 Lesson, hopefully less challenging than most, it's fantastic how the skies are white, maybe a little cospite, a number of mutations, a lot of mutations here. But we have studied it, run it in a global data crisis today, and come up with this essentially a whole whole theory that is actually characterizing very much like the emotional species, exactly like the emotional species almost, except that it doesn't make it all the way to the top, like the ice species that love you a lot in some way, which is most creative. And we know how much of people are in this responsibility. With cancer, we don't know how, we can actually master it. It has caused us all, and it will ruin most of the world. So this is going to be about one thing. Now, briefly, though all of you are in this, the cancers contain individual, clone characters, much like normal emotional species. Not normally carried by these mutations, which you can see here, such as the indefinite carry part, they are also known as indefinite. The carrying parts of the cancer differ from normal cells, diploid cells, in cancer specific, are known, as we call it, to normal cells. Or a diploid is the technical term between the brain and the liver region, not the right flow, not the right flow, it is the number of chromosomes, so on. And here are two examples. On the left is the parallel of evolution, that's the human-matter-span state chromosomes, and here is the behavioral chromosomes, and on the right is the organic, the color code, these chromosomes, it makes it much easier to decide if you have a cancer, so it's better for chromosomes. Objects, on the microscope slide, they have hyperbalancers, how does it work? Both, and they all assume these artificial colors. So this is chromosome 123, all the way to 22 years, X, Y, Y. So that's the normal brain, 26 chromosomes. There's one particular cancer cell, a purified of coral cancer cell, so like, it's a cell with 5 cells, as long as 5 cells are. And you can see the numbers of the cells that they change. And here's the algorithm of so-called creeps, so we're marking them, so they are 5, these are from the helipads, this is the height of the 6, this is the height of the 17, this is the height of the 2, there's 2 colors that are certainly different in terms of everything, and filled with like this one, that is the overall amount of cancer cells. When that happens to us, normally, men who say it's not a bad thing, if you argue it would be more of a mistake of these changes. Only in a cancer cell, I want more of a different approach to it. There are no more examples, that is for breast cancer, not a good one, as you can see, there are lots of market forms of cancer cells, breast cancer cells. And as everybody says, cancer is in vitro, you are more of a caretaker, you get it by speech, and here's the caretaker of a muscle cancer, it's simple, others that are higher in the world. So in contrast to the caretaker types of normal speech, as you can already see from these patterns, the caretaker types and phenotypes of cancers are flexible. I don't like to use the word constable, because constable means they don't fall apart, but they oscillate in a narrow range, like in ways, like in physics. And they are flexible in these limits, and that's able to evolve ever more and they can have phenotypes spontaneously, because it's the only property of cancer, it starts fed by everything that's worse, because it's so flexible, because it's made fast, don't be like a tool, now we need a solution, we have to wait for it to settle, and we need it here. This explains the only ability of cancers to go, to make the world, it's paying dollars to use to call it, which is also termed as cancer protection. Stardust is a management cancer, it's more of a process that's dying, and I'm thinking, as insoluble as you have in flexibility, the caretaker types of cancers are critical also, and the treatments and so on, and we have procedures. Now this is a different way of looking at the instability, it's sort of a thing that is in excel, the students might have figured it out, you can lie up, I'll introduce the metaphases or the chromosomes for 20 cents, in the x-axis, they call it the caretaker, the x-axis here, are the chromosomes numbers, so here's one, two, three, four, five, and six. In this, you can see already, it's made in the normal way, we have two, here's a y-axis, and there's also a coconut here, it's the two, because it's diploid, and in man, there's one more way, it's half a way, but we feel like more of a summary of the x-y chromosomes, the two of those here, or others, I don't know. And so these are the images, or essentially the preserves that claim to be lying up, next to each other, and you could see, we are mentioning that they're completely healthy even though their caretaker types are identical, as they say. It's the same instrument, it's the same guy, and it cancels it, this one is breast-canceled, another breast-cancel line. You can see now, there is a completely different caretaker out in Africa, there is no longer those parallel lines of the normal cell, they go up and down, there are new caretaker types, we see the coconut here, or the jaw, there are three, there is no start to