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What is a precancer?

Who is the author of the term "precancer", is still unknown. Different authors call different surnames of the inventor of this term. In the opinion of T. Venkei and J. Sugar (1962), he first occurs in the work of the dermatologist V. Dyubreil (1896).

Until now, it is also unclear what a precursor is. In terms of meaning and meaning, the precancer must meet two criteria: always precede cancer and turn into cancer inevitably, i.e. in all cases. Otherwise, this is not a precursor.

If the precancer meets these two criteria, then its meaning is clear to everyone: the diagnosis of precancer and its elimination must prevent cancer. This is the only way to reduce the number of cancer patients. At present, this is extremely necessary, because standard methods of cancer treatment - surgical, radiation and medicinal - can remove and destroy only a part of cancer cells, but not all, i.e. prolong the patient's life.

According to the theory of R.Virchov, the basis of any disease is the pathology of the cell or cells. The cell is the smallest unit of life, susceptible to disease. Hence, it will not be a mistake to use the expression "sick cell".

Cancer in the broadest sense is a population of malignant cells from any tissue whose cells possess sinister properties - invasion and metastasis. The process of cancer formation in the form of a scheme can be presented as follows:

1 A non-malignant tumor is formed according to the same scheme.


"Target cell" 1

> Cancer Cell

> Cancer (clone or population of cancer cells)

It can be seen from the scheme that cancer is the end result of the disease of the target cell. But the cancer itself arises from a cancer cell due to its unlimited division. It also follows from the scheme that if there is a precancer, its place should be between the target cell and the cancer cell. What can be in this place, and must be a precancer. Let's call it "something" for now, as we learn from the following presentation.

Aristotle wrote: "To know a thing, you need to know its origin and development." For us, this means figuring out how a normal target cell turns into a cancer cell, i.e. we need to turn to carcinogenesis. However, first some information about the cell and its properties should be given.

The life of a cell and its properties are determined by the genotype. Each gene through its product - a protein, creates some kind of property of the cell. All properties of a cell are its phenotype. The genotype of a cell is disturbed by the effect on the cell of a carcinogen-a chemical, physical or biological-virus. In this case, the phenotype of the cell also changes: the former properties change or disappear, new ones appear. Properties of cancer cells: the ability to invade and metastasize - the main reasons for the difficulties in curing cancer. Thus, the target cell can become tumor only after its genotype is exposed to a carcinogen.

It is now clear that the genetic disorders that result in the target cell becoming a cancer cell can be: 1) the derepression of a number of fetal genes - epimutations in it and 2) changes in the suppressor genes, DNA repair, in the genes of the cell cycle, apoptosis and immune response in the cell - epimutations and mutations.

Although the picture of gene causes is still incomplete, but already available knowledge can be used in practice.

1 "Target cell" is a tissue cell that has been exposed to a carcinogen.

The main method for detecting epimutations in a cell is the methyl-specific polymerase chain reaction (MC-PCR), to detect mutations, the polymerase chain reaction by the molecular colony method (PCR-MMK). Such methods allow us to identify cancer cells by changes in their genes in the biopsy material, as well as in samples from biological fluids from the patient - blood plasma, etc.

Carcinogenesis is the process of converting a normal cell into a tumor cell. It can only involve immature tissue cells and more often when they are in the division stage. There are two ways of carcinogenesis: 1) "de new"

- from the target cell of normal tissue and 2) "on the soil" ("against the background") - from the target cell, altered by one or another exposure to the tissue; In altered tissue, there is more pool of dividing cells than in normal tissue.

In the experiment it is proved that the carcinogenesis in the tissue of any organ consists of two stages: the 1st stage - the initiation and the 2nd - the promotion. These stages were first discovered by I. Birnblom (1947, 1956), G.P. Rush, B.E. Kline (1950), etc. on the skin of mice, and then confirmed on various tissues of other organs and other animals.

