A person’s chromosome set carries not only hereditary characteristics, as written in any textbook, but also karmic debts, which can manifest themselves as hereditary diseases if a person, by the time they are presented for payment, has not managed to change his erroneous perception of reality, thereby paying off another debt. In addition, a person could distort chromosomes not only by errors in his worldview, but also by poor nutrition, lifestyle, being or working in harmful places, etc. All these factors additionally distort a person’s chromosomes, which is easy to see if you periodically undergo studies of the condition chromosomes, for example, on computer diagnostics Oberon. From the same diagnosis it is clear that with healing, the state of a person’s chromosome set improves. Moreover, the restoration of chromosomes, and only partial ones, occurs much later than the restoration of the health of a human organ or system if the person’s healing was carried out without working through the root causes. This means that the first to take the “blow of fate” are the human chromosomes, which then manifests itself at the cellular level, and then in the form of a disease.

So, the accumulated “wealth” of errors is recorded in a person at the level of his chromosomes. Distortions in chromosomes close or distort human superpowers and create illusion of fear, because distort energy and information, cause an illusory perception of oneself, people and the surrounding world.

Large distortions in human chromosomes are the root cause of pride, which arises due to an illusory perception of oneself, starting with 12% distortions. Large distortions of the chromosomal set are usually characteristic of sorcerers and the diverse public who practice magic (because they have little energy), NLP, Reiki, hypnosis, dianetics, cosmoenergetics, “channels”. Such professionals themselves constantly have to use this, because... otherwise, the burden of accumulated karma due to the use of harmful methods of pushing problems into the future can be crushed, and the same can be said about unreasonable patients who agree to use such methods.

The average amount of chromosome distortion in humans is 8%.

Each pair of chromosomes is responsible for its own area of ​​health and life. I will give data on the 5th, 8th, 17th and 22nd, since they contain the main distortions (85% of 100%) for those who will be present at the session on April 19th.

The 5th pair of chromosomes is responsible for childbirth, gender relations, and the transmission of ancestral energies, including karmic retribution for negative ancestral karma (NPK).

The 8th pair is responsible for immunity, cleansing of waste and toxins, the lymphatic system, the defecation and excretion system (including sweat glands), the genitourinary system, kidneys, liver, spleen, small and large intestines.

The 17th pair is responsible for the production of hormones in the body, including endorphins, the thyroid gland, the pituitary gland, and the entire endocrine system.

The 22nd pair is responsible for the musculoskeletal system and movement control (vestibular apparatus, middle ear and poor coordination), the production of lactic acid (fatigue), and the body’s physical endurance.

Let me give you examples:

– Athletes with distortions in the 22nd pair of chromosomes will never be able to achieve significant athletic achievements. More precisely, the magnitude of sporting achievements is inversely proportional to distortions in the 22nd pair of chromosomes.

– A dancer will never become outstanding if she has distortions in the 5th and 22nd pairs of chromosomes.

Distortions in chromosomes are one of the main causes of the appearance of altered cells.

Description

Determination method PCR, sequencing A conclusion from a geneticist is issued!

Material under study Whole blood (with EDTA)

Home visit available

Study of the presence of duplication on chromosome 17 in the region of the PMP22 gene.

Type of inheritance.

Autosomal dominant.

Genes responsible for the development of the disease.

PMP22 (PERIPHERAL MYELIN PROTEIN 22).

The gene is located on chromosome 17 in the 17p11 region. The gene contains 4 exons.

To date, more than 40 loci responsible for hereditary motor-sensory neuropathies have been mapped, and more than twenty genes have been identified, mutations in which lead to the development of the clinical phenotype of NMSN.

Mutations in the PMP22 gene also lead to the development of Dejerine-Sotta disease, Roussy-Lévy disease, inflammatory demyelinating neuropathy, and neuropathy with pressure paralysis.

Definition of disease.

