Cancer Immunotherapy Doesn't Work? Read This

Dr. Dino Prado argues that patients with KRAS-mutant tumors labeled untreatable by standard oncology can respond to immunotherapy when doctors use precision medicine. Standard PD-1 inhibitors work long-term in only 19% of patients, but analyzing thousands of molecular markers per tumor can reveal hidden immune pathways and guide personalized drug combinations and cellular vaccines.
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What is the single most terrifying statement an oncologist can deliver? Your cancer is invisible to your immune system and immunotherapy won't work for you. This message comes coded by your oncologist like this. You have a crass mutation with microsatellite stability, meaning you have no access to immunotherapy in the sense of PD1 inhibitors. That your tumor is cold and it's evading your immune system and there's nothing else you can do. This isn't the truth. About 80 to 85% of the cases that are classified as low immunotherapy responsive tumors are consider not treatable with immunotherapy in the one size fits all model standard oncology. The microsatellite stability label is often the kiss of death for approved immunotherapy access. It means you're not eligible to the PD1 inhibitor. But this isn't the whole story. This is standard of care oncology only, looking at 24 data points, not over a thousand. With custom drug design build and custom immunotherapy. Even if you had a PD1 inhibitor that was approved for you as an immunotherapy, you're going to see that it only works long term for about 19% of the patients, according to frontiers in oncology. For the major, it only helps partially in short term and maybe for 10 months. So we're going to get into it in this episode and we're going to talk about how really what's going on. Here is another form of big pharma management, and there's a lot more to the story. I'll show you how precision oncology works to completely change the picture, because without your immune system being fully engaged, you're only managing the cancer. Remember, I've said this before. The first and last defense against cancer is your immune system. And it needs the knowledge to shut the cancer down. That's the goal of precision oncology. I'm Dr. Dino Prado, founder of Envieda Medicine Medical centers. For the last 25 years, my team and I have worked with patients who've failed the top cancer hospitals across the country. It's been my life's work with my team to solve a lot of these problems with immunotherapy. And we go way beyond the one size fits all because each cancer is unique. It has a different blueprint. It's heterogeneous. When you test thousands of markers, they are different. Two colon cancers, pancreatic, endometrial, gastric, breast. All the cancers have unique Markers but with deep N of one precision targeting multiomics, next generation sequencing DNA, hundreds of markers, RNA transcriptomics. Now we're getting into a thousand plus markers, spatial biology and immunity. Now we can build custom immunotherapies and change the tumor's information. To deliver the right powerful treatment. You need all the markers. A lot of patients think they've already done genetic testing with a few of these DNA markers that looks for let's say a crass mutation or it says oh, you are micro satellite stable, therefore no access to immunotherapy. This is standard of care thinking, but in precision oncology that is just telling us a little information of the tum we need to work around. Before I get started this episode, remember I'm just giving you educational information here. Make sure you're always working with a doctor before you change any type of treatment plan. So why are the new crass targeted drugs spelled Kras powerful? They're mostly cytostatic, meaning they slow the cancer down. They really don't kill the cancer, they buy time, maybe seven months. But when we can use multiomics with detailed testing, transcriptomics, ngs, DNA, full maps with spatial biology, we can get a GPS map of the cancer's hidden defenses and and this helps us to build immunotherapy. We'll use an example here. We'll call him Mark as a fictitious patient, but it's an example we see over and over again. Patient comes in with a crass mutation and microstatellite stability with a colon cancer and he was deemed hopeless until we were able to go direct to tumor, change the tumor microenvironment and turn the immune system on. And this is all part of precision oncology. So before we get started, I want to give you some history here and we're going to break this down. You're going to become an expert in these areas of crafts and microsatellite stability. Just understanding immunotherapy in general terms. There are all of mutations today. I'm focusing on one. But you could look at all the different types of mutations that there are now what they call specialty drugs designed to treat and most of them just slow things down. And when you're told that you don't have an immunotherapy option and the standard of care, one size fits all model, we can custom build it if we understand the details of the tumor. So 95% of the problem occurs when people have, let's say a metastatic colon cancer that spread to the liver and they have a crafts mutation and microsatellite stability tumors. That sentence is crushing because it tells. Well, there's nothing else we can do. And the oncologist can't prescribe their beloved PD1 inhibitors, which we've been using on and off label for well over a decade. And we know their limitations. Like I've said before, it may work 19% of the time