PATHOPHYSIOLOGY OF TISSUE GROWTH.. Definition of tumor Tumor − typical pathological process, which...

PATHOPHYSIOLOGY OF TISSUE GROWTH.

Definition of tumor

Tumor − typical pathological process, which is characterized with an unlimited (uncontrolled, independent and endless) icreased tissuel growth and cellular anaplasia

Pathophysiologicalcharacteristic of tumor

Unlimition of growthUnregulation of growthAnaplasia of tumor cells

Pathophysiological chracteristic

Universal and obligatory property of benign and malignant neoplasms – is their capacity for unlimited growth.

In base of the growth lies uncontrolled surplus proliferation of cellular elements.

Neoplastic cells mitoses speed does not exceed the one of normal cells – embryonic bone marrow cells, bowels epithelium and other.

Tumor cells differ from normal not by the cell division speed, but character of proliferation.


Neoplastic cells acquire ability to cell-fission boundless.

Growth unlimitation carries the fact, that the tumor cells are not able to exhaust division resources.

In each cell there is genetic program, which limits its division amount.

Tumor cells do not have limiting program. They lost it owing to somatic mutation.


Tumor cells fiss to death of the organism.

Tumor can be carried into the other biological kind of organism (that is from mouse to mouse, from rat to rat etc.).

Tumor living and growth to organism-recipient’s death.


Transfer of neoplastic cells from one organism to the other is called transplantation.

Tumor cells can also be carried into culture medium, where its can also fiss endlessly for a long time.

Cultivation of tumor in culture medium is called explantation.

Neoplasms, which support artificially, are called neoplastic strains.

Methods of tumor cultivation

1. Transplantation 2. Explantation Transplantion stains1. Erlich сarcinoma in mise2. Crocer сarcinoma in mise3. Sаrcoma M-1 in rats4. Carcinoma Braun-Pirs in rabbit Explantation stains1. Cells of HeLa- cervix cancer


Tumor cells have autonomous growth. Cultural growth is controlled at two levels

– organismal and tissue ones. Organismal level of control is realized with

aid nervous and endocrine systems. Tissual level – with aid biologically active

substances - mitogenes and keylones.


Autonomy of tumor cells develops gradually.

The first tumor cell gets partially hormonal regulated (hormone dependent tumor).

Later it is perfectly irresponsible for hormones (hormone independent tumor).


The third characteristic feature of tumor cells – is anaplasia.

Structural and biochemical organization simplification of tumor cells, coming back to embryonic state.

Neoplastic cells lose a capacity to differentiation and can not form the specific tissue complexes.


Tumor arises from one mutational maternal cell.

Mutated cells differ from their general ancestor by much parameters.

These distinctions concern of cell structure, its organelles, metabolism, specific properties and functions.

There are following kinds of anaplasia: morphological, biochemical, physical and chemical, functional, immunological.

Kinds of cellular аnаplasia

•1. Моrphological•2. Biochemical•3. Physic-chemical•4. Functional•5. Immunological

Characteristic of the anaplasia

• The essence of morphological anaplasia is in appearance of atypic cellular and tissue.

• In base of cellular atypism lie polymorphism of cell,nuclear size increase, polynuclear state, nuclear hyperchromatosis, nucleoles amount increase, mitochondrial changes – decrease of its amount,crests disappearance.

• Tissuel atypism – changes of sizes and shapes of tissue structures, sometimes is the total loss of morphological tissue signs.

Morphological anaplasia

Polymorphism of cells Increase of relation

nucleus /cytoplasma Multinucleonic Hyperchromatosis of

nucleuses Increase of quantity

nucleoles Changes of cell оrganels

Changes of mitochondrias

Decrease of amountDecrease of sizesThinning of mitochondriale

membranes Decrease of amount crestThinning of mitochondriale crest

Biochemical аnaplasiaFeatures of protein metabolism

1. Dysfermentosis2. Unification of isoenzymic spectr3. Activation of nucleonic acids synthesis4. Activation DNA-polymerase5. Increase of protein synthesis 6. Decrease of protein catabolism

Chracteristic of the anaplasia

Biochemical anaplasia – is the tumor cells metabolism peculiarities.