Charcot-Marie-Tooth disease (CMT), or Charcot-Marie neural amyotrophy, also known as hereditary motor-sensory neuropathy (HMSN) is a large group of genetically heterogeneous diseases of the peripheral nerves, characterized by symptoms of progressive polyneuropathy with predominant damage to the muscles of the distal extremities. NMSI are not only the most common hereditary diseases of the peripheral nervous system, but also one of the most common hereditary human diseases.

Pathogenesis and clinical picture.

The occurrence of the disease in most cases is due to overexpression of peripheral myelin protein (PMP22) due to gene duplication, which accounts for 2% to 5% of myelin proteins in peripheral nerves. The appearance of signs of the disease in the presence of point mutations in the PMP22 gene is associated with disruption of the processes of degradation of Schwann cells and their inclusion in compact myelin. The disease occurs in the 1st or 2nd decade of life. In 75% of patients, the first signs are detected before the age of 10, and in the remaining 25% - before the age of 20. The first to be involved in the pathological process are the foot flexors, which is clinically manifested by their hypotrophy and gait disturbance in the form of stepping. As the disease progresses, foot deformities occur in the form of Friedreich's, cavus or equinovarus, and the shins take on the appearance of inverted bottles. Damage to the distal parts of the arms usually occurs after several months or years. The first to be affected are the interosseous muscles of the hands and the hypothenar muscles. As the disease progresses, the hand takes on the appearance of a “clawed paw” or “monkey paw.” In the area of ​​the affected muscles of the arms and legs, disorders of superficial and deep sensitivity are found. In 56% of cases, patients have sensitive cerebellar ataxia and intention tremor of the hands. Tendon reflexes decrease in the initial stage of the disease and quickly fade as the disease progresses. A characteristic symptom of this form of the disease is thickening of the nerve trunks determined by palpation. Most often this symptom can be noted in the ear and ulnar nerves. Involvement of the proximal muscles of the arms and legs in the process is not typical and is observed only in 10% of elderly patients. The course of the disease is slowly progressive, not leading to severe disability. Patients retain the ability to self-care and move independently until the end of their lives. Several patients with clinical manifestations of peripheral neuropathy in combination with mental retardation, dysmorphic facial features and vision pathology have been described, in whom the deletion in the region of the short arm of chromosome 17 was more extensive and could be determined using cytogenetic methods. Currently, this variant of hereditary motor-sensory neuropathies includes Roussy-Levi and Dejerine-Sottas diseases, which until recently were classified as independent nosological forms.

Electroneuromyographic signs of peripheral nerve damage occur long before the appearance of the first clinical symptoms. The presence of these signs can be noted starting from the age of two, and in homozygotes for the mutation (in the presence of four copies of the PMP 22 gene) - from the age of one. The main electromyographic signs are: a sharp decrease in the speed of impulse conduction along the peripheral nerves, which averages 17-20 m/sec and ranges from 5 to 34 m/sec; decrease in the amplitude of the M-response; prolongation of distal latency and F-wave; absence or sharp decrease in the amplitude of sensory potential.

In a biopsy of peripheral nerves, specific onion-like thickenings of the myelin sheath of peripheral nerves are determined, formed by processes of Schwann cells and the basement membrane, alternating with areas of de- and remyelination.

Frequency of occurrence:

For all forms, NMCH varies from 10 to 40:100,000 in different populations.

A list of mutations studied can be provided upon request.

