Can We Switch Off Cancer? The Latest Research on Survival Rates

What if I told you one of the deadliest cancers, pancreatic, finally has a drug that nearly doubled median survival from 7 months to 13 months? Now, it doesn't sound like a lot, but there's a lot more to the story that could help even more cancers. And that's what I want to get into in this episode. It's important to understand that this drug attacks a cancer off switch, and this off switch scientists have been trying to find a drug to treat. They finally found something that may have very good benefit in other cancers as well. And that's important in the area of precision oncology. So I want you to pay attention. You're going to learn about this drug that's called daraxinib, or commercially called RAZIQ. And I'm going to take you through this drug so you can understand a little bit more about the RAS family, because we're talking about particular mutations in KRAS. And we're going to understand how this precision oncology drug could be very good, not just for pancreatic cancer, but a number of colon, lung, and really other cancers that have these RAS and they have these KRAS mutations. So we're going to get through going into this drug and understanding why this is such a big deal. It gives us a target that may be very helpful to slow things down so we can get the immune system involved and shut the cancer down even deeper. So that's why I want you to listen to this, because it's more than just a drug. You know, we know that this drug has a mechanism. Yes, it can slow cancer down if these mutations are present in the patient. So it's not just pancreatic, even though 90% of pancreatic cancer patients have this type of mutation that can be actionable. Other cancers do too. And so it becomes a cytostatic drug, a little bit slowing things down, but it also helps the T cells get into the immune system. And that's the conversation no one is having, and I'm going to show you in this episode how we can combine that with precision oncology and make 1+ 1= 11, or multiply the benefits, because deep mapping matters. I'm Dr. Dino Prato, founder of Invita Medical Centers. For the last 25 years, my team and I have worked to help thousands of patients who've failed some of the top cancer hospitals across the country, and we've done that by precision oncology. Now, in this episode, this is such a great example for you to Learn more about what precision oncology is because see this one drug, this daraxinib that works on this RAS and KRAS mutation. It's a very interesting drug and slow down the gas pedal for the growth of cancer, but it doesn't do the job all on its own because this is one marker. With deep precision targeting, we can map out everything including immunotherapy and start combining things for patients. That's the power of precision oncology. Now, before I get started, make sure you're working with a doctor before you change anything in your healthcare plan, and let's get. So why does this RAS mutation even matter? It's an on switch, you know, where this daraxinib new drug that's coming to the market is going to sell billions of dollars. It's going to grow because it's an important actionable target in certain cancers. These RAS mutations and KRAS mutations, these are molecular switches inside of cancer cells. Normally the switch turns on the cell's need to grow and the growth signal of the cancer. So it makes a difference. If we can shut that switch off, we can really help. So if a patient has this on switch, obviously we can still treat it. There's other things we can do, but this is a specific drug that slows down that growth and lets the immune system get involved. So the scientists knew that they've been working on it for decades. And, you know, like many things, these drugs have probably been available and a lot of patients have been ordering it through Right to Try, but pharmaceutical companies are not that easy giving out the drugs because they want to get it approved and get it fast-tracked for pancreatic, but it's going to move into other targets. The most important thing for you to know is, It's not just a pancreatic drug. Yes, 90% of cancer patients have these mutations, so that's why it's helpful. But when we think of somebody's life being extended from, you know, 7 months to 13 months, you're saying, Dr. Prato, that's not that big of a deal. 6 months. And you're right. But in the world of oncology and in the world of drug discovery, that is a big deal. I like to think of helping people live a lot longer than that, many years. And with the goal of remission, that always should be the goal. So think of this as a potential piece of the puzzle and not the full solution. That's something you won't hear anywhere else because you're going to hear in the media, great drug, wonderful data, people will invest in it, all those great things. But I'm going to tell you from a precision oncology perspective, our 26 years experience of developing and hitting these targets, that this is one good step in the right direction. But if you combine it with other things, you can see potentially even better responses. So this RAS mutation, this is a relatively small protein. In size, but its surface is really smooth and shallow. So traditional drug targets, really hard to fit this pocket of this drug, right? So that's why it became very important when they decided to finally develop a tool that could get to this drug through a downstream regulation. So now it's a treatable target. So daraxinib approaches