It is characterized genetic system changes. Enzymic spectrum of tumor cells changed. All cells get alike by enzymic admission (unification of

isoenzymic spectrum). The most typical biochemical feature of neoplastic cells

concern proteins and carbohydrates metabolism. Proteins metabolism peculiarities are: synthesis

activation of nucleinic acids, DNA-polymerase inactivation, increase of proteins synthesis and decrease of proteins disintegration

Biochemical аnaplasiaEnergy supply

1. Activation of anaerobic glycolysis 2. Present of aerobic glycolysis 3. Activation of glycolic enzymes

- pyruvatkinase

- hexokinase

- fruitkinase 4. Inhibition of Krebs cycle

Chracteristic of the anaplasiaCarbohydrates metabolism and energetic of

tumor cells is also differ of norm. The main energy sources in normal cells are

anaerobic and aerobic carbohydrates disintegration, that is glycolysis and Krebs cycle.

Neoplastic cell also receives the energy owing to glycolysis and Krebs cycle. However glycolysis role in tumor cell is more, than in normal one.

The tumor cells energetic supply include: anaerobic glycolysis activation, aerobic glycolysis presence, oppression of Krebs cycle by powerful glycolytic enzymes system.

Physic-Chemical аnaplasia

Acidosis Intracellular hydration Accumulation of potassium Increase of electroconductivity Decrease of colloid viscosity Increase of membranes charge Decrease of surfase tension


Physical and chemical peculiarities of neoplastic cells:

1. Acidosis owing to lactic acid accumulation;

2. Intracellular hydration;3. Raised electroconductivity;4. Colloid viscosity decrease;5. Membranes surface-tension decrease;6. Negative membranes charge increase.


Functional anaplasia displays in loss or perversion of tumor cells function.

In neoplastic thyroid cells, for example, a surplus amount of hormones thyroxine and triiodothyronine can be synthesized, thyrotoxicosis arises.

In other cases separate functions of tumor cells fall out, for example, bilirubin does not get conjugated in hepatome.

In very malignant neoplastic cells functions are totally lost. Sometimes such cells begin doing the functions, which are not specific for them (bronchus cancer synthesizes the gastrointestinal hormones).


Immunological anaplasia – is change of tumor cell antigen properties.

In tumor cells antigen admission is changed.

There is antigen simplification, antigen divergence and antigen reversion.

Antigen simplification – is the general number of neoplastic cells antigens decreased. For example, the cells of normal tissue synthesize up to 7 typical antigens, while same tissue tumor cells synthesize only 2-3 antigens.


The idea of antigen divergence is in the fact of neoplastic cells starting to synthesize heterologous antigens. For example, hepatoma (liver tumor) begins synthesizing organospecific spleen antigens, or other organs antigens.

Antigen reversion means neoplastic embryonic antigens synthesis. For example, human liver cancer synthesizes a special embryonic protein, which is -fetoprotein.

Immunological аnaplasia

Antigen simplification Antigen divergence Antigen reversion

Tumor etiology

Tumors are caused by carcinogens, which include such groups: chemical, physical and biological.

Chemical carcinogenesis. The first clinical supervisions in this direction had been done by Pott. He described scrotum, internal thighs surfaces and stomach cancer in young chimney-sweepers.

Yamagiva and Ichikawa proved a carcinogenous of chemical matters in experiment at first. They drifted carbonic resin onto the rabbit ear for fifteenth months. This process was followed with skin cancer in rabbit. In 1930-1932 pure carcinogenes were extracted out of carbonic resin, including benzoapyrene, dibenzanthracene, methylcholanthrene.

Tumor etiology Chemical carcinogenes. The main groups are: polycyclic aromatic hydrocarbons,

aromatic amines and amides, nitrosamines and nitrosamides.

Substances, that contain three or more benzoic cycles belong to the first group. More than 200 of them are known. But the only one of them, which is 3,4-benzopyrene is carcinogenic for a human.

Carcinogenes of this group, are usually of antropogenous origin. They are in tobacco smoke, car-petroleum gases, blast-furnaces smoke, chemical productions wastes, overfried food. They cause cancer or sarcoma by their injection way. Polycyclic aromatic hydrocarbons exude from organism by kidneys, skin, mammal glands, therefore are followed with the neoplasms of these organs.