Scheme of a two-stage concept of carcinogenesis

(J. Berenblum, P. Shubik, 1947)


1) for the induction of the tumor, it is necessary to follow the sequence of effects - carcinogen, then the promoter;

1 These stages occur in any type of carcinogenesis. On them there is also a non-cancerous tumor cell.

2) initiation is reversible and can be carried out in a matter of hours or days;

3) the promotion is reversible, but requires a prolonged and repeated exposure of the agent;

4) later in the study at the genetic level, it was shown the inclusion of various genes in the stages of carcinogenesis (H. Land, IF Parada, RA Weinberg, 1983).

The concept of carcinogenesis will be more understandable from the example of animal experiment.

Experience on the skin of mice. Once lubricated skin area subthreshold, i.e. a minimal dose of a carcinogen, which does not in itself lead to the appearance of a tumor. After a while - from a week to several months, the same place on the skin begins to lubricate not carcinogenic substance

- croton oil, which also does not itself cause cancer. This lubrication is carried out for a certain minimum period of several weeks. As a result, the skin develops multiple papillomas and cancer.


1) in the experiment, a croton oil, a nonspecific stimulus, was used as a promoter, causing irritation of the tissue, leading to a marked proliferation of the cells of this tissue;

2) if a carcinogen is used as a promoter, then tumors occur at an earlier time than from a nonspecific stimulus.

The initiation stage is caused only by a specific stimulus, i.e. carcinogen, so it is called the initiator. The time period from the first exposure of the carcinogen to the tissue before the appearance of a visible tumor is called latent. The stage of promotion can be caused both by a carcinogen - its non-specific part of properties, and various nonspecific stimuli. The irritant causing the promotion step is called the promoter. The role of the promoter is twofold: an increase in the proliferation of "dormant" tumor cells or an increase in the proliferation of immature cells of the original tissue.

In the first stage, exposure to a carcinogen causes genotype disturbances in the target cell, i. E. tumor genotype, and then a tumor phenotype, i.e. the cell becomes a tumor. It carries out not less than one division cycle, and these cells remain in the tissue in such a state - as if they "doze"; to activate them, the action of the promoter is necessary. This concludes carcinogenesis. This is the stage of "dormant" tumor cells.

In the second stage, activation of the "dormant" tumor cells and their proliferation, leading to the formation of a visible tumor, occur only under the influence of a promoter, not even a carcinogenic one, for example croton oil. From these data, I. Birnblom concluded that "dormant" tumor cells are a precancer.

However, later a number of authors (VV Khudoley, 1985, Ya. G. Ehrenpreys, 1986-1987, IF Seitz, 1986) made additions to the essence of the stages: the target cell does not immediately become tumor. In the 1 st stage in the cell under the influence of a carcinogen there are epigenetic changes - the tumor genotype. This condition persists after the cessation of the carcinogen, but a change in the signs of initiation is possible, the cell still retains a normal phenotype, i.e. it is a precancerous cell. It is divided at least once, and the cells are formed until the promoter acts on them. This is the stage of the initiated cells (Ya.G. Ehrenpreis, 1986).

In the second stage, under the influence of the promoter, the initiated cells, i. precancerous, acquire a tumor phenotype, i.e. turn into cancer cells. This concludes carcinogenesis. After that, cancer cells divide unlimitedly, forming a tumor. With the number of cells 108-109 in the tumor, it differs with the naked eye.

From the analysis of the essence of the stages it follows that in the 1 st stage the target cell first becomes precancerous, and in the second stage - the stage of promotion, acquiring a tumor phenotype, turns into a cancerous one. So, "something" is the initiated cell or cells in the tissue, i.e. precancer (1st stage - stage of initiated cells). In connection with this, in the scheme of cancer formation between the "target cell" and the cancer cell, it is necessary to add the missing stage -

stage of the precancerous cell:

Normal "target cell"

> Precancerous cell (s)

> Cancer>

cage (s)

Cancer (a clone or a population of cancer


Evaluation of experiments in mice I.
Birnblom (1947, 1956) was conducted on the final result, i.e. on the formation of cancer. Hence the logical conclusion was that the precancer is a "dormant" tumor cell.

