. But let me continue with the study. So you're looking for many ways to shut the cancer down, and they found this— 3 major targets that help the survival of these patients and knock the pancreatic cancer out. Now, these are in mice, and when you're treating humans, it is a little bit more complicated, but the theory is very important. It's not random, it's strategic, and that's what precision oncology is about. It's moving away from this one-size-fits-all model to getting patients what they need. So let's talk about how they did this. Here was the main engine. Most pancreatic cancers are driven by some mutations, some of them being called KRAS. KRAS is like a gas pedal that's stuck on the floor that lets the cancers drive. They shut down the KRAS mutation, and there's many drugs that can do that. They selected one, but it depends on each patient. Secondly, they looked at the bypass route. So when that's shut down, when you block KRAS, it often will create a detour. It's called EGFR. This is a different signaling. So they used another drug, an EGFR inhibitor family drug, to block that, and this cuts off that escape route. So you already have two drugs. And third, the backup. So they called it the backup generator in this case. When the cancer is under attack, it turns on stress signaling called STAT3, and so the cancer cells stay alive when everything else is failing. So they shut that down using a drug, SD-36, and it destroyed it. And this removed the tumor's backup generator, and that's where they got the success. Now, this is what I want you to look at. When you look at precision oncology, that's exactly what we're doing with our deep algorithms. We're looking at all the maps, the escape routes, the shutdown generators, all the components so that we can shut it down. But we add another component that was not added here: immunotherapy. Because in the end of the day, the long-term remissions always require immunotherapy in our clinical experience, meaning you'll get maybe a longer remission, but if you want long, long-term remission, years and years, dare to say a cure, we need immunotherapy to be involved. So in this study, when all 3 locks were applied, the tumors regressed completely. Resistance didn't develop, affected later 200-day survival, which is a big deal. And that's why the study made the headlines, because you had mice living that long. There's something to this. And of course, this particular regimen should not be seen as a management to treat pancreatic cancer patients, but the strategic modeling and precision oncology, which we have been doing with our patients, should be seen, in my opinion, more commonly used with patients. Now listen very carefully. Just because something works in mice doesn't mean it's going to work in every human being. But because every patient has different cancer profiles, different mutations, different pathways, different immune escapes, all these different targets, we can address those in precision oncology and greatly enhance the patient's outcomes. This isn't just for pancreatic cancer. It's breast, it's colon, it's prostate, it's lung, it's you name because all cancers have that. They have escape routes. They grow, they mutate. Now pancreatic does that in the most aggressive of them, but this can be used on many cancer types. So this Spanish study didn't just prove one drug cures pancreatic cancer. It proves that you must identify the blocks, the cancer escape routes. That's exactly what precision oncology does, but customized for each patient. Simply put, here's how we do that. First, we look at the DNA. So that's the biomarkers, the next generation sequence, hundreds of markers. And that's where you would find, let's say, a KRAS mutation or a TP53. Or other mutations. RNA transcriptomics— this tells us the escape routes. We can look at literally 1,000+ markers here to show what the next pathway would be if this one doesn't work. So already working on the blockade down the street, if you will, to the pathway. So I always like to say the DNA is the car driving in the street, the RNA is the roads or all the escape routes that it's going to take, and then finally the immune profiling tells us, is the immune system going to take it out like a sniper? Is the immune system exhausted? Is it blocked? Does it have a tumor microenvironment that's blocking your T cells and natural killer cells from doing work. And in my opinion, you have to turn this on for the long-term results that people really want, and as clinicians, we want for our patients. So this gets us out of this one-size-fits-all. So here we are, standard oncology, no matter which top hospital you go to, and even if you do integrative care, it's one-size-fits-all on both ends. You're going to get a pretty much a one-size-fits-all— here's the treatment based on tumor marker, biopsy, and imaging, we're going to put you on this protocol. If you fail it, you go on another regimen. If you fail it, another regimen, to clinical trial. Instead, this is custom-built. If you go to integrative care, high-dose vitamin C, ozone, immunomodulator. It's all one size, Escadar, you know, whatever they want to use, mistletoe. And they'll throw these regimens in. There's nothing wrong with that. They're trying to help their patients. But again, it's just throwing something at it without having the mapping. That's the genius of precision oncology. For each patient, we want more than just a triple threat. The Spanish study used these drugs, and this was impressive. But precision oncology can go way beyond this 3-drug limit. It can map it out. It can custom build the combinations. We can go on-label, off-label, repurpose drugs, natural treatments, phytotherapeutics to target all pathways using these approved drugs and these various combinations on and off label and custom build them in the pharmacy. We can bring them direct to the tumor so we get 95 to 100% absorption without hurting the body. We can stimulate it through the body with microdosing so the immune system stays strong. So it's important to know that whenever you use this precision modeling, then what we want is adaptive monitoring. So now we're not just waiting for tumor markers or imaging, but we're actually looking at circulating tumor cells, methylation scores, CT-free DNA, which tells us way before the cancer is going to return, if it's going to return. So that's the power of precision oncology. So I hope you found this helpful to help you see that precision oncology and the strategy is the most important part, and working with a doctor or facilities that do this is critically important. So what should you ask your doctor? Number one, what's the strategy for treating my cancer? Are you looking at the DNA biomarkers? Are you looking at the RNA transcriptomics, the escape pathways? Do you have treatments for that, on-label, off-label, repurposed drugs, immunotherapy? That's the question you want to ask. Can we go straight to tumor? Can we turn my immune system on? And can Custom target my immune profiling with my immune spatial biology to help the cancer stay at bay. If the doctor says yes, we can do that, great. If they can't and they say we don't know, we haven't heard about this, this isn't available right now, find another doctor. Because in my opinion, with late-stage complex cancers, you need this targeting. It makes the world of difference. So we're not just looking at there's going to be a cure tomorrow with one single pathway. It's the ability to find the resistance. It's so important to use a strategy that combines all the best to get to the heart of the question. Here is what the patient needs. To build their immune system and shut the cancer down once and for all. That's the goal of the therapy. So I know that currently over 90% of you that are watching are not subscribed yet. Please support the channel. We want to get the word out on precision oncology so people aren't stuck in the one-size-fits-all model, and we change the way doctors think and patients think so we can improve people's quality of life. I hope you found this episode helpful, and may the Lord bless you on your journey to healing.