Chemical carcinogens 1. Polycyclic aromatic hydrocarbons 3,4-benzopyrine 1,2,5,6-dibenzoantracene 9,10-dimethyl-1,2- benzoantracene 20- methylcholantren 2. Aromatic аmines and amides monoаzоbenzol 2-аminofluoren 2-naphtylamine chlornaphthisine benzidine

3. Nitrosamines and nitrosamides

N,N-dimethylnitrosamine

N-nitrosopyrolidine

N-nitrosomethylаniline

N-nitrosomorpholine

N-methyl- N-nitrosourine

Tumor etiology Aromatic amines and amides. Monoazobenzene; Benzidine; Chlornaphthisine These substances are usually used for

natural or synthetic fabrics colouring, polygraphy, cosmetics production, colour-photography processes, medications or eather insecticides synthesis that is followed with neoplastic growth attached to skin or gastrointestinal contacts. Tumors are usually located in liver, urinary cyst, bowels, kidneys.

Tumor etiology Nitrosamines and nitrosamides cause

neoplastic processes in 40 animals species.

Their carcinogenous effects upon the humans are not proved, however the experimental data are of the great attention.

Nitrosamines and thear productions in man digestive channal transfer in nitrogen.

Tumor etiology Almost all of carcinogenic matters are not

active. But they acquire carcinogenic properties due to their entering the organism. them.

Carcinogenes react with purine bases of DNA obligatorily.

The most frequent target – is guanine, which gets methylated or eather alkylated by cancerogenes.

Changed guanine is unable to bind with cytosine, but gets associated with thymine. The sequence of bases in DNA molecule gets disturbed. In a result arises gene mutation.

Tumor etiology Physical carcinogenesis. To physical factors belong

ionizing and ultraviolet rays. The ionizing rays cause genetical and chromosomal

mutations. They cause neoplastic growth almost in all of organs.In

skin, bones, lungs, thyroid, mammal gland neoplasms arise in case of external irradiation. In case of ionizing radionuclides entering inside, the tumor arises at their local accumulation. For example barium, calcium, strontium radionuclides cause the bone neoplasms. Caesium, thorium radionuclides, able to cause liver, bone marrow, stomach, thick bowel tumors.

Tumor etiology Viral carcinogenesis. Tumors can be caused by viruses. There are some neoplasms examples of viral

origin: Rauss sarcoma in chicken, Shope papilloma in rabbits, mammal gland cancer in rats, which arises in case of Bittner milk factor.

Viruses, which cause neoplastic growth, are called oncogenous. They belong to the group of retroviruses.

Not many human tumors, which get caused by viruses are known. They are Burkitt’s lymphoma (Central Africa), nasopharyngeal cancer (China), cervix cancer

Tumor pathogenesis Conception of oncogen A special theory was

formulated in the end of last century,due to the foundation of contemporary knowledge, which united all of known carcinogenesis forms (chemical, physical, biological) into a single universal mechanism. It had been called as conception of oncogen.

Appearance of neoplastic growth is related to genetic system somatic cells changes. Tumor is a hereditary phenomenon at the cell level. There are many causes of cancer and all of them get DNA damaged. This damage must be located in that area DNA, where cellular oncogenes are situated. These genes are the usual components of the cell genome. They control growth and cells differentiation.

Tumor pathogenesis Cellular oncogenes are also called as cancer

genes. Carcinogenic agents damage either oncogenes

or genes-repressors, which are serial located. In effect of chemical, physical and viral factors,

their activity gets raised sharply and they turn the normal cell into the neoplastic one.

Cellular oncogenes activative mechanisms: viral transduction, chromosomal mutation, genetic material insertion, genetic amplification, point mutations.

Tumor pathogenesis Viral transduction. Retroviruses are the cause of

cellular DNA damage due to the transforming genes invasion, they are called viral oncogenes and have cellular origin.

The cellular DNA areas, which were seized by virus into the own genome occasionally. Now more than 20 viral oncogenes are known. All of them have cell twins.

Cell twins (cell oncogenes) are situated in different chromosomes. Examples are: Raus sarcoma virus in hens is located in 20-th chromosome, Molone sarcoma virus in mice – in 8-th chromosome, Rorru-Donal virus in cats – in 5-th chromosome, sarcoma virus in hairy moukeys – in 22-th chromosome

Tumor pathogenesis Viral oncogenes differ from their cell

predecessors. Viral oncogene preserves an ability to stimulate

cells growth and differentiation, but at the same time loses genes-repressors and becomes uncontrolled.