However, in the experiments:

1) the state of the cells in the interval between a single lubrication of the skin with a carcinogen and the action of the promoter has not been studied. This is the reason that the stage of the precancerous cell was not noticed;

2) the precancerous cell has a tumor genotype, but a normal phenotype. Therefore, morphological methods can not be distinguished from a normal tissue cell. This requires a PCR method, which was developed only in 1983.

Hence it follows that today's pre-cancer is a precancerous cell, but the definition: a pre-cancer is a "dormant" tumor cell, now it's not certain.

Thus, for such a long period of time - from the proposal of the term "pre-cancer" to the present, many scientists tried to find out what a precursor is, but they did not succeed in achieving this goal. The main reason is that the precancer was searched in isolation from carcinogenesis. At the heart of this approach lay the principle: if there is cancer in any local tissue change, for example, leukoplakia, then such a change is a precancer. On this and with regard to the degree of atypia of tissue cells - A, B, C (T. Venkei and J. Sugar, 1962), classifications of "precancerous diseases" - skin, mucous membrane and red border of lips prof. A.L. Mashkileyson (1970) and the "Committee on the Study of Head and Neck Tumors" (1977), as well as by other authors. But this is an erroneous approach.

Currently, any local tissue change is not considered a precancerous disease and is referred to as the "background process".

In oncology, for the time being there are two criteria for a precancer: a lesion of grade III dysplasia that occurs in some part of the background process and is detected by morphological methods, and a precancerous cell. But dysplasia of the third degree does not meet the criteria of precancer by some features. This is clear from the characteristics of dysplasia:

- it is treated differently - the focus of immature cells or the focus of immature cells with atypical cells and tissue structure;

- by morphology - this is the closest change to the cancer cells, and often dysplasia of the third degree turns into cancer;

- it is found in tissue by morphological methods, but they can not determine the genotype of its cells;

- in each specific case, its fate is unknown: turning into cancer or regression;

- the center of dysplasia of III degree as a precancer is recommended to be used for any tissue. The question arises: if the center of dysplasia of the third degree is a precancer, then why does no one say that its cells are precancerous?

ON. Krayevsky and co-authors (1993) write: "A pathologist sees under a microscope either a normal cell or a tumor cell, and in a picture that is considered a precancer, he does not have four morphological data to ascertain his true nature." What is the genotype of cells of dysplasia of the third degree is not yet clear. For this, dysplasia cells need to be examined by PCR-MMK and MC-PCR methods. It is clear that without the tumor genotype of the cells of the focal point of dysplasia of the third degree, it can not be considered a precancer.

A new approach to answering the question of what a precancer is was with the discovery of stages of carcinogenesis. From the analysis of stages, the precancer is the initiated cell

in this or that fabric. Its characteristics meet the two criteria of precancer, which we mentioned at the beginning of this section.

In the stages of carcinogenesis, not tissue, but only the cell of this tissue participates. If it has a tumor genotype, but a normal phenotype, it is a precancerous cell. It is also important that in any tissue the pre-cancer is a precancerous cell of a given cell type. Hence: there is a precancer, but there are no precancerous diseases. (AI Rukavishnikov, 1994, 1999).

About the connection of the precancer with the 1 st stage - the stage of initiation, before us prof. V.M. Dilman (1986). He stressed: 1) "the presence of the initiation stage can be treated as a state of biological precancer, since during this period the cell is already genetically different from normal, but is not yet cancerous";

2) "... after the action of the initiating agent on the cell, it is no longer normal, since the initiation phase is, in the main, irreversible. But this cell is not malignant, because the tumor process is not manifested outside the promotion. Consequently, the cell that underwent changes under the influence of the initiating agent is already precancerous "(cited in: IF Seitz, 1986).