Literature

1. Milovidova T.B., Shchagina O.A., Dadali E.L., Polyakov A.V. , Classification and diagnostic algorithms for various genetic variants of hereditary motor-sensory polyneuropathies // Medical Genetics. 2011, vol. 10. N 4. p. 10-16.
2. Tiburkova T.B., Shchagina, O.A., Dadali E.L., Rudenskaya G.E., Fedotov V.P., Polyakov A.V., Clinical and molecular genetic analysis of hereditary motor-sensory neuropathy 1- type // Materials of the VI Congress of the Russian Society of Medical Genetics, Medical Genetics, supplement to N5, 2010, p. 178.
3. Shchagina O.A., Dadali E.L., Tiburkova T.B., Ivanova E.A., Polyakov A.V., Features of clinical manifestations and algorithms for molecular genetic diagnosis of genetically heterogeneous variants of hereditary motor-sensory polyneuropathies. // Molecular biological technologies in medical practice, "Alfa Vista N", Novosibirsk, 2009 p.183-193.
4. Tiburkova T.B., Shchagina O.A., Dadali E.L., Rudenskaya G.E., Polyakov A.V. , Clinical and molecular genetic analysis of hereditary motor-sensory neuropathy type 1. // Medical genetics, 2009, No. 12, pp. 34-35.
5. Mersiyanova IV, Ismailov SM, Polyakov AV, Dadali EL, Fedotov VP, Nelis E, Lofgren A, Timmerman V, Van Broeckhoven C, Evgrafov OV. (2000) Screening for mutations in the peripheral myelin genes PMP22, MPZ and Cx32 (GJB1) in Russian Charcot-Marie-Tooth neuropathy patients. Hum Mutat. 2000 Apr;15(4):340-347.
6. G.E. Rudenskaya, I.A. Shagina, N.N. Wasserman, I.A. Mersiyanova, E.L. Dadali, A.V. Polyakov. Hereditary motor-sensory neuropathy with X-linked dominant inheritance. Journal of Neuropathology and Psychiatry named after. S.S. Korsakova. - 2001. - No. 10. - P. 8-13.
7. Milovidova T., Schagina O., Dadali E., Fedotov V., Polyakov A., Charcot-Marie-Tooth disease type I in Russia // European Journal of Neurology, vol. 18, supp. 2, p. 656, T206. September 2011.
8. OMIM.

Preparation

No special preparation is required for the study. Required to fill out:

*Filling out the “molecular genetic research questionnaire” is necessary so that the geneticist, based on the results obtained, firstly, has the opportunity to give the patient the most complete conclusion and, secondly, formulate specific individual recommendations for him.

The process of accumulating knowledge means not only the emergence of new connections between neurons, but also the removal of old connections. In the embryonic brain, nerve cells form a much more complex network of connections, many of which break down and disappear as they mature. For example, in newborns, half of the cells in the visual cortex of the brain receive impulses from both eyes at once. Soon after birth, as a result of radical pruning of excess axons, the visual cortex of the cerebral hemispheres is divided into areas that process information only from the left or right eye. Removal of non-essential connections leads to functional specialization of brain regions. In the same way, a sculptor chips away excess parts in a block of marble to release the hidden work of art. In mammalian infants who are blind from birth, specialization of the visual cortex does not occur.

Eliminating unnecessary connections between nerve cells means not only breaking synapses. The cells themselves die. We have heard so many times the sad story that nerve cells die and are never restored. You can lose up to 1 million nerve cells per day. But a mouse with a defective gene ced-9 nerve cells do not die, which does not make her smarter. On the contrary, such a mouse will meet a sad end with a huge but completely undeveloped brain. In embryos in the later months of development and in breastfeeding

These nerve cells die in the brain at an incredible rate. But this is not the result of the disease, but a way of brain development. If cells did not die, we would not be able to think (Hakem R. et al. 1998. Differential requirement for caspase 9 in apoptotic pathways in vivo. Cell 94: 339-352).

