In this discussion, Dr. Shiva Ayyadurai shares the findings of CytoSolve’s recent results in mapping out the molecular systems architecture of Acute Myeloid Leukemia – a rare by deadly disease. The results were just published in the journal Cancers with co-authors from Stanford University.
The original research in this video is made possible by generous contributions from supporters of the Dr.SHIVA Truth Freedom Health® movement. Please contribute so we may continue to bring you such original research, valuable education, and innovative solutions.
- Dr.SHIVA Ayyadurai, MIT PhD – Inventor of Email, Systems Scientist, engineer, educator – presents a CytoSolve®Open Science Institute Project on the Molecular Systems Architecture of Acute Myeloid Leukemia (AML).
- CytoSolve® has published the complete systems architecture of acute myeloid leukemia (AML).
- AML is a cancer of the cells that would normally develop into different type of blood cells, which starts in the bone marrow and moves into the blood.
- There are 20,050 new cases of AML in the United States every year, rare but deadly with a 50% mortality rate.
- CytoSolve® publication of the molecular systems architecture of AML provides a blueprint for understanding the complex interactions occurring in the AML microenvironment.
- CytoSolve® research enables the identification of targets to treat AML.
- CytoSolve® enables a systems view of AML to understand off-target (adverse) interactions.
- A systems approach leads to a much better drug development paradigm that can minimize side effects and maximize efficacy of treatment.
CytoSolve, systems, cells, aml, cancer cell, science, support, research, shiva, created, stromal cells, literally, immune cells, suppresses, discovered, signaling, cancer, people, molecular architecture, systems approach
Hello, everyone, it’s Dr. Shiva Ayyadurai. It is a little bit after 6pm. On Tuesday, today, we’re going to be doing a science discussion from the CytoSolve® of Open Science Institute project, which many of you know, we have launched recently. And the Open Science Institute project allows everyone in the world to basically use the infrastructure that we’ve created over the almost two decades now, that came out of my PhD work at MIT – an infrastructure, called CytoSolve®
CytoSolve®, which will do a couple of videos, today, you’ll understand what CytoSolve is, you’ll get a practical understanding of how CytoSolve® can actually help. It will support research, you’ll get an understanding of how CytoSolve® can be used to do product development.
But most importantly, we want to invite all of you to start becoming innovators and start recognizing that this infrastructure CytoSolve® that we’ve created, took many, many decades to create is now here for all of you to essentially start asking scientific questions and using this infrastructure to actually start coming up with answers. Supporting it, right? Essentially, being an agent for change. As many of you know, what we do here at VAShiva is not only to provide you with a scientific framework, which we call the Science of Systems, through the Foundations of Systems course.
So, all of you can actually become system scientists. We’ve created a whole course curriculum, which you can go to TruthFreedomHealth.com, and learn about. I’ll come back to that before the end of this. But you can also not only learn how to be critic, critical about understanding how systems work, be your body, beat the world around you, be political systems, you can get very, very adept at doing this.
But more importantly, you yourselves can start using system solutions to help change the world. And if you go to me, go over here. By the way, today’s talk is Molecular Systems Architecture, Acute Myeloid Leukemia. And this is brought to you by CytoSolve®, Open Science Institute project, as you can see right here, and our slogan is science by the people for the people.
So it’s through people’s support and contributions, this research is possible. So if you want to support this, you can go to TruthFreedomHealth.com. And when you support this research, I actually want to support your education.
So please, take someone. Someone just said here, this is a very sad story, someone just said, AML killed my father in a matter of weeks horrible disease. Yeah, it’s a horrible disease. And you’re gonna learn very soon that this is a rare disease, but it’s a very deadly one over 50% death rate.
So we’re going to learn about an article we just published in the leading journal in cancer. And we’re going to talk to you about that. Those of you who want to learn more about the work that we do, our Institute does, VAShiva does, go to VAShiva.com. And at VAShiva.com, you will get an amazing set of tools and opportunities to actually become an agent of change. So please go check it out.
Molecular Systems Architecture
Let me begin by walking you through what we’re going to cover today. As you can see, you’re going to learn this diagram really well. But we’re going to walk you through the systems architecture that CytoSolve® has discovered, we worked actually with Stanford on the Stanford actually came to us and believe it or not many, many universities come to CytoSolve® because we can do the work of probably 20 or 30, PhD or postdocs because of the technology.
But what you’re seeing here is the architecture that we have discovered, by taking a Systems Approach, by bringing together the disparate work that’s been done in science. So you see, here’s, here’s the AML cell over here, which we’re going to talk about: the AML cells survives by three different processes, what’s called cell proliferation.
