Pancreatic Cancer Breakthrough | How Multi-Target Strategy Stops Tumors Dead

A Spanish research team achieved remarkable results, making pancreatic cancer tumors disappear in mice by targeting multiple escape routes simultaneously. This approach prevented tumor recurrence and resistance, highlighting a design strategy central to precision cancer medicine.

Dr. Dino Prato discusses how this mirrors the principles of targeted cancer therapy, emphasizing the importance of understanding the tumor microenvironment for effective cancer care.

🎯 What You’ll Learn in This Episode:
- Why pancreatic cancer is so difficult to treat
- What KRAS, EGFR, and STAT3 do
- How tumors develop resistance
- What the triple-lock strategy means
- Why mouse data doesn’t always translate to humans
- The difference between one-size-fits-all and precision oncology
- Why immune activation matters for long-term control
- Questions to ask your doctor about pathway targeting

📍 Envita Medical Centers – Scottsdale, AZ
🌐 Learn more: www.envita.com
📞 Speak with a care coordinator: 866-830-4576

“Cancer adapts — so treatment must adapt faster.”

Disclaimer

This podcast is for educational purposes only and is not a substitute for professional medical advice, diagnosis, or treatment. Always consult your licensed healthcare provider before making any medical decisions. Individual results will vary, and Envita Medical Centers does not guarantee outcomes. Some treatments discussed may not be FDA-approved or available in all locations. Testimonials are shared with patient consent and may not reflect typical results. Do not delay or disregard professional medical care based on the podcast's content. Certain treatments may be available only at Envita’s international clinic in Hermosillo, Mexico. No specific outcomes are promised or implied

Outcomes Disclaimer
The results referenced from Envita's Precision Cancer Care: 35-Fold Improvement in Response Rates are from a retrospective analysis of 199 late-stage cancer patients treated at Envita Medical Centers between 2021 and 2023, as published in the Journal of Cancer Therapy. These outcomes are not guaranteed and will vary based on individual factors such as cancer type, stage, genetics, immunity and prior treatments. Any comparisons to standard care or clinical trials are based on published data and internal analysis, not head-to-head studies. Individual results will vary.

You can read the full peer-reviewed study at: 

https://www.scirp.org/journal/paperinformation?paperid=132493

Transcript

SPEAKER_00 0:08

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 Prado, founder of NVITA Medical Centers. For the last 25 years, my team and I have treated thousands of patients who've 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 three 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 NCCNN guideline, National Comprehensive 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 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 five year 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 block 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 three 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 a thousand plus markers and block it on multiple fronts. But let me continue with the study. So they're looking for many ways to shut the cancer down. And they found this three major targets that helped the survival of the patients and knocked 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 mutation, some of them being called Crass. Crass is like a gas pedal that's stuck on the floor that lets the cancers drive. They shut down the CRAS 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 CRASS, 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 signalings called STAT three. And so the cancer cells stay alive when everything else is failing. So they shut that down using a drug SD36 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 and 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 three 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 headline, because you had mice living that long, there's something to this. And of course, this particular regimen should not be seen as a regimen 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 long, it's you name it, 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 CRASP mutation or a TP53 or other mutations. RNA transcriptnomics. This tells us the escape routes. We can look at literally thousand-plus markers here to show what the next pathway would be if this one doesn't work. So we're 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 gonna 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 their 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 gonna get a pretty much a one size fits all. Here's the treatment. Based on tumor marker, biopsy, and imaging, we're gonna 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 therapy, immune modulator, it's all one size, Escodar, 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 three 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 the 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 gonna return if it's gonna 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 transcriptnomics, 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 you 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 gonna 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.