one, here is after four, here is after five, and you can see the lines are not on the combing arrow, but they oscillate along this path, and this family is actually in the heart, we see, it's a stability within the instability, there is a characteristic of the neck, if even if you have a breast-cancel, 60 generations, in other countries, when I go, and I say, you can go more or less the same, unless you put on some some sort of pressure, a pressure, a pressure, then you change the caretaker, which has a cell, you know, non-self-care, when you have a cancer, it's the cancer that becomes persistent, you let it go. So, as the service is in flexibility, the caretaker's cancer, and the service tumors are, and it continues, and it is therefore still remaining, and it has been remaining, for nearly 100 years now, it has been really close to just becoming so many, and it's also a cancer, such as cancer, it's a maturity, it's a geneticist, it's favored, you know, there's mutations, it's still remaining, because of the flexibility, but, rather specifically, the caretaker has shown you, or whether stable, and specific mutations are causes of cancer, that we are not seeing, for the normal genes now, they would, as a consequence of the cancer, cause cancer, and also, it's taken as a caretaker. So, the caretaker, it's taken as a caretaker, it's randomized, it feels like the patient, although, you can hardly find it in modern textbooks anymore, you don't see a caretaker anymore, everything is expressed in genes, or genes, the caretaker is considered, something particular on days, or people of the last year, they say, it's true life is broken, working in real life, but, for the caretaker, it's very, so, cancer research, you've got a gene, or a cell, it's a piece, and it shows, right now, the cells, the response, to the caretaker, to the surgeon, whether they were alive, that's the best, that's the most difficult, we take down, that's what they say, and, I don't know, how they seem, but they do see it right. So, this is the, the question that has, has not been said that, in 100 years, what we did, is that, all the cells, there's a mutation, because of cancer, and we are solving it, by now, makes it 50 years old, that's what we do. Well, I don't know, so, so the mutations, CLA holds, that, a set of six, three, six mutations, or specific genes, that are, kind of, oncogenes, as a result of these mutations, meaning that the cells, transformed all the cells, to cancer cells, independent of care, it's all there. They recognize, by seeing, yes, a lot of variation, by disease, it's a consequence, so, I see that, things across the cell, it's transformed. Popular components, or the mutations here, we, all of them have, our friends, we, current friends, there's some, like, visual, balance, so, all of them. And, they have these versions, so, the mutations. No correct function, for the mutations here, despite, stirring in, of this version, and decided that, despite, gene technology, that is, models, you know, put, any gene in the cell, if you want, if you want, and they have done that, these oncogenes, put it into normal cells, also, as you can see, the results are, best of details, if not, there's so many more, and more. What happens, when you take, a, conflict, a convenient, or whatever you call it, consensus, number of opportunities, that is, certainly, sufficient for cancer, one of them, published in Nature, this is, you know, one here, and by all of this, it's the same thing, it takes three, four, put it into normal cells, and then, you see, three or four minutes, after seven months, there is a true message coming, as it goes. What they don't tell you is, if you put millions of cells, into this culture, that all have the same oncogenes, that are not transformed, out of which, all the months, comes from age, age, flow, or transformed cells. So, what that means is, when you get, for, for transfectiness, that's called, millions of cells, these oncogenes, they're also called, because of the passive, you get, putting one, two, five to transform, that means, these genes are not sufficient, to do the job, something else is required. And there is more, let's hope, to be acknowledged. So, they're not sufficient, for two inches, and the answer, of the mainstream is, we need another gene, yet, that we aren't found. But, they have never found a company, to say, yet, although, the Nobel Prize, was given to us, so, that we catch up, soon, to justify, what happens, for the next week. So, the oncogenes that, induce transformation, another, the sound of these experiments, in one of the ten to the five cells, are not necessary, to maintain, the transformed field. They do their job, actually, because, tools and leukemias, induced by oncogenes, persist, even if the oncogenes are lost, or turned off experimentally, with, with experimentally, to control the promoters, this, hand-on, head-off, the, the cyclic, the promoters in the U.S., the last cyclic, of the gene cells, or sharon, once, the tumor is established, in a couple of weeks, it is no longer dependent, on the oncogenes. The oncogenes, in other words, is not, maintaining, the transformed field of life, and it's not sufficient to issue. And all cells, that