Therefore a recurrent entrance into the infected cell DNA is followed unrestricted cell division.

Cell oncogen itself gets changed also in its seizure by retrovirus process. It consists of exones (encoding areas) and intrones (unencoding areas) in the cell. It combines exones only (encoding areas) in virus genome. Therefore it is very active.

Formation of carcinogenes

Precarcinogene ↓

Proximal ↓

carcinogene ↓

Final carcinogene

VIRAL VIRAL carcinogenesiscarcinogenesis ANIMALSANIMALS:: 1. 1. RaussRauss sarcomasarcoma inin henhen - 1910 - 1910 2. 2. Shope fibroma in rabbitsShope fibroma in rabbits - 1932 - 1932 3. 3. Shope papillomaShope papilloma in rabbitsin rabbits - 1934 - 1934 4. 4. BBііttnerttner milk factormilk factor - 1936 - 1936 PEOPLEPEOPLE:: 1. 1. BurkittBurkitt lymphomalymphoma– – Central Central ААfricafrica 2. 2. NasopharyngealNasopharyngeal cancercancer – –ChineChine 3. 3. CervixCervix cancercancer

Activation ofActivation of protooncogeneprotooncogene

PointPoint mutationsmutations ChromosomalChromosomal translocationtranslocation ViralViral transductiontransduction Insertion ofInsertion of geneticgenetic materialmaterial Amplification of genesAmplification of genes

Mechanisms of oncogene Mechanisms of oncogene activationactivation

Point mutations.Point mutations. All cell oncogenes All cell oncogenes activation mechanisms, which were activation mechanisms, which were characterized earlier, obligatorily characterized earlier, obligatorily related to cell DNA changes. related to cell DNA changes. Eventually, all of them are of Eventually, all of them are of mutational origin. Now it is admitted, mutational origin. Now it is admitted, that point mutations are a major that point mutations are a major carcinogenesis mechanism. carcinogenesis mechanism.

Mechanisms of oncogene activationMechanisms of oncogene activation Chromosomal aberration.Chromosomal aberration. Translocatons are observedTranslocatons are observed in human in human

neoplastic growth cells more often. neoplastic growth cells more often. Translocation is one of the cell oncogenes Translocation is one of the cell oncogenes

activation ways majority.activation ways majority. Chromosomes breaking takes place close Chromosomes breaking takes place close

to the cellular oncogenes frequently. They to the cellular oncogenes frequently. They get activated after the breaking.get activated after the breaking.

Such tumor example is Berkit lymphoma. Such tumor example is Berkit lymphoma. Mutual translocation between 8 and 14 Mutual translocation between 8 and 14 chromosomes is typical for such chromosomes is typical for such lymphoma.lymphoma.

Mechanisms of oncogene activationMechanisms of oncogene activation Insertion of genetic material. Insertion of genetic material.

Neoplastic growth arises not only, in case Neoplastic growth arises not only, in case of viral oncogene injury into the cell DNA. of viral oncogene injury into the cell DNA.

Cell oncogene activation is also possible, Cell oncogene activation is also possible, when any heterologous (viral) genetic when any heterologous (viral) genetic material encroaches into the cell DNA material encroaches into the cell DNA close to it . It is not suppose to keep close to it . It is not suppose to keep oncogene. oncogene.

Any viral DNA is able to activate cell Any viral DNA is able to activate cell oncogene, due to its incorporation into oncogene, due to its incorporation into the cell DNA beside the oncogene. the cell DNA beside the oncogene.

Mechanisms of oncogene activationMechanisms of oncogene activation Amplification of cell oncogene.Amplification of cell oncogene. Usually, Usually,

cell oncogenes are represented by one cell oncogenes are represented by one copy.copy.

Amount of copies can increase as a result Amount of copies can increase as a result of spontaneous DNA replication anomalies. of spontaneous DNA replication anomalies. Such phenomenon is named amplification. Such phenomenon is named amplification.

DNA copies amount augmentation causes DNA copies amount augmentation causes their summary expression augmentation.their summary expression augmentation.

Supplementary RNA and oncoalbumen Supplementary RNA and oncoalbumen amount gets synthesized on amount gets synthesized on supplementary DNA matrices. supplementary DNA matrices.