Pushed by certain genes to which the gene belongs ced-9, healthy cells of the body commit mass suicide. (Different genes of the family ced cause the death of cells in other organs.) Cell death is carried out in strict accordance with the predetermined plan. Thus, in the microscopic nematode worm, the embryo before birth from the egg consists of 1,090 cells, but then 131 of them die, leaving the adult organism with exactly 959 cells. These cells seem to sacrifice themselves for the sake of the prosperity of the body, like soldiers who, shouting “For the Motherland,” go into a deadly attack, or like worker bees who die, leaving their sting in the body of an uninvited guest. The analogy, by the way, is not so far-fetched. The relationships between the cells of the body really resemble the relationships between bees in a hive. The ancestors of all cells in the body were once free-living single-celled organisms. Their “decision” to organize a cooperative, made once 600 million years ago, was a consequence of the same reasons that forced the ancestors of social insects to unite into families (only this happened much later, about 50 million years ago). Genetically related creatures, in one case at the cellular level, and in the other at the level of organisms, turned out to be much more resistant to the vicissitudes of fate when they distributed functions among themselves, leaving the reproductive function in one case to the sex cells, and in the second to the queen of the family (Ridley M. 1996. The origin of virtue. Viking, London; Raff M. 1998. Cell suicide for beginners. Nature 396:119-122).

The analogy turned out to be so good that it allowed scientists to better understand the nature of many non-infectious somatic diseases. Mutinies often arise among soldiers against the command, and among bees, discipline is maintained not only by instinct, but also by collective vigilance and the expulsion of lazy people from the hive. At the genetic level, the loyalty of worker bees to their queen is maintained by the fact that the queen bee mates with several males at once. The genetic heterogeneity of the offspring does not give the opportunity to manifest genes aimed at breaking up the family and returning to a solitary lifestyle. The problem of rebellion is also acute for the cells of multicellular organisms. Some cells constantly forget about their patriotic duty, which is to provide the reproductive cells with everything they need. Instead, they begin to divide and behave like independent organisms. After all, every cell is a descendant of free-living ancestors. The cessation of division goes against the basic tendency of the development of all living organisms, or rather, their genes, to reproduce themselves. In all tissues of the body, rebellious, randomly dividing cells appear every day. If the body cannot stop them, a cancerous tumor occurs.

But usually the body has the means to suppress the rebellion of cancer cells. Each cell contains a system of genes that guard the body and turn on a self-destruction program at the first signs of uncontrolled cell division. The most famous cellular suicide gene, about which many articles have been written since the day it was discovered in 1979, is the gene TR 53, lying on the short arm of chromosome 17. In this chapter we will talk about the problem of cancer from the point of view of genes, whose task is to ensure the self-destruction of cancer cells.

At the time Richard Nixon declared war on cancer in 1971, scientists knew virtually nothing about their enemy, other than the obvious fact that cells were dividing rapidly in the affected tissues. It was also obvious that in most cases, oncology is neither an infectious nor a hereditary disease. It was generally accepted that cancer is not a separate disease, but a manifestation of a wide variety of dysfunctions of the body, often associated with exposure to external factors that lead to uncontrolled cell division. Thus, chimney sweeps “earn” scrotal cancer as a result of constant contact with tar; X-ray or radiation exposure leads to leukemia; smokers and builders working with asbestos develop lung cancer, etc. etc. It was also clear that the influence of carcinogenic factors may not be direct, but associated with a general weakening of the body’s immune system.

It was possible to look at the problem of cancer from a different angle thanks to the discoveries of several competing groups of scientists. Thus, in 1960, Bruce Ames from California showed that what carcinogens such as X-rays and tar have in common is their ability to destroy DNA. Ames suggested that the cause of cancer lies in genes.

Another discovery occurred much earlier, back in 1909: Peyton Rous proved the infectious nature of chicken sarcoma. His work went unnoticed for a long time, since infection was quite difficult to reproduce in the experiment. But in the 1960s, many new animal oncoviruses were described, including chicken sarcoma virus. At the age of 86, Rous received the Nobel Prize for his early discovery. Soon, human oncoviruses were discovered and it became clear that a whole group of oncological diseases, such as cervical cancer, should be considered to some extent infectious (Cookson W. 1994. The gene hunters: adventures in the genome jungle. Aurum Press, London).