long term. And that leaves one out of five patients that has a decent respond. The rest have partial responses and they don't get the long term response we need. So we need to do precision testing anyways. So let's shatter that narrative today. So not with wishful thinking, but with a revolutionary science of precision oncology. Transforming the invisible enemy to a visible one. That's the tumor. Making it vulnerable again to your immune system. If you've been told your tumor is too cold to fight, this episode's for you. It doesn't matter what type of cancer you have because we want to manifest a strong immune system and we can do that with the right data. But let's give a little bit of education here. Think of a crass protein as a growth signal to the cancer. It's like having your foot on the gas pedal while you're driving. You're going really fast. The cancer's growing and there's this mutation that's making other therapies not work. Well, this is the gas pedal. It's jammed, it's on go the whole time. The cell receives this constant unrelenting message. Grow, bread, divide. If you were a big pharma looking at the problem, you say, okay, let's develop a drug to sl that down. Sounds good, right? These drugs by 2030 are multi billion dollar drugs. Right now they're well over a half a billion a year in sales. And they're being sold by little companies like amgen, Bristol Myers squig, Bayer's getting involved, all the big pharmaceutical companies. And this is a huge step forward in molecular oncology. So when you're looking at standard of care oncology, and you have these mutations, these smart drugs, they buy you time, maybe seven months of life on average for these kind of medications, but they don't solve the cancer. But big pharma likes managing cancers instead of solving it. I'm not saying drug is good or bad or whether it's helpful or not, but it's not the whole picture. What I want to get across to you is it's buying us time. For what? To get the immune system involved. Because the immune system has to do the job. So let's just go through this. There's two types of drugs. There's cytostatic or better cytos slow things down meaning it's going to slow the cancer cell down. Or cytotoxic or another term would be cytosmash. Destroy the cancer and kill it. The best way to go after cancer is in my clinical experience with immunotherapy. And yes, there are micro dose targeted chemotherapies that are good matches for patients that I like to use within our GTF platforms that are custom and microdosed which kills the cancer instead of just managing it. But we must distinguish the difference between the two because there are different types of anti cancer treatments. One is managing the cancer and the other one is the goal of long term responses. I think it's fair to say everybody wants a long term response but we need to change our strategy in testing and treatment to get there in my clinical opinion. So this is the mechanism of the modern multinational drug companies. Let's make a drug that manages one marker and then if we got another marker, we got another drug and eventually we get blockbuster drugs that sell billions a year. Managing patients really not curing the cancer. That sound familiar? That's what we have today in specialty drugs and that in the conventional model is termed precision oncology. No, no, no. What I'm talking about is a different level of precision oncology. It's n of 1 where we custom build everything around the patient. It's groundbreaking with drug design on label, off label, repurposed phytotherapeutic cancer cell biology cancer vaccine. To go after it and kill it. That's the goal. It's to be an immunogenic cell death is the goal of every treatment. Slow the kill the cancer. That's the perfect setup. That's what we want for every patient. Doesn't matter if you have early stage or late stage because the sooner we do that, the sooner we get to the goal of a better longer term response. This helps us to better eliminate the cancer with targeting now big pharma's, crass inhibitors. Let's just get a little background. It's a $475 million market as of 2024 expected to surpass 2 billion by 2030. Now this is great for Amgen, Bristol Myers Squid who bought out one of the inventors and Bear who's getting into the space. But when you look at a seven month survival, this can't be the best we. I'm not blaming them for discovering a beautiful drug that can be helpful but it's not curing anything. So we have to have a doctor or a medical system that builds the care around the patient to say if that mutation is in place, it's buying us time. And I'm going to say this again, for what? So we can get the immune system involved and have a goal of long term remission. We want people to live and live long. So big pharma approves these drugs that are actionable on these DNA mutations. And I'm not even talking about testing all DNA NGs or full RNA transcriptomics. They use a few markers because they commonly see this in pancreatic or colon, colon or endometrial or gastric, whatever, cancer types that commonly will have crass mutations. And they're like, oh, here's a drug we can give you that'll slow things down. And that's precision oncology. But no, the type of precision oncology I'm talking about shatters this entire form of thinking. It uses thousand plus data points to look at all the pathways. So if the DNA is mutated and you have your foot on the gas pedal and it's pushing the crass mutation, meaning other drugs aren't going to work. The cancer is growing uncontrolled. There are other offshoots. The difference with using