Amplification is typical for some human Amplification is typical for some human tumors. Neuroblastoma and thick bowels tumors. Neuroblastoma and thick bowels carcinoma arises due to such mechanism.carcinoma arises due to such mechanism.

Stages of carcinogenesisStages of carcinogenesis Neoplastic growth beginning and Neoplastic growth beginning and

development in multistage process. The development in multistage process. The main three stages are: transformation, main three stages are: transformation, promotion and progression.promotion and progression.

Transformation.Transformation. The first stage is followed The first stage is followed with the cell oncogene activation. with the cell oncogene activation.

The cell acquires unusual property, which is The cell acquires unusual property, which is called immortalisation. This is a potential called immortalisation. This is a potential unlimited division, immortality ability. unlimited division, immortality ability. However, the presence of active oncogene is However, the presence of active oncogene is a readiness to division only. a readiness to division only.

A cell with active oncogene can resist in A cell with active oncogene can resist in latent (condition) for years. It does not latent (condition) for years. It does not display itself with anything.display itself with anything.

Stages of carcinogenesisStages of carcinogenesis

Promotion.Promotion. Supplementary influences Supplementary influences upon immortalisated cell, are necessary upon immortalisated cell, are necessary to exit it out of the latent state, for giving to exit it out of the latent state, for giving a push to irrepressible division.a push to irrepressible division.

Provoking factors, which are Provoking factors, which are supplementary doses of chemical supplementary doses of chemical cancerogenes or x-rays, retroviral cancerogenes or x-rays, retroviral superinfection. They are named superinfection. They are named promotors. promotors.

Stages of carcinogenesisStages of carcinogenesis ProgressionProgression is the very last and the most protracted is the very last and the most protracted

stage of neoplastic growth development. stage of neoplastic growth development. The clearest determination of this notion Fulds has The clearest determination of this notion Fulds has

given: “given: “Progression is a neoplasm development in Progression is a neoplasm development in a way of constant, irreversible, qualitative a way of constant, irreversible, qualitative changes of its one or a few signs".changes of its one or a few signs".

Progression is not just quantitative tumor growth, but Progression is not just quantitative tumor growth, but native change of its biological properties. native change of its biological properties.

One of the major Fuld’s principles is an independent One of the major Fuld’s principles is an independent progression of separate neoplastic signs. progression of separate neoplastic signs.

Its essence is the following: each tumor sign Its essence is the following: each tumor sign (morphological anaplasia degree, hormones (morphological anaplasia degree, hormones dependence degree, invasive growth capacity, dependence degree, invasive growth capacity, metastasing ability) evolutionizes irrespectively to the metastasing ability) evolutionizes irrespectively to the other signs, however to the malignisation side always.other signs, however to the malignisation side always.

Stages of carcinogenesisStages of carcinogenesis Neoplastic growth progression reflects tumor admiring Neoplastic growth progression reflects tumor admiring

to autonomy. It holds a neoplastic cell much more to autonomy. It holds a neoplastic cell much more further from maternal. further from maternal.

The main progression index is organs and tissues The main progression index is organs and tissues structure loss by the tumor with simultaneous cell structure loss by the tumor with simultaneous cell differentiation lowering. differentiation lowering.

Neoplastic growth progression reflects in its clinical Neoplastic growth progression reflects in its clinical symptoms and therapy possibilities. symptoms and therapy possibilities.

Some tumors (mammal gland cancer, uterius corpus, Some tumors (mammal gland cancer, uterius corpus, prostata) on the definite development stages react to prostata) on the definite development stages react to hormones. These neoplasms are hormone dependent. hormones. These neoplasms are hormone dependent.

Tumor cells lose the specific receptors and stop Tumor cells lose the specific receptors and stop reacting to the hormones influence during the reacting to the hormones influence during the progression. Neoplastic growth becomes hormone progression. Neoplastic growth becomes hormone independent. It is not sensitive to hormonal therapy. independent. It is not sensitive to hormonal therapy.

MetastasingMetastasing The final progression stage of any tumor is its The final progression stage of any tumor is its

transformation into the malignant neoplasm. transformation into the malignant neoplasm. The major criteria of malignant tumor is its ability The major criteria of malignant tumor is its ability

to generalisation, that is – to metastasing. to generalisation, that is – to metastasing. Metastasing includes three stage: neoplastic Metastasing includes three stage: neoplastic

invasion into the surrounding tissues, tumor cells invasion into the surrounding tissues, tumor cells transport with the blood and lymphatic vessles, transport with the blood and lymphatic vessles, their implantation in different organs and tissues. their implantation in different organs and tissues.