As soon as it became possible to sequence (read) the genomes of organisms, scientists learned that the well-known Rous sarcoma virus carries a special gene called src, which is responsible for the oncological transformation of cells. Their own “oncogenes” have been discovered in the genomes of other oncoviruses. Just like Ames, virologists saw the genetic nature of oncology. But in 1975, the emerging theory about the role of genes in the development of cancer was turned upside down. It turned out that the terrible gene src It is not of viral origin at all. This is a normal gene of any organism - chicken, mouse and ours - which the harmful Rous sarcoma virus simply stole from one of its hosts.

More conservative doctors have long refused to acknowledge the genetic basis of cancer - after all, with the exception of some rare cases, oncology is not a hereditary disease. They forgot that the genome has its own history not only from generation to generation, but also in each individual cell of the body. Genetic diseases in individual organs or individual cells, although not inherited, still remain classic genetic diseases. In 1979, to confirm the role of genes in cancer, tumors were experimentally induced in mice by injecting DNA from cancer cells into cells.

Scientists immediately had hypotheses regarding what class of genes oncogenes might belong to. Of course, these must be genes responsible for cell growth and division. Our cells need such genes for prenatal growth of the embryo and for the development of children, as well as for the healing and healing of wounds. But it is extremely important that these genes remain turned off most of the time. Uncontrolled inclusion of such genes leads to disaster. In a “heap” of 100 trillion constantly dividing cells, oncogenes have plenty of opportunities to bypass restrictions and remain turned on even without the help of mutagens such as cigarette smoke or solar ultraviolet light. Fortunately, cells also have genes whose role is to kill rapidly dividing cells. The first such genes were discovered in the mid-1980s by Henry Harris of Oxford, and they were named tumor suppressors. Their action is opposite to the activity of oncogenes. They perform their function in different ways. Typically, the cell's development cycle is blocked at a certain stage until internal control mechanisms check the cell's condition. If the alarm was false, the cell will be unlocked. It became clear that for a cancer cell to arise, two events must occur in it: the inclusion of an oncogene and the destruction of a suppressor gene. The likelihood of both conditions being met is quite low, but that's not the end of the story. Having deceived the suppressor genes, the cancer cell must now undergo yet another more stringent genetic control. Special genes are activated as a result of unnatural cell division and instruct other genes to synthesize substances that kill the cell from the inside. This role is taken on by the gene TR CHG

Gene TR 53 was first discovered by David Lane in Dundee, UK. At first it was mistaken for an oncogene. Only later did it become known that its role is to suppress cancer cells. Lane and his colleague Peter Hall were once arguing in a pub about the purpose of a gene. TR 53, and Hall proposed using himself, like a guinea pig, to prove the anticancer role of the gene. To obtain permission to conduct experiments on animals, one had to wait for months, and a volunteer was nearby. Hall irradiated a small area of ​​skin on his arm several times, and Lane took tissue samples for biopsy over the course of two weeks. A significant increase in the content of the p53 protein in cells, the product of the gene, was found TP following irradiation. The experiment showed that the gene is turned on in response to the action of a carcinogenic factor. Lane continued his research into the p53 protein as an anticancer drug. By the time this book was published, clinical trials of the drug on a group of volunteers under the supervision of doctors were to begin in Dundee. A small Scottish town at the mouth of the Tay, which until now was famous only for burlap and marmalade, is gradually turning into a global center for cancer research. The p53 protein has become the third promising anti-cancer drug developed by Dundee scientists.

A mutation in the TP, 3 gene is one of the necessary conditions for lethal cancer. In 55% of human cancers, a defect in this gene is found in cancer cells, and in lung cancer the mutation is found in more than 90% of cases. In people with a congenital gene defect TR 53 on at least one chromosome, the probability of developing cancer at a young age reaches 95%. Take, for example, colorectal cancer. This disease usually begins with a mutation in the APC suppressor gene. If the following mutation in the oncogene occurs in the developed polyp R.A.S. then an adenoma tumor appears in place of the polyp. The disease enters a more dangerous phase after the third mutation in one as yet unidentified suppressor gene. But the tumor becomes a lethal carcinoma only after the fourth mutation in the gene occurs TR 53. Similar developmental patterns apply to other forms of cancer. And the mutation in the TR gene is always the last to occur.