This is the disease layer through cell survival and inhibition of apoptosis. Apoptosis is a big big word if you want to write it down, which means cell death. So remember, cancer cell doesn’t die. So, it learns how to evade apoptosis. So it survives by inhibition of cell death. And then the third way that the AML cell survives is by suppressing your own immune system.
And these are all the molecular pathways we’ve integrated and put together to understand these processes. And each one of these molecular systems, you notice there’s 1,2,3,4,5,6,7,8- 8 major subsystems, each composed of different molecular pathways, which are taking place in your different cells, what are called your stromal cells, these stromal cells are hijacked in many ways, or what we call the micro environment that is used by the cancer cell to support cell proliferation, cell survival and immunosuppression.
Journey to Systems
Okay, so you can see it’s a very complex system, and the technology CytoSolve®, and our Systems Approach has helped uncover this and the same Systems Approach, we can use to uncover many, many other things, including how your body functions. So before I go, as people are joining, I want to encourage everyone to recognize that I want to encourage all of you to take a Systems Approach to everything you want to do in life.
So if you go to TruthFreedomHealth.com You can learn that I’m going to play a quick video, hopefully to inspire you about why we need to take a Journey to Systems and this is my own personal journey. Here we go.
Alright, so let’s go back to our discussion today we’re going to take a Systems Approach to share with you the recent paper we just published in the January 2022 issue of the acclaimed journal called Cancers. So it took us about, let’s say two years to get the paper published. As you can imagine, when you’re doing this, and you’re not part of the academic establishment, it takes a lot more effort to get papers published.
But we did get it published in one of the leading journals. We’re going to walk you through that – you’re going to learn a lot today, on the Molecular Systems Architecture of Acute Myeloid Leukemia. So, you’re going to before the end of this discussion, is clear to those of you who are listening on our podcast, I’ll try to describe visually, but you’re going to learn how the different cells in your body get hijacked by what’s called the AML cell to basically hijack your own system.
So the AML cell gets to support itself through three major processes, what’s called cell proliferation, where it essentially proliferates itself through cell survival where it survives, by ensuring it never dies. And by suppressing your own immune system, okay, so that’s what we’re going to learn shortly.
But in order to get there, we got to build this up, by the way, this is the journal Cancers. It’s a journal that publishes, you know, scientific articles on what’s going on in the field of cancer. So that’s what the journal does.
Let me go back here. And you will see that this is a paper we just published, you can see the article, it says Molecular Systems Architecture of Interactome, in the Acute Myeloid Leukemia Microenvironment. So key things , let me zoom in, it’s the system’s architecture systems.
Architecture is literally a blueprint of the disease. The interactome is literally all the integrated molecular pathways. And AML is a disease and we’re looking at the microenvironment, what the micro environment means is you’re you have the cancer cell, and you have all this other stuff around it.
And this other stuff, the microenvironment supports the cancer cell. But you can see, I was the lead author, with my colleague, Dr. Deonikar , Kevin McLemore and Dr. Sakamoto, who’s a professor out of Stanford. Okay, so, and we want to thank our colleagues at Stanford University, it was a pleasure working with them.
What You Will Learn
So let’s go right into this. So what are you going to learn? First, you’re going to learn what is AML? You’re gonna learn what is Acute Myeloid Leukemia, you’re going to also learn the systematic bioinformatics methodology that we use to apply the CytoSolve® methodology. We’re going to talk about the interactions of all the different bio molecular pathways in AML.
And then we’re going to look at the interactions between the different cells in AML, in the microenvironment. And then, why this architecture that we discovered is a breakthrough for science, we want to share that so you can share that with your friends.
Before I begin, some of you may already know what is CytoSolve® and some of you may not, but CytoSolve® is literally an architecture – thank you to online call. Someone just donated US $10 to our Open Science Institute. And by the way, the research that we do here is funded by the people for the people we’re not waiting for, you know, the Fauci is of the world to fund us, we go direct, because of CytoSolve®.
But CytoSolve®, as you can see, is a technology framework that helps us model very complex diseases and understand scientific questions. So you can also ask very probing questions, but we’re literally taking, you know, in any field, in this case, we looked at all the papers in AML. We funnel them through a process of figuring out which ones had molecular mechanisms, then we created the Molecular Systems Architecture and then we are in a position now to actually model it.
But today we’re going to talk about the architecture we created. And as some of you may know, I’ve talked about the fact that CytoSolve® really came out of my efforts nearly about 19 years ago, when I started my PhD on this, to understand the way that drug development works is really, really sort of a medieval Stone Age model. They can only work on a single drug compound. They spent about five years in test tubes and killing a lot of animals, which I don’t think is necessary. And then they go do clinical trials.