this totally different. Instead of looking for a traditional, you know, lock and key model to shut off a drug, it's going after proteins like Cyclophosphamide. So these types of things activate these RAS, these, you know, if you will, growth or gasoline to the tumor, and it helps to shut 'em off. I mean, that's really what you know through the molecular mapping. This is only one piece of mapping, and the RAS mutations are just one pathway. But what happens is when you shut these off, after these few months, new pathways open up. How do we know this? Well, in colon cancer, there are drugs that treat KRAS mutations, and what you see is that it'll turn on another pathway called EGFR. So I'm just getting into the little bit of the stuff I like to talk about here, which is molecular targeting. So think of it as like you're seeing a map and in the road you have the DNA mutation. So you can see the road you're on and you might treat that mutation. But after a little bit of time, you're going to open up new roads, new escape pathways, and those need to be shut down. That's why we need DNA, which is next-generation sequencing, which gives us this information. But then we need to go to the next level, which is what we do, which is RNA transcriptomics, which allows us to look at thousands of markers, all the escape pathways, and then another level called immune profiling, because then we can get the immune system to get on board and get after this cancer. Now, this drug, draxinib, is more cytostatic. It slows things down, but it has a particularly unique thing. It helps the T cell infiltrate the tumor. Why am I saying that? Because remember, the first and last defense against cancer, really shutting it down with the goal of long-term remission so people can live and not die, is a lot of it to do with immunotherapy. And so you have combinations here that are really important. So just imagine colon cancer, lung cancer, doesn't matter. It could be ovarian cancer. It could be a gastrointestinal cancer that has this marker. It becomes really It's really important now to treat it. And if you slow it down and it helps the immune system for this window, it's opening up a small window of opportunity where maybe with that genetic information and immunological information, go to the tumor directly. Maybe we use chemo-immuno precision injection through interventional radiology oncology and get right into the pancreatic tumor, kill it, stimulate the immune system to have what's called a Scopple effect. That means a systemic immune response to go after these cells everywhere in the body. And In the meantime, the drug is keeping things slow and nice so they don't grow outta control while the immune system finally hits the antigen or the target of the tumor. See how precision oncology is a game changer? It's not just about one drug. So a lot of people say, Dr. Prato, this drug is a precision drug, but it's one marker. And that's the complexity of cancer. That's how far behind we are in oncology. We get excited, we find one marker. Yes, we get extension of life, but We're not putting all the pieces together, which is what I would call a comprehensive architectural deep mapping of precision oncology. That's how we work. We want to see the bigger picture. Yes, it can help pancreatic. Yes, it can help colon. But do you have the right markers? And these are only one marker. So now if we know all the other markers and we can slow those down, and now we have tools to kill the cancer because we have the information that says these are cytostatic, meaning to slow it down. These are cytotoxic that kill the cancer, and these are Immunological active pathways that changes the entire game. I'm really telling you probably what you're going to see in 10 and 15 years in oncology, but we're doing that now. That's why I'm saying these drugs are nice, but they're one tool and the combinations are important. Now I'm going to add another thing. There can be combination integrative agents, which we call adjuvant care, which may support these pathways to work even better. Because remember, like I said, it's like you put a block In the road, so this mutation stops, but new roads open up. Well, there are integrative agents that in the literature, in published literature, has assistance in shutting those other escape pathways. So we get to a deeper healing and even a better response for patients. So yes, KRAS is huge. There's already some drugs in that. But when you block these pathways, it opens up others. Like I said, in colon cancer, the more classic example is you give somebody a KRAS inhibitor. Well, it opens up EGFR, just another target, and you need to have combinations that go even deeper than that. That's one tool. Layer. We're talking about going 7, 10 layers deep with immunotherapy. That's the power of precision oncology. That's why we see the results we see in combination therapy, because it's custom built for each patient. Each patient is different. And so we go deeper. The mapping is so important. I say, look at the DNA mutation. So when you're talking to your doctor, this is what you want to know. If your doctor isn't running DNA mutations by now, you just need to find a new one, because I've been talking about this for, you know, almost 2 decades. DNA mutations has been around, and finally they're starting to run them because there's drugs to treat them. But it's still Playing the one drug, one target game. What we need to do now is also run RNA transcriptomics, which I don't know anybody