Now you can see why early diagnosis of cancer is so important for successful treatment. The larger the tumor becomes, the greater the likelihood of another mutation becomes, both due to the general theory of probability and as a result of the ever-accelerating frequency of cell division, which leads to errors in the genome. People predisposed to cancer often have mutations in so-called mutator genes, which leads to an increase in the number of random mutations in the genome. These genes most likely include breast cancer genes, BRCA/ And BRCA 2O which we spoke about when considering chromosome 13. Cancer cells are under pressure from the same evolutionary process that weighs on the rabbit population. Just as the offspring of a rapidly reproducing pair of rabbits soon displace their more passive neighbors, in a cancerous tumor lines of rapidly growing cells displace moderately growing cells. Just as in a population of rabbits, only those who skillfully hide from owls and foxes survive and leave offspring, in a cancer tumor, from the many mutations, only those are selected that help cancer cells successfully resist the body’s defenses. The development of a cancerous tumor occurs in strict accordance with Darwin's evolutionary theory. Despite the huge variety of mutations, the course of cancer is similar in most cases. Mutations are random, but the direction of the selective process and its mechanisms are the same for all people.

It also becomes clear why the likelihood of cancer doubles with every decade of our age, being predominantly a disease of older people. As a result of random mutations, some people in the population sooner or later experience mutations in suppressor genes, such as TP g or in oncogenes, which leads to irreversible and often fatal consequences. The share of oncology among the causes of death of people ranges from 10 to 50% in inverse proportion to the level of development of medicine. The better doctors cope with other diseases, the longer the average life expectancy becomes and, accordingly, the more mutations a person manages to accumulate, and the more likely the occurrence of cancer becomes. The likelihood that, as a result of random mutations, important suppressor genes will be damaged and dangerous oncogenes will be activated is extremely low. But if we multiply this probability by the number of cells in the body and the number of divisions, then by a certain time this probability will turn into a pattern. “One fatal mutation per 100 trillion cell divisions is becoming not so rare,” Robert Weinberg said on this occasion (Robert Weinberg 1998. One renegade cell. Weidenfeld and Nicolson, London).

Let's take a closer look at the gene TR 5G The gene consists of 1,179 “letters” and encodes a fairly simple p53 protein, which is quickly destroyed in the cell by other proteins and “lives” on average for no more than 20 minutes. Moreover, all this time the p53 protein is in an inactive state. But as soon as certain signals arise in the cell, protein synthesis rapidly increases, and its degradation by cell enzymes stops. What these signals are is still not clear. Certainly, fragments of DNA resulting from the destruction or incorrect copying of chromosomes are one such signal. Broken DNA fragments also affect the activity of the p53 protein itself. Like special forces soldiers, protein molecules rush into the fray. One can imagine the dashing protein p53 walking onto the stage and declaring, “From now on, I am in charge of the operation.” The main function of the p53 protein is to enable other genes and proteins to function. Further events develop according to one of the following scenarios: either the cell stops proliferation and DNA replication until the situation is clarified by special repair proteins, or a self-destruction program is activated.

Another signal that activates the p53 protein is a lack of oxygen in the cell, which is typical for a cancer tumor. Inside a rapidly growing tumor, the blood supply is disrupted, and the cells begin to suffocate. Malignant neoplasms cope with this problem by producing special hormones that force the body to grow new arteries to feed the tumor. It is to these arteries, reminiscent of the claws of cancer, that the tumor owes its name, used in Ancient Greece. An entire direction in the development of cancer drugs is devoted to the search for substances that block the process. angiogenesis- formation of new blood vessels in a cancerous tumor. But usually the p53 protein understands the situation even before the tumor begins angiogenesis and destroys it in the early stages of development. In tissues with poor blood supply, such as skin, the lack of oxygen signal is not clear enough, allowing tumors to develop and neutralize the p53 protein. This is probably why skin melanoma is so dangerous (Levine A. J. 1997. R 53, the cellular gatekeeper for growth and division. Cell 88: 323-331).