over a thousand markers is we can look at all of the pathways and shut down many, many more of them. But the most important part is getting the immune system involved. And this is critical. So oftentimes what patients will hear is oh, I have micro satellite stability, therefore I can't use an immunotherapy drug. Now for some of you don't know that microsatellite stability is basically code for PD1 inhibitors aren't going to work for you. What patients are told is better is microsatellite instability, which means you have higher amount of broken DNA, if you will, in these tiny little pockets that are neoantigens, these little antigens. So let think of it this way. Your cancer, like a snake, has skin on it and it sheds it every now and then, right? Mutating cancer shed very quickly. The antigens are the fingerprint that tells your dendritic cells, which is the detective who gets the mug shots, gathers all the information, checks everything out and then passes that onto your natural killer cell to go out and sniper and kill the cancer. Right? That's the, that's the fundamental goal. So if you have microsatellite instability, you have more of this information that's out there saying to the immune system like a bright Red flag. I'm here and now if I give you a PD1 inhibitor, I'm gon better response. But here's what nobody's telling you. Even if you are a candidate for a PD1 inhibitor, it doesn't work long term on most patients. Frontiers in oncology tells us about 19% of patients respond long term, which means the majority maybe get another 10 months and the cancer will grow again. Because it is not the full picture of immunotherapy, I'm going to repeat this. PD1 inhibitors are not the only form of immunotherapy. We have many ways to custom build immunotherapy when we have all the information. You remove the gangs around the tumor that are blocking it from your immune system. We can take a cold tumor that's hiding, make it hot, which means now the immune system can see it, and we can get the immune system to target it. That's the key. So immunotherapy will not work if you don't know those details and you aren't able to custom build the treatments long term. That's the genius of precision oncology, where everything's custom designed for each patient. So it's not about getting a diagnosis of you have microsatellite stability and you can't do immunotherapy or you have a cross mutation or not, and you're limited. It's way more than that. And I'll give you an example here in a little story. Let's call him mark. Mark's about 50 years old, diagnosed with metastatic colon cancer, spread to the liver. His original tumor tested and confirmed combinations of both crash mutations and microsatellite stability. So low tumor mutational burden. Right. That's what he has going on. So after two lines of standard chemotherapy, he failed them. And he was told there was nothing else he could do. There was no immunotherapy options for him. That phrase is what gets patients. Because now the oncologist says, well, we're just monitoring and quality of life or clinical trial or hospice. But there's a better way. Way. In my clinical experience, Mark did not get full testing. So the oncologist stated he had a crass mutation. So he'll give him a precision drug and he'll give a crash drug. And that crass drug will slow things down, maybe buying seven months, slow down the pathway. But Mark isn't happy. He starts looking around. He doesn't want to go on the 24 markers, tumor marker biopsy and imaging to design his care with the national Comprehensive cancer network guidelines and a few DNA mutations that recognize the crass or the microsatellite stability, which tells them they're not a candidate for PD1 inhibitors. Those are limitations. So what did we do? We tested him and we told him, let's take a look at your immune system and let's look at the targets that are there. And so we were able to unmask the immune system because we looked at a thousand plus markers, we did spatial biology, we were able to take a drone essentially over the tumor and look at the gangs around the tumor that were blocking the immune system. We were looking at the blockades, we were looking at the transcript nomics, RNA within the tumor, the DNA next generation sequencing, full mapping, not a few DNA markers. Then we custom built paths, pathways. Now to explain what we did so you can understand this, Mark got excited because just like most of the patients we see, 90% of the patients that we see were on the wrong chemotherapy. They had failed. They were given too high of a dose of chemo, it was the wrong type. They wiped out their immune system. So now they have a problem of not only are they not having an immune system that will respond to an immunotherapy, it's wiped out, it's exhausted. So making everything more difficult. We were able then, with that data, thousand plus markers, using our algorithms, deep learning, and our information with precision oncology, to build on label, off label adjuvant phytotherapeutics, nanoparticle delivery direct to tumor, cellular immunotherapies, and even a cancer cell vaccine. See, this is Star Wars. This has opened up options that weren't even there before. This helped to unmask a tumor. Now Mark is on his way to responding because now we have targets. We now have the GPS of the tumor and we can do several things to help that cancer. One of the most important things we were able to do is go straight to the tumor with chemo immunoprecision injections. Let me explain what that is. So that's using interventional radiology oncology. So imagine we