This takes about 13 years, and only 20% of the stuff ever even comes out of here that makes it through phase one. And this is why pharma companies have been a lot of people don’t know as pharma companies over the last many, many years, they’re not getting new drugs approved, even though they spend more and more money. This is why the jab is so important to them. Pharma needs the jab, you say because the jab was done. So you don’t have to go through testing. And you can’t sue pharma companies.
So the entire pharmaceutical industry saved itself from this process by just going to by shifting the goalposts. But anyway, CytoSolve® is a very powerful technology, which allows us to, in a revolutionary way, do development and discovery of medicine. So here’s a little bit of background on CytoSolve®.
Acute Myeloid Leukemia
Because of all people’s support, over the last many years, we’ve been able to do this research. So we want to thank you. So let’s go right to Acute Myeloid Leukemia. So what is it? First of all quick overview, it’s a cancer of the cells. So you have cells that would normally develop into different types of blood cells, okay. So think about it this way.
There’s a whole research we’ll do a presentation will do on stem cells. So you have a whole bunch of cells that are going to become different types of blood cells. And what happens here is that this cancer starts in the bone marrow because that’s where your red blood cells are produced, and then it moves into the blood.
And there’s 20,050 new cases of AML every year in the United States. And as you can see, 11,540 deaths come from AML. So we want to thank Beth, to support the Open Science Institute. Thanks, Beth Levine. So again, this research was just published in the leading journal – Cancers. But this results in 11,540 deaths from AML in the United States that’s in the US alone. And that count accounts for a rare type of cancer, but it’s deadly. But the total number of people that get this cancer is only about 1%. So 1% of people get this cancer, but guess what? It has a death rate of unfortunately 50% Okay.
So let’s go right into this now, how do you get AML? Okay, so I’m sure everyone’s wondering about this. How does how do people get AML? So there’s a couple of different sets of risk factors. One is its age and sex, it’s prevalent in adult males. Smoking is one of the big things, long term exposure to chemicals, benzene, which is a carcinogen, formaldehyde, chemotherapeutic drugs, so think about as chemotherapy leads to AML. So benzene, formaldehyde, chemotherapeutic drugs, exposure to radiation. Okay, these are the risk factors of AML.
But there’s others family history, exposure to electromagnetic fields, workplace exposure to diesel, gasoline and certain other chemicals and solvents, and exposure to herbicides and pesticides. Okay. Michael says here, that one of my brothers died of leukemia 1979 at 21 years old, sorry to hear about that, Michael.
So these are the different risk factors. Again, let me review that. If you go here, age and sex prevalent in adult males, smoking, long term exposure to chemicals, benzene, formaldehyde, chemotherapeutic drugs, exposure to radiation, sometimes it’s family history, exposure to electromagnetic fields, workplace exposure to diesel gas, gasoline and other solvents.
And obviously, exposure to herbicides and pesticides. So those are all documented. So you don’t have to be a health nut to believe in this. This is what’s been documented that we uncovered.There are a bunch of gene mutations that are paper uncovered that we’ve itemized here.
So there are four types of gene mutations that are observed in AML. And you can see the four columns here, Class I Genes affect what’s called signal transduction, that’s signaling communications between the cells, okay. And as you can see, there are FLT3, KIT, NRAS, KRAS, JAC2 , PTPN11, those are the class one genes, and there’s about six genes there that get affected that the mutations lead to AML.
Class ll Genes
Class ll Genes are involved in the function of differentiation when your cells actually differentiate into different kinds of cells. And you can see RUNX1, CBFα, CEBPα, NPM1, PU1, MLL, and RARα, okay. Again, you don’t need to memorize any of this, but I just want to let you know there’s a whole bunch of other genes that control differentiation of cells and when they go awry, you get mutations observed in AML.
Class lll Genes
Next is Class III Genes, epigenetic regulation, which is fascinating. Remember, I’ve talked about this before epigenetics is based on what you do in the world, what you’re exposed to. There are certain genes which get affected by that. And these are TET2, IDH1, IDH2, DNMT3A, ASXL1, EZH2, Cohesin and NPM1. So these are the genes that affect these epigenetic regulation.
And there are two others, there are a bunch of genes involved in the other genes. Category One is Tumor Suppressor genes, WT1 and TP53, there are genes that your body has, believe it or not, to suppress tumors. And when those genes are mutated, you also are open to getting AML and then Oncogenes PML-RARα, FLT3-ITD, AML-ETO and CBFB-MYH11. So, these are the gene mutations observed in AML. So, this is from the genetic standpoint. Okay.