It is not surprising that the p53 protein was given the name “Defender of the Genome,” or even “Guardian Angel of the Genome.” Gene 7P 53 is something like a capsule of poison in the soldier’s mouth, which dissolves only at the first sign of treason. This cell suicide is called Stoppuiss, from the Greek word for autumn leaf fall. It is the most effective natural remedy against cancer and the body's last line of defense. Nowadays, information is increasingly accumulating that almost all modern successful cancer treatments in one way or another affect the p53 protein and its colleagues. It was previously believed that the effect of radiotherapy and chemotherapy was reduced to the destruction of DNA in rapidly dividing cells. But if this is so, why is treatment effective in some cases, but has no effect in others? There comes a time in the development of any cancerous tumor when its cells stop responding to radiotherapy and chemotherapy. What is the reason for this? If the therapy simply kills growing cells, the effectiveness of the treatment should only increase as the tumor grows faster.

Scott Lowe from Cold Spring Harbor Laboratory found the answer to this question. "Anticancer therapies do damage some DNA in growing cells," he said, "but not enough to kill them." But fragments of destroyed DNA are the best stimulators of the activity of the p53 protein, which triggers the process of self-destruction of cancer cells. Thus, radio and chemotherapy are more reminiscent of vaccination - the process of activating the body's internal defenses. Experimental data soon appeared confirming Lowe's theory. Irradiation, as well as the chemicals 5-fluorouracil, etoposide and doxorubicin, often used in chemotherapy, caused aioitosis in a laboratory tissue culture infected with oncovirus. And in cases where, in the later stages of the disease, cancer cells stop responding to therapy, this is always accompanied by a mutation in the gene TR 5G In untreatable tumors of the skin, lungs, breast, rectum, blood and prostate, a mutation in the TR ChZ gene occurs in the early stages of disease development.

This discovery was important for the search for new means to combat cancer. Instead of looking for substances that kill growing cells, doctors should look for substances that trigger the process of cell suicide. This does not mean that chemotherapy is useless, but its effectiveness was the result of a coincidence. Now that the mechanisms of therapeutic effects on cancer cells are becoming more clear, we can expect a qualitative breakthrough in the creation of new drugs. In the near future, it will be possible to at least spare patients from unnecessary suffering. If the doctor, using genetic analysis, determines that the TP 53 gene has already been destroyed, then there is no need to subject the patient to painful but useless therapy in the last months of his life (Lowe S. W. 1995. Cancer therapy and p53. Current Opinion in Oncology 7: 547-553).

Oncogenes, in their normal unmutated state, are necessary for cells to grow and divide throughout the life of the body: the skin must regenerate, new blood cells must form, bones must grow together, wounds must heal, etc. Mechanisms to suppress the growth of cancer cells must be regulated so as not to interfere with the normal growth and development of the body. The body has means that allow cells not only to quickly divide, but also to quickly stop growing at the right time. Only now is it becoming clear how these mechanisms are implemented in a living cell. If these control mechanisms were developed by man, we would marvel at his inhuman genius.