So, the precancerous cell has a defective genotype, but a normal phenotype. Normally, in an organism such a cell must be destroyed by apoptosis, i.e. suicide, as defective, and cells of the immune system, as an alien.

Acad. V.P. Skulachev (2002) writes about this: "Precancerous cells destroy themselves with the help of apoptosis. In half the cases, the cancer appears when it breaks down? the wt53 gene encoding the p53 protein that "watches" for the breakdown of DNA. When they are found, he sends a precancerous cell with a modified genetic material the signal "to commit suicide?".

Immune cells of the body - cytotoxic T-lymphocytes "recognize and destroy foreign precancer cells." "But if suddenly the changes in the genetic apparatus of the cell have gone too far and occur

failure in the immune system, a precancerous "cell degenerates into a cancerous cell".

The focus of precancerous cells in the tissue under the experimental conditions (1st stage of initiation) is similar to the focus of dysplasia of the third degree, revealed by morphological methods in the tissue from the patient. Both of them at the very beginning of the process represent a small group or nodule from the cells into tissues 1-2 mm in diameter. It is tempting to find out whether they will be identical in genotype and phenotype of their cells. Such an assumption can be verified by PCR-MMK and MC-PCR in such cells of the biopsy material from suspicious locations in the background process. In the case of coincidence of genotypes and phenotypes of their cells, it can be concluded that the precancer in the experiment is the same as the focus of grade III dysplasia from precancerous cells, but under macroorganism conditions. Until we met the works in which the cells of grade III dysplasia from the background process from the patient were checked by PCR-MMK and MC-PCR methods.

A.V. Liechtenstein, G.I. Potapova (2005) write that "the established practice of identifying and destroying an existing cancer is the moment when? The battle? largely lost. From this point of view, a much more grateful target for therapeutic effects is the cancer array preceding the cancer, which does not yet possess all the properties of malignancy. " Such mutant cells are nothing but precancerous cells. - A.R.

Oncology is still used terms: obligate and optional facial. They are included in monographs and in all textbooks in which there is a section of oncology.

In this case, the precancer is understood as the altered tissue as a whole, and not the focus of dysplasia of the III degree and not the precancerous cell in the tissue. The term "obligate" means that this altered tissue in all cases turns into cancer, and "facultative" - ​​not always. These concepts of precancer, as well as the terms that signify it, do not correspond to the level of knowledge about precancer and therefore should be excluded from the medical literature.

The search for precancerous cells and cancer in suspicious locations in the background process is carried out on the material of a tissue fragment from these places taken from a biopsy. Any background process on the skin or mucous membrane, or elsewhere in the body and the precancerous cell in the tissue, is oncopathology, and such a patient belongs to the clinical clinical observation group of the oncologist.

In our opinion, for patients with a background process and precancer, a precancerous center should be organized in each major city. In such a center, a PCR laboratory, a cell culture laboratory, a stem cell laboratory, etc. should be organized.

In the presence of a precancerous center, the contribution of a dentist or a doctor of a different profile of polyclinics to patients with a background process and a precancer will be reduced to two tasks: 1) diagnose the patient's background process by clinical methods and send it to the precancerous center. In the absence of a precancerous center, the patient must be referred to a specialist in the oncology dispensary. In it, an oncologist will make a biopsy from suspicious places in the background process and the material is examined by morphological methods, and in the future PCR-MMK and MC-PCR methods.

To treat a patient with a background process and precancer on the mucosa and skin, two methods are used: cryodestruction with liquid nitrogen and excision. Иссеченный материал направляют на исследование в патогистологическую лабораторию. Такое лечение должно выполняться в условиях онкологического учреждения. Это уже закреплено в лечебно-диагностической тактике врача-стоматолога выпускника в «Программе по хирургической стоматологии для студентов стоматологических факультетов медицинских учебных заведений. М., 1996 г.»:

Лечебно-диагностическая тактика врача-стоматолога выпускника

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