And again, to those of you joining us, we are sharing with everyone the results of our breakthrough research that was just published in the Leading Journal Cancers. And this is part of the CytoSolve® Open Science Project. This is science by the people, for the people, we didn’t take money from the government for this, we didn’t take money from universities, this research was supported by you, high end, world class research brought to you for the people, by the people, okay, and those of you who want to support it, go to TruthFreedomHealth.com and support the efforts.
So now, how did we, what was the process, we did identify these genes and the research, I’m going to walk you through what we use the CytoSolve®, bioinformatics process, let me walk you through that. And some of you are commenting on mV25™. So the technology that we used, that we use as the infrastructure for the Open Science Project allows us to look at all the little pieces of knowledge that are out there, organize it, extract out the molecular pathways and figure things out.
You see, the problem in academic research is people work in their little cubby holes. And they don’t want to work together because everyone wants to win the Nobel Prize. So they don’t want to work together because they don’t want to hide their research or get their government grants.
The approach that we take is where we collaborate, we’ve created what we call a Collaboratory. We can bring this research together, some of you may know in a very practical way. Several years ago, we used CytoSolve®, to actually discover a very powerful combination of ingredients to lower inflammation, and pain. And we had been helping many, many companies for many years doing research.
But mV25™ was a product that came out of that. And if you want to know more about it, you can go to our shop, and I’ll talk to you about this. But let me just play a quick video here. That’ll let you understand that beyond just doing research. And again, I want all of you to start brainstorming. Because with this infrastructure, we can take a complex disease and mathematically model it like we’re doing like we just did with AML. Look at all different ingredients out there. And without killing animals – it figures out what works. And this will give you an idea of practically what we can do.
And here’s mV25™, a product that we created. Using this technology millions of people suffer every day from painful discomfort and swelling. But most pain medications come with harsh side effects, and many alternative supplements have little scientific backing.
Alright, so you guys, if you want to know more about mV25™, just go to VAShiva.com. A couple of people are texting me just go there. And you can find it there. And you’ll understand that, as I mentioned our entire things, we’ve optimized this by executing trillions of molecular pathway reactions. And one of our promises is that as the science improves, we’re gonna keep reformulating this. It’s Certified Clean – Made in USA.
Systematic Bioinformatics Literature Review
Let’s talk about how we did this analysis on AML. We literally did what’s called a bioinformatics review. This is what CytoSolve® allows us to do, where we create a list of the medical subheadings, keywords, and optimize the recall of the literature. And then we search. And we retrieved all the relevant peer reviewed articles out there published between January 1980, to June of 21. So that’s over nearly what, 41 years. So we looked at every paper that’s out there. And then we screened the titles in the abstract. And then we performed a full length review of the final set using domain experts.
If you look at this, these are some of the keywords that we use, right? Human acute amyloid, right human acute. So there’s nearly 12 Different subject headings, but these are all the possible sort of from an AI standpoint, that typical keywords that could be out there for acute myeloid leukemia, and then you can see, we identified out of all of those 1000s of literature 602 that were relevant, we remove duplicates, and then we found eligible 529 of those articles when we excluded 276. Out of these, the studies included anything having to do with you know, the subsystems of AML.
Molecular Systems Architecture
Let’s look at the molecular systems architecture here, what we discovered, what we discovered here that you can see, and to those of you listening on podcast, I will, I’ll try to explain this there really, four types of cells in the AML micro environment. What do I mean by micro environment?
Think about here’s a cancer cell, let’s say it’s in the center, and it’s surrounded by a bunch of other cells, okay, and structures, that’s called the micro environment. So remember, the cancer cell doesn’t exist on its own. It can’t survive on its own, it needs Its microenvironment. Now, in the case of AML, there are four cells that it recruits or hijacks to support itself.
One of them is called immune cells. Okay. And I’ve talked about some of those, but these are the cells that support your immune system. The second is stromal cells, and we’ll walk you through those. So, if you look at the immune cells, by the way, you have dendritic cells, these are in the bone marrow, you have TH-1 cells TH-17, NK natural killer cells, TFF cells and T reg cells.
So 1,2,3,4,5,6. 6 Different kinds of immune cells are involved, then you have stromal cells, what are stromal cells? Well, those are the cells that are involved in the stroma, okay, fibroblasts, MSC, blood vessels, endothelial, and what’s called the BMSC cells here, okay. So these are the immune cells over here. These are the stromal cells, fibroblasts, MSCs, blood vessels, BMCs, endothelial cells, these are the cells that line your blood vessels, like your arteries.