else that's doing that. Thousands of markers. Remember, this drug improves the tumor microenvironment so T cells can better, meaning your natural killer cells can better infiltrate the tumor. Nice. But why not making sure that that immune system is built and targeted to your tumor so that when the infiltration opens up, meaning the soldiers can attack the tumor, they're going to do it in big numbers with power and authority? Well, that changes the game from. Little bit of remission to longer-term remission. Dare I say the goal of long-term remission? And this is important because this is just one aspect of cancer signaling. Drugs have these ability to slow things down and buy us time. You'll you'll see this with breast cancer. This is a good conversation to have here. Like a Herceptin, it slows it down, but then years later, it finds an escape route. It doesn't cure; it buys us time. What are we doing with that time? That's what I want you to grab in this conversation. Are we building the immune system? Are we targeting the other causes of cancer? Do we see all the other roadmaps? And can we build an N of one, which is custom treatment for each individual based on their mapping. So this is when you hear me talk about everybody has different maps with the same types and stages of cancer. They have totally different maps. And so this KRAS and RAS mutation is great, new drug, very exciting, but it's one important aspect. And we want to take that 7-month or 13-month, we want to take that to multiple years. How do we do that? By deeper combinations. This is why I'm saying oncology is changing. Now marry that to deep learning, which is what we're doing in our tools. And now we have, you know, what I call Star Wars of oncology, the future. And we can do it with less toxicity and greater precision because we know what the patient needs. We're not just shotgunning drugs, hoping they work on, you know, a certain percent of the population. And then those cancers grow back. It's about understanding these pathways. Now I'm going to add another thing. It's not just about treating these mutations. It's understanding that we have to do what's called adaptive monitoring. That means while we're treating the patient, it could be 3, 4, 6, 8 weeks. And these targets change. These dirty, difficult cancers, pancreatic being one of them, can change every 6 to 8 weeks, mutations along these pathways. So if we can use adaptive monitoring, our circulating tumor cells, ct-free DNA, methylation scores, potentially other tools, and those allow us to look at the cancer's evolution. That evolution is very important. Now, let's get back to pancreatic cancer for a second, because that's what Draxinib is prescribed for mainly today. These pancreatic cancers have dense stromal barriers. So think of a tumor that has all this, you know, Collagen fibrosis, cancer-associated fibroblasts all around the tumor. So trying to get chemo in there and not easy, but if we can get directly into the tumor with the right genetic chemo, right immunotherapy, see, the secret here isn't even the interventional radiology, but it's the drug targets. So building those, I don't know anybody else that's doing that, that custom builds those drug targets and then delivering them in an elegant manner where you don't have to have chemo throughout the whole body. You can spot treat the tumor. And now you've got 1 plus 1 equaling 11. You're treating the biology of the patient. Understanding what the causes were, changing the diet and lifestyle components so we can build a treatment that is the true architecture that's appropriate for the individual patient. This is why combinations matter. It's not just direct-to-tumor, or it's not just a new smart drug, or it's not just a, a, you know, targeted care. It's the combination that changes from patient to patient. And this is how, whether you're dealing with colon, breast, you know, prostate, pancreatic, lung, these are the combinations that That really can make a difference. And this continuous monitor, knowing if you're improving or not, and then continuing to hold that with the right architecture is what we're pursuing. That is the goal. And that's when I say I see an end of cancer coming, because as you can see this mapping like we do, and you see where things are going in the next few years, it's so powerful. New drugs, new technologies. But how do you combine these? How do we get beyond just a 13-month or 7-month extension? It's the combinations. I want you to think like 4D chess, not checkers, right? A new drug, new target. I want you to think of the deeper mapping, deeper environment, deeper immunity. What caused your cancer? How do we monitor those changes? And can we change the trajectory of the entire disease? That's exciting. That's the bigger question. Can we really shut this down? Can we pursue deeper mapping instead of a one-size-fits-all protocol, which, you know, can help, but can we go deeper and customize the architecture for the patient? That's next-level care. I don't know anybody else doing that at this level. And that's what I think the key is. So the next question for you is not what the next protocol is going to be. You've heard me say that, but it's What is the right targeting for the individual patient? Now, I hope you found this helpful and this episode helped to kind of give you some information so you can better understand cancer treatment at an entirely different level. I hope this was helpful and may the Lord bless you on your journey to healing.