have been studied, for diuretiles, and that's only very few, have done that, as you can imagine, one, who did, and, who have found to be, another, and that is not mentioned, in Asia, when there was a problem, with the, the, the virus, I even said, with diuretiles, isn't that, the information, is, there's no, we don't need that, it's enough, we're not taking the six mutations, that they have, seven chromosomes, we said, that's the six mutations, that come, that are, we're not allowing, not taking 20,000 genes, it's not right, that we want, we're not having, we're not taking, so, they're not taking, the spread, so, what is not the role of mutations, of the genes, in cats? The conclusions, from these three types of, experiments are, of the genes, are not sufficient, and are not necessary, to maintain, the cancer cells, so, what is the role, of the, that is, what is not, how is it, 5,000, 10,000 child, the caret, you see, here's the theory, that we see, how it works, for the doctor, the cancer is, the, generating the gene, in, in efforts to explain this, we have recently proposed the two-step, carrier-driven, cancer theory, that's, once you have seen that, then it's almost, I'm almost done. The, the first step, in this, positive, customer genesis, is that, the synergents, and also, the opportunities, which function by synergents, destabilize the caret, by inducing, random and employee, some of them might also, induce with patients, but as, say, the, initial point for cancer is, that they, stabilize the caret, and then, you see, then it explains, in the same form, about half of all known, synergents, that are not clinicians, are the specialists, that's, what we're describing, what we're saying. So, once you have an annuloid cell, the employee destabilizes, the caret, automatically, automatically, by unbalancing, the use of proteins, that segregate, and synthesize, in the caret, the concept. Imagine, you had, with most parents, because the physical complex analysis, is a spin analysis itself, segregating, 46 chromosomes, eventually, any adults, if it hasn't, and their points, 99% of cancer, actively, if there's a slight imbalance, if there's a little bit more, of 2 million, instead, probably, you know, at the end, of my thing, or something, then, it's out of bounds, and it's like, you have a long, long, long, short, you start living, and you become healthy, and you have, the annuloid cell, constantly, changes itself, you know, because of these, many, physical analysis, is a spin analysis, which is, very, very sensitive, to change, or even, yes, as I said, for example, they've made tricks in DNA, if you have a big translation, there's a name, there's a, DNA is, for whatever reason, the light is, it makes, if you change that balance, a little bit, it's, it's, you're hypnotizing the DNA, or stop spinning it, if there are the right balance, if they're not going to give, that's, their balance has been changed, by the balance of genes, because of, that has been balanced, for three billion years of life, now, if you change that, if you change thousands of genes, thousands of genes, thousands of genes, in most cases, in fact, they have to go inside that, it has to find it, it can lift it, it can retain it, so on and so forth. So, the employee, it stabilizes, the parent, I want that to be changed, it does, keeps changing, the parent, it does, it machines, it maintains, it carries to the conclusions, they constantly, they go to change, because they have, they have stability. Most of these newly-evolving kind of types, are again, random employees, that are functionally inferior to normal sets, or at least, they don't. Occasionally, I look, like, play over there, and play down, the real cancer-causing, kind of, type of loss. It's a long way from the will, of how much species has to buy now, and just run it up with the plane, or flying, or to go. That's not it yet, but it's good enough to be in a problem's path, that it has continued to this life, for which it just goes. These kinds of causes, carry back, then stabilize, by the inherent instability, against the inherent instability of unfolding, by selection to a transformative function. So they keep, as you can see, on this plane, that's a short period, they keep fluctuating, also they can't, clone the value, but as soon as they go, too far outside of it, they will not be capable of, because they may take, not be able to take, as fast as they can be lost. And that's a typical phenotype, it passes in all of them, the one who knows where they are, the one they cause this, you get, it's a death sentence, that that makes you have to be killed. Suicide. So this plane, you can see, with the postulates, the drone, yet flexibly carried out, are the chinos, of the chinos, of the cases, not the cases, but chinos, and we know, that power of the console, of the chinos, very, it makes it, it has itself. It's the kind of type, as a whole, just as the kind of life, as a whole, it makes us, you know, not be a pig, or a dog, or a cat, or a pig, or a pig, it's not a violation. If you take us, as long as you want to, you'll never take a mother, we have to reunite the consoles, or like you, let's say, for us, what we want to make, all of us, we