So there’s four different kinds of cells here, then you have the cancer cells, okay. Which are, this is actually the AML cell itself, and the MDSC cells up here, okay, as well as Quiescent HSC cells. So 1,2,3 different types of cancer cells. And then you have the bone cells down here, the osteoclast and the osteoblasts. Osteo is in reference to bone, okay, so you got four different cell types. And that’s what I want you to think about stuff in the marrow, immune cells, cancer cells and stromal cells. So it’s literally, it’s a community. It’s a system of a bunch of cells that work together, that the AML cell right here is using to protect itself.
So what is the AML cell do? You can see what this little red arrow – it suppresses the immune system. That’s one way it works. Next thing is it. It uses the stromal cells for cell proliferation and to stop itself from dying. And then it also evades – it evades immune system you using MDSC’s. Okay. And that’s how this all works, okay.
Now, what we discovered here, is, after many, many years using CytoSolve®. This is one of the heart of the papers we literally discovered. And you don’t need to, again, learn this. We’re going to walk you through this, this is what’s called the Molecular Systems Architecture.
So imagine that, you know, you’re building a home, you’re building a home, you have all the different rooms, you create the blueprints, how the wiring is going to be, how the electricity is going to run, how the plumbing is going to run. That’s the architecture of your home.
Well think about what we’re trying to do, we are showing up as scientists after the fact. And we are looking at different pieces in a – what we do from a Systems Approach at CytoSolve® was we’re finding all those pieces. And it’s almost like we’re reverse engineering how nature did this. And this is what we found. So we put all those pieces together with all this painstaking work. This is what we’ve published that we have figured out the molecular systems architecture of all the pieces, as we know now that are involved in AML.
So think about how valuable this is, knowing the molecular systems architecture of AML, produced by the CytoSolve®, Open Science Institute project, we’re now able to take this architecture, and then we can now use it to figure out okay, if I take this medicine, what will I do? If I take this medicine – without having to kill animals, but we get the blueprint, the map, okay, without this map, this is the way science is working, right? They try this. And then they try that. And they try this. And they take a lot of government funding to just sort of shoot in the dark.
But now we have a map. And what we’ve done is we have published this map, we didn’t keep it secret or just to ours, to ourselves, we published it. So we can allow other researchers to use this map to accelerate scientific discovery. This is what the CytoSolve® Open Science Institute project is all about.
We are going to, you know, directly allow everyone out there to support us. And then we go do science versus a government taking your tax dollars. Then it goes to some NIH NSF and they support their buddies in academia. And it takes 10-20 years and there’s really no incentive for them to solve anything. Because many of those people are like this with Big Pharma, where there’s really not an intention to even try, let’s say combinations of natural products. But with CytoSolve® with the map that we’ve just discovered, it helps us do this.
I’m going to walk you now, through this map, step by step. Okay. Someone said, Without torturing animals, yes. That’s one of our goals. So let’s walk through this okay. What is this? So, what you see here is in the center here, this purple is the cancer cell around it, all of these other cells are the micro environment.
So anything in white are the immune cells, okay, that are involved in the microenvironment, okay, By in large, okay. And some of them like the TH-17, NK, N-17. Okay, the fibroblasts and the adipocytes are part of the stromal cells, okay, but by in large, most of the white ones are the immune cells.
So let’s walk through this, I’m going to walk you through pieces. So here is the cancer cell. Here’s the endothelial cell here, fibroblasts, here’s an immune cell. So everything in here is the immune system right here. This is a bone cell, this is fat over here, over here is your bone marrow and stromal cells. These are MDSC’s. Okay. And we’ll come back to those but those are the major cells that are involved here. Okay.
Now, let’s go to one of the subsystems. So what we’re going to do is we’re going to look at the interactions of some of these cells in a little more microscopic way. So now we’re going to look at three types of cells as stromal cells, the cancer cells in the bone cells, again, here is a cancer cell. The bone cells are over here, and the stromal cells there’s a class of cells there, the mesenchymal, the bone marrow, and the endothelial. Okay. Now, what’s interesting is these signaling promotes metastasis, which is cancer by increased cell survival and proliferation and increased vascularization.
What do I mean by that? Think about a cancer cell invades your body, and it literally lays down its own blood supply. That’s called vascularization. So what we’re showing here, and hopefully, everyone can track this, which I’m trying to do here – to help everyone understand this and you can explain it to others. Angiogenesis, a big word down in this lower left corner means and you can if you want to write this down, angiogenesis is a term used to mean when a cancer cell literally lays down highways within your body so it can sustain itself through getting blood to the cancer cell.
That’s called vascularization. But angiogenesis, a process in which our cancer cell invades your body to support itself by basically hijacking your body’s blood supply. Okay, so that’s angiogenesis. And what you can see here is that the endothelial cell supports angiogenesis. And all of these cells supports cell survival and proliferation of the cancer cell, which is in the middle. So, this cancer cell uses your other cells to support angiogenesis, which has increased vascularization as well as to proliferate itself.