have image guided pro using a catheter the size of your hair, very small, goes into the blood vessel, into the tumor and delivers the targeted immunotherapy. So get your T cells awake to release the antigens. Did you hear what I just said? So the tumor was cold. Now we're releasing the antigens, we're changing the tumor microenvironment. And now the immune system's engaged. It's hot chemo, immunoprecision, injection is similar to fracking. If you know anything about getting oil, you drill down into the ground and there's these sheets of rock in which the oil is there. And so it blasts a high pressure water and it eventually releases the oil. Well, with sippy immunotherapy, custom drug design, we go into the tumor so that we not only kill the cancer, which is great and seal the blood supply so it dies, but we release the antigens. It's like the oil, we release the antigens, which is the fingerprint and the information that the dendritic cells now can use to recognize a tumor everywhere else in the body. So it's not uncommon that we treat one area and another area responds even if we don't treat it because of the systemic immune response. This is what helped Mark and many patients that we see like Mark in that situation. See it's the targeting and the custom and the directed tumor. Now we went a step further. Now that we have the antigens and we know the peptides of the tumor and the damage associated molecular patterns which you can look up my other videos on it is a concert we're able to use to build a custom cellular vaccine for the patient in our international facility. In this case, he was a candidate for AIT A. Toggless adopted immunotherapy in where we were able to expand the cells using this information and now create a systemic response to the body where the immune system is doing the work. So in the first spot with chemoimmunopre injection we were able to create a vaccine at the tumor level, teaching the body what these antigens look like in killing the cancer. Then we were able to develop a systemic treatment for the whole body to be immune centric. This is the difference of precision oncology. You are N of 1. The treatment is built on you and 1000 plus markers not on the standard of care NCCNN guideline because he already failed that. And that's what I mean when we're saying we're 10 or 15 years ahead with precision oncology is because it allows us to get past the suppression that's trying to block your immune system. See, oftentimes these patients with the microsatellite stability will have t suppressor cells, FoxP3. These are all fancy markers, MDSC, Myelo derived suppressor cells that are all blocking the immune system from doing its work right. The wrong types of macrophages and this microenvironment needs to be shifted at the same time of releasing the new antigens. The neo Antigens from the tumor, creating a immune response that the body can recognize. Because this is how the body naturally gets rid of cancer. It gets this information and it shifts it from cold to hot. One is so important and it doesn't promise cures for everybody, but it just changes the trajectory to treatment to an entirely new level where, yes, we've seen patients in our clinical experience respond better, better quality of life, length of life, when all these combinations are put in play. So instead of just measuring the shrinkage of the tumor, which is great, which we saw, we also want to measure the longevity and quality of life of the patient. So we use circulating tumor cells, CT free DNA methylation scores, monitor how they're responding, stay on the mutation of the cancer, stay on the immuno markers, and then help the patient. Your immune system is the key. It's the key to recognizing the cancer. And so just by taking a specialty drug, like a crass drug or any other one, because I'm just picking colon cancer here, it could be anything. It's just slowing things down. It's buying us time. For what? To get your immune system involved, get the immunotherapy moving, getting the spatial biology maps revealed so we can custom build the treatment and get your immune system so it's not paralyzed, it's active and can fight the cancer everywhere in your body. This is the key, in my opinion, to ending cancer. Because as we get better at this, which we do every year, we get more and information. These cold tumors become hot. The immune system does what it normally does, which is eradicate the cancer and we get better responses. That's the goal of precision oncology. So I recommend that you don't just fall into the standard of care only, but look at the idea of precision testing. You want to ask certain questions to your doctor. Number one, are we using immunotherapy for my cancer? And if the answer is no, or just a PD1 inhibitor, ask the doctor, what other combinations can we use to help with my cancer? What other testing are we using? Can we go beyond microsatellite stability? Can we go beyond the crass mutation? Do you have any other target? You look at transcript nomics. Can you custom build on label, off label integrative agents to support me? And if the answer to that is no, look for another doctor. You can find somebody that knows how to work in that space. That can give you the advantage with precision care. I hope this episode was helpful. You can tell I'm passionate because I hear this all the time. And it really in many ways is false information. There is always hope when we have n of one care that's custom built for each patient. May the Lord bless you on your journey to healing.
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