want the SOV, it cannot mutate the console, we have to reunite, set the console, let's say, for consoles, that's what it's about, or whatever it was, it's a variation of stuff. Here's a copy, of the whole system, here's the long, kind of type, this different state of cells. In step one, I'm applying the devices, reduced either part. Casino chip, shall be called, I'm deploying it here, I'm deploying it here, there are times, it's only a few, or sometimes, my previous paper accident, and then, you have, I'm deploying it, and then, you've got to deploy it, you've got to do the job, see, and they, keep changing the cells, but there are two states, there's the console, this one is the most famous, there's the most famous, there'll be copies, because sooner or later, the console is missing, there's the sense to provide you with the set, and it does, and sometimes, and occasionally, it's that size of the neck, it's that width, send it to that region, to come up with the cancer cell, and that would be, the cancer cells, sort of, carry on, but who wants to, you know, do the production, and once this happens, it has a kind of type, it's a kind of continuous, we won't fear it, it was, which made it, in a new way, a pool of carrier types, is the cancer cell, and now, it has a certain degree of, flexibility, depending on the carrier type, and moves on, over many generations, and occasionally, again, it makes it, it makes it, a digital, a revolutionary step, when it's challenged, by chemotherapy, then the pharmacocystic combination comes up, the tickles from the parenter, carrier type, or the pharmacocystic, from the styrofoam, from the cancer, then again, it differs from the, from the carrier type, although, the basic carrier type, is maintained, is adjusted, very much like, we look for, monkey, two, we don't look for, four, we don't look for. So, here's this, one experiment, I was going to mention it, then a, torture, to test the cancer cell, carrier type cell, we are asked, for the activated oncotines, that have been, tested for so long, now, do it, you do it, you do it, you do it, you do it. So, there's this, the initial cancer-specific carrier, types, much like those pieces. Well, we will be asked, whether it is different, tumor-economic cell lines, rising from human cells, transmitted, with the same oncotines, a cell in this experiment, to inspect millions of cells, to get a few, transformed cells. So, it's very low efficiency, we would predict, if it's an, a motion, spontaneous motion, Each of these new ancestors comes out of a homogeneous group of human cells, all transfected. It's the same on machines, but each has their own language. Like, unfortunately, of the original man, it also has a language that is in parts that is conserved in all these languages. Again, it would have, again, like individual species, it would only be the same as the parent, individual, parent also. So the relevance of this for testing mutations here is that if individual two-organic lines from the same parent cells with the same organ genes have individual parent types, phenotypes, it would follow that the organ genes have played only an indirect role in conservation as postulated by our system. It's the kind of object that makes it a cancer cell that the whole machine grows essentially like a casserole. It's like a human brain. And that gives you 30 years before you get the cancer from the machine on a casserole. By contrast, the mutations here, we would predict that two-organic cells would show up on these transfected cells with only carrier types. They don't spell it out, but they don't say it should change in time. And it would have the same phenotypes, because the home machines, the end, are including these phenotypes. So, indeed, we found that the carrier teams here, the police, that we've shown on the last slide now, we found a different two-organic cell that's surprising for human cells to affect it. It's the same set of organ genes. They have individual clonal carrier types, phenotypes. That's essentially my experiment here. So, here you see two cells, but the cell lines, that's just on the microscope. You have to look at it manually before we get more different phenotypes, but you can see these cells are phenotypically more often. They're quite easily the same, yet they're generally by exactly the same amount of genes you can see in the cell, longer than you can see in the cell. So, these phenotypes cannot be so different from the same amount of genes. Here you can see what it is. It's these two carrier types that you have that belong to the two cells. They came from these sort of cells that were transfected. The organ genes, in general, are the ones that you can see. The right one is the one that you showed here. And then, in isolation, they come in columns. The other one is like this. And these are the ones that come in columns. So, here is a similar example of two different products that they generated with the same cell. As it's like in some of our experiments, we've come from the theory that the genomes of cancer cells are flexible. Two carrier types are the same. Thank you for all your attention. Please don't leave the room. We just opened the questions and answers session.