Okay, so that’s one of the discoveries that came out of our work. The next thing is, and by the way, that’s done through this process called CXCR-4/CXCL12 signaling. This signaling process, you can see right here, the stromal cells and your bone cells use CXCL12 signaling, to have the cancer cell through a series of processes support a cell proliferation, and survival, okay. And once this occurs, this H1F1 signaling, through this process enables the endothelial cells to do angiogenesis.
And you can also see through this process, if you follow this line through CXCL12 signaling, it supports the bone marrow. So all these things are interconnected. This is why we need to take a Systems Approach, because you can see how one thing affects another. They’re all intimately connected. But the major takeaway is that there’s one type of signaling that the cancer cell is able to lay down its pipeline. Okay.
The next thing that you’re seeing here is TGF-β signaling. If you go just go on Google and search for TGF-β, you’ll see that this cytokine, a signaling molecule, has a lot of deleterious effects. So let me go over here. And you can see here, and there’s two types of cells involved here. The stromal cells, the bone, and the endothelial again, these are endothelial cells are the things that layer your arteries.
For example, bone marrow cells are obviously in your bone marrow. And again, here, these cells work through TGF-β signaling. So here’s TGF-β. It comes in here and here, and through the TGF-β signaling, it then goes up here and supports endothelial but TGF-β signals, again, to support angiogenesis, as well as cell survival and proliferation.
The other aspect here is the cells that are involved in your bone, your cancer cells and the immune cells. Again, here’s a bone cell. It works with your bone cells right here, and through this other signaling RANKL R,A,N,K,L to suppress your immune system through your NK cells. And then it also works directly to support cell survival and proliferation of the cancer cells. Okay? Now, this is very interesting, if you think about fat, okay.
If you think about fat, what you’re seeing is a fat cell. And this is what I want you to think about here. Here’s a cancer cell here. And the fat cells produce something called FFA, free fatty acids, and they are literally fueling the cancer cell. So the big takeaway here is, here’s a fat cell. Here’s a cancer cell, the adipocytes, which are a type of stromal cell fuel your cancer cell, and this interaction promotes cancer cell survival, hijacking the adipose tissue, to provide free fatty acid.
So, here’s your cancer cell. It hijacks your fat cells, and the fat cells create FFA, which fuels the cancer cell. So this is this very nice vicious process that the cancer cell is using for its own survival. Okay, so it literally hijacks key takeaway is cancer hijacks your fat cells to produce free chain fatty acids.
Alright, Okay ,there we go. Let’s go to another example here. And look what happens here. Then, again, stromal cells, cancer cells and immune cells are involved. And this is how cancer cells actually suppress your own immune system. So, cancer works by its own survival. Remember, if your immune system works solidly, you prevent cancer, that’s a big takeaway, but what cancer does, it suppresses your immune system.
Well, how is it doing that? So let’s go over here and look at this process. So here is the MDSC’s which are part of the cancer cells, okay. MDSCs. Here are your different immune system cells, T cells, monocytes, natural killer cells – called NK cells. And Teff cells.
The red lines mean suppression. If you follow this red line back, for example, the Teff cells, they’re being inhibited right here by the IDO production within the cancer cell. So IDO production suppresses the Teff cells, IDO productions suppresses your natural killer cells. IDO production suppresses through this process of ROS, which is a reactive oxygen species, the T cells. And what’s happening here is the IDO cells proliferate the M2 cells through arginase.
Okay, so they’re suppressing that, coming over from your myoblast, you have two cancer cells involved, the MDSC’s, on the myoblast, the myoblast, through arginase, suppress your monocytes. And then also your T cells are getting down regulated from the arginase here, from the IDO here, and from the ROS here, so your T cells get destroyed pretty big. Remember, the T cells, as we’ve talked about in other lectures, are very, very important to your immune system. Remember, when people get ”AIDS”, it’s a suppression of the T cells. So if your immune system is weak, you’re going to get “AIDS” okay, which is when your T cell counts drop to a very, very low amount.
So again, you’re seeing ,to those of you joining us, we have literally mapped out the molecular pathways of AML.
This is a breakthrough paper we just recently published from the CytoSolve® Open Science Institute. The next thing I want to show here is IFN-α. In many of the lectures I’ve shared with you for the last two to three years, I’ve talked about the immune system, I’ve shared with you a very important chemical or a cytokine, called interferon alpha. Interferon alpha is extremely important to support your immune system, okay.