Once again, the key element of the system is apoptosis. Oncogenes cause cells to grow and divide, but at the same time, surprisingly, some of them act as triggers of cell suicide. For example, gene MYC is responsible for both cell growth and death, but its killing function is temporarily blocked by external factors called life signals. If life signals stop coming, and the gene protein MYC is still in active form, cell death occurs. The Creator, knowing the unrestrained nature of the gene M.Y.C. provided it with two opposing functions. If in any of the cells the gene MYC gets out of control, the same gene leads the cell to commit suicide immediately after growth signals stop coming. The creator also took additional precautions by linking three different oncogenes together, MYC, BCL-g And R.A.S. so that they control each other. Normal cell growth is possible only if all three genes coordinate their work with each other. According to the scientists who discovered this phenomenon, “as soon as the proportions are violated, the shutter of the trap is triggered, and the cell is dead or in such a state that it no longer poses an oncological threat” (Huber A.-0., Evan G. I. 1998. Traps to catch unwary oncogenes. Trends in Genetics 14: 364-367).

My story about the p53 protein, like my entire book, should serve as an argument in a dispute with those who consider genetic research dangerous for humanity and propose in every possible way to limit scientists in penetrating the secrets of nature. All attempts to understand the workings of complex biological systems without touching them are flawed and fruitless. The dedicated work of doctors and scientists who have studied cancer for centuries, while worthy of recognition, has yielded little compared to the achievements of the last decade, when doctors got their hands on genetic research methods. Italian Nobel Prize laureate Renato Dulbecco was one of the first to voice the idea of ​​the Human Genome Project in 1986.

(Renato Dulbecco), who simply stated that this is the only way to defeat cancer. For the first time, people have a real opportunity to get a cure for cancer - the most common and terrifying cause of death for modern people. And this opportunity was provided by geneticists. Those who scare people with mythical monsters of genetic experiments should remember this (Cook-Deegan R. 1994. The gene wars: science, politics and the human genome. W. W. Norton, New York).

Once nature finds a successful solution to one problem, the same mechanism is used to solve other problems. In addition to serving the function of eliminating cancer cells, apoptosis plays an important role in resisting infections. If a cell discovers that it is infected with a virus, it will be better for the body if it self-destructs (sick ants and bees also leave the colony so as not to infect their fellows). There is experimental evidence of the suicide of infected cells, and the mechanisms by which some viruses attempt to block cell apoptosis are known. This functionality has been noted for the membrane protein of the Ebstein-Barr virus, which causes mononucleosis. Two proteins in the human papillomavirus, which causes cervical cancer, block the gene TR 53 and other suppressor genes.

As I noted in Chapter 4, Huntington's syndrome causes unscheduled apoptosis of nerve cells in the brain that cannot be replaced. In an adult, neurons do not recover, so damage to the brain and spinal cord often leads to irreversible consequences. Neurons lost their ability to reproduce during evolution, since during the development of the organism, each neuron acquires its own unique functional uniqueness and special significance in the network of neurons. Replacing a neuron with a young, naive and inexperienced cell will do more harm than good. Therefore, apoptosis of neurons infected with viruses, unlike apoptosis in other tissues, only leads to escalation of the disease.

Some viruses, for as yet unknown reasons, actively stimulate apoptosis of nerve cells, in particular encephalitic alphavirus (Krakauer D. S., Payne R. J. N. 1997. The evolution of virus-induced apoptosis. Proceedings of the Royal Society of London, Series B 264: 1757-1762).

Apoptosis plays an important role in the elimination of active transposons. Particularly strict control over selfish genes is established for germ cells. It was clear that control functions were assumed by follicular cells in the ovaries and Sertoli cells in the testes. They induce apoptosis in maturing germ cells if they show any signs of transposon activity. Thus, in the ovaries of a five-month female embryo there are up to 7 million eggs. By the time of birth, only 2 million of these remain, and only about 400 eggs will be produced by the ovaries during a woman's lifetime. All other cells, which strict controllers consider not perfect enough, receive a command to commit suicide. The organism is a totalitarian despotic state.

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A special qualitative state of the world is perhaps a necessary step in the development of the Universe. A naturally scientific approach to the essence of life is focused on the problem of its origin, its material carriers, the difference between living and nonliving things, and evolution... ... Philosophical Encyclopedia