Separate cells evacuation out of the neoplastic Separate cells evacuation out of the neoplastic node takes place in case of intercellular contacts node takes place in case of intercellular contacts relaxation. Tumor loses calcium, which must turn relaxation. Tumor loses calcium, which must turn intercellular spaces cementated in malignisation intercellular spaces cementated in malignisation process. Diminished amount of desmosomes, process. Diminished amount of desmosomes, which create the intercellular contacts arises in which create the intercellular contacts arises in pernicious neoplasms. pernicious neoplasms.

MetastasingMetastasing The definite role in neoplastic cells abruption The definite role in neoplastic cells abruption

from the tumor node belongs to mechanical from the tumor node belongs to mechanical factors. factors.

The part of abrupted cells is carried with blood The part of abrupted cells is carried with blood and lymph channel. 95-99,9 % get necrotiesed. and lymph channel. 95-99,9 % get necrotiesed.

An important role in their elimination the anti-An important role in their elimination the anti-neoplasm immunity mechanisms has. neoplasm immunity mechanisms has.

They are performed by Т-lymphocytes and They are performed by Т-lymphocytes and natural killers (NК-cells). Natural killers natural killers (NК-cells). Natural killers recognize and kill the mutante cells without recognize and kill the mutante cells without preliminary sensibilization. The tumor cells lysis preliminary sensibilization. The tumor cells lysis gets realized with proteolytical and lipolytical gets realized with proteolytical and lipolytical blood enzymes also. blood enzymes also.

MetastasingMetastasing

The secondary tumor nodes form at the The secondary tumor nodes form at the third stage. third stage.

Neoplastic cells delay by the vessel Neoplastic cells delay by the vessel intima and thrombus forming around intima and thrombus forming around them arises firstly. them arises firstly.

Tumor cells accumulation in capillaries is Tumor cells accumulation in capillaries is sometimes provoked by mechanical sometimes provoked by mechanical causes: capillary lumen happens to be causes: capillary lumen happens to be more narrow, than neoplastic cells more narrow, than neoplastic cells diameter. diameter.

MetastasingMetastasing Tumor cells exit into the out of vessels space Tumor cells exit into the out of vessels space

after their adhesion to the endothelium. after their adhesion to the endothelium. This exit is related to capillaries This exit is related to capillaries

penetrability rising. Cells fate out of blood penetrability rising. Cells fate out of blood channal is different. channal is different.

Many cells get perished. Other cells are Many cells get perished. Other cells are staying in a latent condition for a very long staying in a latent condition for a very long time, pending of years. time, pending of years.

Only small part of cells receive the further Only small part of cells receive the further development. They reproduct and establish development. They reproduct and establish a new neoplastic node (metastasis). a new neoplastic node (metastasis).

Neoplastic growth and human Neoplastic growth and human organism correlationorganism correlation

Tumor appearance and growth depends on Tumor appearance and growth depends on the organism state. Two system perform the organism state. Two system perform the primary role: endocrine and immune.the primary role: endocrine and immune.

Endocrine system and oncogenesisEndocrine system and oncogenesis..

NeoplasmsNeoplasms divide into two groups: divide into two groups: dyshormonal tumors and unendocrine ones. dyshormonal tumors and unendocrine ones.

Dyshormonal neoplasms totally depend on Dyshormonal neoplasms totally depend on the organism hormonal status. Endocrine the organism hormonal status. Endocrine glands and organs-targets tumors, which glands and organs-targets tumors, which underlie hormonal influence belong here. underlie hormonal influence belong here. Human dyshormonal mammal gland, Human dyshormonal mammal gland, uterus, prostate neoplasms are the most uterus, prostate neoplasms are the most expanded. expanded.


In case of mammal gland and uterus tumors In case of mammal gland and uterus tumors development an important role belongs to the development an important role belongs to the surplus production of estrogens, which surplus production of estrogens, which stimulate cells proliferation in these organs. stimulate cells proliferation in these organs.