And what you’re going to see here is that when you have interferon alpha, you can actually suppress the survival of the cancer cells. So that’s one of the findings we came up with. So here is what you see the cancer cell right here. Okay, here are the natural killer cells in the dendritic cells and the T cells, part of your immune system, these three boxes here. And what you’re seeing here is that IFN-α, when you have proper amounts of these guess what it does, it activates your NK cell in the NK cell, following this red line, stops the cell survival and proliferation of the cancer cell.
Similarly, if you look at the IFN-α, and you follow this wiring diagram, it activates the T cell, which then stops the cell survival and proliferation of the cancer cell. Similarly, if you have IFN-α here, it activates the dendritic cells, which stops cell survival and proliferation. More importantly, IFN-α literally works through the IFN-α receptor, right in the cancer cell, it results in fast cell signaling, which also stops the cell survival and proliferation.
I’ve talked about before there are certain nutrients like glutathione, right, food is very, very important proper food to support your interferon alpha system. So one key takeaway from this research is that interferon alpha is very powerful in suppressing the survival and proliferation of cancer cells, alright, interferon alpha, then I want to talk about the fact that the myoblast uses it, it actually can promote the cancer cell survival by a couple of other mechanisms that uses the ability to knock out your dendritic cells growth. The and this leads to the ,and by the way, this leads to knocking this out, which leads to IDO’s formation production, which suppresses your T cells and your monocytes see how this cascade happens.
Cancer Cell screws up your dendritic cells, your dendritic cells Go and screw up your T cells in your monocytes and these then knockout your Teff cells. And then the unfortunate reality is that these also knock out your Treg cells, which and when you knock this out, so basically your entire immune system, all these white 1,2,3,4,5,6 cells are involved in your immune system. And this cancer cell attacks all five subsystems. And it also keeps proliferating. So think about what it’s doing. It is lowering your immune system, and it’s expanding itself. And that’s what this shows.
And then the last piece here is how another way that the myoblast creates PD-L1, which literally stops tumor suppression in your own immune cells. And it produces Galactin 9, which kills one of your own immune cells. So the myoblast, this is a cancer cell in purple, attacks your own cells, so you’re your own immune cells right here.
So your own immune cells don’t even stop cancer anymore tumor formation, and it also knocks out your TH1 cells right here, and they kill themselves, which means they lead to apoptosis. Again, a big word apoptosis means cell death. So the cancer cell basically makes your own immune cell commit suicide. And that’s how you get immune suppression.
So going back to what I talked about, you can rewatch this video. So we’ve shown you all the different subsystems that we’ve discovered from taking a Systems Approach. And now we’re going to put it all together. So what we find we put it all together, here’s the system’s architecture, here are the fibroblasts.
And if you look at this a fibroblast is involved in collagen synthesis and TGF-β signaling. And when this gets affected, you get cell proliferation. The MSC cells are involved in CXCR12, and IL-8 signaling, and that affects cell proliferation. Well, the cell survival, okay. And the endothelial cells affect these three subsystems, which affect the proliferation of the cancer cell, as well as the ability for the cancer cell to survive.
The BMSC’s here affect CXCR12 signaling, as well as the adipocytes signaling here. And these all contribute to against cell proliferation, and cell survival, the cancer cell. And again, you can see the bone cells here, they’re supporting both these systems on left side as well as immunosuppression. And then you have the MDSCs, and your immune cells, which are getting hijacked which suppresses the immune system. The key takeaways, the bottom layer here is the anatomy of all the different cells that are getting involved in AML. This is why it’s such a deadly disease, because it’s affecting all the cells. So even though 1% of people get it, unfortunately, when people get it 50% survival rate only.
16 molecular systems are involved. All of these. And these molecular systems affect three different disease progression mechanisms. So this is what we call an architecture. Okay, so I hope that’s clear. We’ve identified all the different cells, we have identified all the molecular systems, and how these 16 Molecular Systems affect three different disease mechanisms.
And what you’re seeing here is that when you suppress the immune system, when you stop the cancer cell from dying, and then you support cell proliferation, it’s a great environment for cancer to come around. So the key takeaways, the significance of this research is that what we have created here is a blueprint for understanding the complex interactions occurring in the AML micro environment, right, all those other cells, this now enables us to identify targets.
Okay, why is this important? So those of you who want to support this research, now that we have the map, we could actually start looking at all the different compounds in nature, let’s say, imagine itemizing all those compounds. And we could say, oh, this compound may go here. Like we’re literally finding out all this molecular pathways like all the different doors, we can find out oh, well, this key go here into this lock. Will this key go here? And that’s what CytoSolve® can do. Now. This is what’s so significant with this map, we can start testing all different ingredients in nature. Okay, that’s called target identification.
Pharma companies will give you billions of dollars if you identify a target, okay? And they don’t and the NIH always keeps us contained. But with our Open Science Institute, think about what we can do now. We’re going to start mapping out all the ingredients just like we did with mV25™ and start testing them on the computer. We can do this faster and cheaper and better.
We’ve taken a systems view of AML to understand off-target and also adverse interactions, right? So we can now use a saying, Okay, if you give this drug, what will be the side effects long before we spent all that money and time in test tubes and killing animals, we can do it using this map that CytoSolve® has discovered, okay. And it’s a much better development paradigm that can have minimum, minimize side effects and maximize efficacy.
Open Science Institute Project
So think about the revolution that all of you can be part of, we’ve mapped this pathway out. And by the way, all of this was done through your support for maybe hundreds of 1000s of dollars. If that Stanford and all these other major institutions, they taken billions of dollars in NIH funding, billions.
But we did this at a fraction of the cost. This is why you know, I have the ticker running before, it’s time that everyone recognize that you can start supporting CytoSolve® Open Science Project, if you go to VAShiva.com, scroll down, you’ll see the CytoSolve® Open Science Institute, go support research, and you can even come to me at VASHIVA, VAShiva.com and say, hey, look, I would like you guys should do research on this, I’m willing to go do crowdfunding to support it, and we’ll go do it. But we can do this at a fraction of the cost.
Okay. So that’s the other piece. The final thing is, this has been published. So this is what we’re proud of, because typically, you have a lot of Grifters on the internet, talking all sorts of stuff, right? But they can’t really do anything, you know, and get it actually do the research and get it published. What’s important here is we’ve actually gotten it published, it took us quite a bit of time.
But this is now published in one of the leading journals in Cancers. And we got Stanford even as a part of this, okay, so we’ve really, if you believe in the establishment, scientific institutions, even they have put their seal of approval on our research. So that’s what’s so powerful about this. It’s not some fringe research, but we’ve literally mapped out all the molecular pathways of AML. And it’s ready.
So what I want to ask all of you to do is support the Open Science Institute. And let me give a couple of ways you guys can do that. If you go to VAShiva.com. I want to share our websites. If you go to the website here, and you scroll down, you can see that we have a video on the journey to the systems to help. But we have launched this Open Science Institute, you can literally go here, you can contribute whatever you want, you can contribute overall to the institute, you can contribute to a particular area of research, like we just launched this.
So you can say, hey, I want to contribute to leukemia research. And you can literally go here and you can donate $1, you can donate no money, you can just see what we’re doing here. It’s up to you. But we’ve created a way because a lot of people have been saying, Oh Dr. Shiva, we want to donate. So if you click on the contribute button here, you can literally go here. And if you want to give $1 $2 $100, whatever you want to give, you can literally go here and contribute to this.
And what I want to say here is when you contribute to us, I don’t want to take your money for nothing, I actually give you back hundreds of dollars worth of gifts. So we give you back all the gifts here to become a Truth Freedom Health Warrior. So for example, if you contribute 100 or more, you get not only to contribute, but you get to become a member of the Truth Freedom Health Warrior movement. So it’s up to you. But do so if you wish to.
But it’s a way for you to be part of this revolutionary approach to doing science, Science by the People for the People. Okay, let me see if there’s any questions. In silico is greater than in vitro animal testing. Yep. What about asparagus? Someone wants to know if we can test that. But think about what we can do is with this capability now we can literally do – you can be a research director.
You can send us an email say I want you to guys to do this research. I’m willing to go crowdsource and we’ll go do that research. So It’s not waiting for the government to do it. We do direct research using this infrastructure. Most importantly, I want all of you to learn the Science of Systems.
Truth Freedom Health®
We’ve created a whole educational platform, we’ve created a community and we’ve created an activism movement. So before I come back to close, I want all of you to go to TruthFreedomHealth.com , become a Warrior-Scholar, learn the Science of Systems, or just support research or just keep watching videos whatever you want to do. So let me just play the video which will tell you what is the Truth Freedom Health movement is and how you can be part of it and all the different things that you get when you become a part of it.
Alright everyone, I hope that was helpful. And this was one of our science presentations. Tomorrow we’ll be coming back and looking at something in the political world. Again taking a Systems Approach. So please take advantage of the Truth Freedom and Health movement, go to TruthFreedomHealth.com and keep an eye out. Thank you, everyone. Have a good evening.
It’s time we move beyond the Left vs. Right, Republican vs. Democrat. It’s time YOU learn how to apply a systems approach to get the Truth Freedom Health you need and deserve. Become a Truth Freedom Health® Warrior.
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