Follicle stimulating hormone role in mammal Follicle stimulating hormone role in mammal gland cancer formation is proved. it activates gland cancer formation is proved. it activates estrogens synthesis and renders the straight estrogens synthesis and renders the straight influence upon the gland tissue. influence upon the gland tissue.

The high estrogens synthesis regulation tension The high estrogens synthesis regulation tension is observed in case of menopause. Menopause is observed in case of menopause. Menopause in women is followed with high hypothalamo-in women is followed with high hypothalamo-hypophyseal system activity. A big amount of hypophyseal system activity. A big amount of gonadotrophic hormones get producted. gonadotrophic hormones get producted.


Sexual steroids synthesis get Sexual steroids synthesis get increased accordingly in ovaries. But increased accordingly in ovaries. But they are out of hormonal properties they are out of hormonal properties already in this age, and still already in this age, and still preserved their ability to stimulate preserved their ability to stimulate proliferation. proliferation.

Therefore the tumor appearance risk Therefore the tumor appearance risk is very high in this period.is very high in this period.


Immune system and neoplastic growth.Immune system and neoplastic growth. Tumor Tumor cells are heterologous for the organism. They cells are heterologous for the organism. They synthesize the proteins, which are not characteric for synthesize the proteins, which are not characteric for normal cells. normal cells.

Neoplasms product specific swelling antigen. Their Neoplasms product specific swelling antigen. Their specificity is conventional, but it is still sufficient for specificity is conventional, but it is still sufficient for immune reaction development. a final result depends immune reaction development. a final result depends on immune attack intensity greatly: that means, if the on immune attack intensity greatly: that means, if the transformed cell is going to reproduct,or not; is the transformed cell is going to reproduct,or not; is the tumor going to arise, or not. tumor going to arise, or not.

Neoplasms are observed in people with congenital Neoplasms are observed in people with congenital immunodeficiency 10000 times more often, than in immunodeficiency 10000 times more often, than in persons with normal immune system. The malignant persons with normal immune system. The malignant neoplasms arise in patients, with transplanted organ neoplasms arise in patients, with transplanted organ (for example, kidney) veryoften. (for example, kidney) veryoften.


Immunodepressive drugs are beeng prescribed with Immunodepressive drugs are beeng prescribed with the purpose of transplanted organ rejection the purpose of transplanted organ rejection prophylaxy in such patients. Tumors in are observed prophylaxy in such patients. Tumors in are observed in such cases 100 times more frequent, than in the in such cases 100 times more frequent, than in the rest of population.rest of population.

These facts testify, that the transformed cells These facts testify, that the transformed cells underlie the organism immune system supervision. underlie the organism immune system supervision. In most people they eliminate in time. a In most people they eliminate in time. a transformed cell exists, reproducts, and produces transformed cell exists, reproducts, and produces the neoplasm in a fact of immune supervision the neoplasm in a fact of immune supervision insolvency.insolvency.

Tumor renders an oppressive action upon the Tumor renders an oppressive action upon the organism immune system in its own way. organism immune system in its own way. Immunodepression gets developed. Immunodepression gets developed.


The matters with immunodepressive action The matters with immunodepressive action produce neoplastic cells. Low-molecular produce neoplastic cells. Low-molecular metabolites (oligopeptides, unsaturated fatty metabolites (oligopeptides, unsaturated fatty acids), embryonic antigens (acids), embryonic antigens (-fetoprotein), -fetoprotein), glucocorticoids belong to them. glucocorticoids belong to them.

Т-suppressors activity in patients with tumors Т-suppressors activity in patients with tumors is increased. They slow down antineoplastic is increased. They slow down antineoplastic immunity. immunity.

One from more main reason of One from more main reason of immunodepression in oncologic patients is immunodepression in oncologic patients is the disparity between neoplastic growth the disparity between neoplastic growth speed and immune answer development speed and immune answer development speed. speed.

Lymphoid cells reproduct slower, than tumor Lymphoid cells reproduct slower, than tumor cells do. Adequate immune answer is late.cells do. Adequate immune answer is late.

Stages ofStages of carcinogenesiscarcinogenesis

TransformationTransformation − − expression of expression of cell oncogenecell oncogene

PromotionPromotion − − division of cellsdivision of cells ProgressionProgression− − development ofdevelopment of

tumortumor in a way in a way

of malignisationof malignisation

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