Epidemiology. Tumours of CNS make, after different data, 2-8,6% of the total number of all neoplasms of the man. Among the organic diseases of CNS tumours make 4,2-4,4%. The amount of revealed for the first time tumours of CNS annually increases by 1-2%. At that, for adults the index of lethality by reason of tumours of the brain takes the 3rd -5th place among all reasons of death. For children lethality as a consequence of the development of the oncologic process of CNS occupies the 2nd place after diseases of the hematogenic and lymphatic systems.
In Ukraine, the occurrence of brain tumours in men is 10,2 per 100 thousand of the population. Among women this index is 7,6 per 100 thousand. In the USA, the occurrence of brain tumours among men reaches 12,2 per 100 thousand, and among women - 11 per 100 thousand of the population. The amount of brain tumours in women at the age of 40-50 years is 1,5-1,8 time more than in men. In men there occur mainly tumours of the glial origin, while meningioma’s and neurinomas prevail in women.
The distribution of neoplasms by their histological structure in many respects depends on the average age of patients of the sample under study. Thus, in adults gliomas account for 40-45% of primary tumours, 18-20% are meningiomas, 8% are neurinomas of VIII nerve, 6-8% - adenomas of the hypophysis. In children, gliomas make 75% of all tumours; meningiomas - 4%, while neurinomas and adenomas occur extremely rarely. In patients over 70 years, meningiomas make 40% of tumours of the brain .
Lately, the tendency persists towards the increase of the occurrence of the appearance of metastatic tumours of the brain of such a type.
Etiology and pathogenesis. At the basis of the development of brain tumours, as well as of any other localization, there lies a persistent disturbance of the integrity of the genetic apparatus of the cell, above all things of those its parts which are accountable for the control of the initiation and progression of a cellular cycle. As a rule, here belong genes encoding albuminous factors which form the basis of the mechanism of progression of cellular division (Rb, E2F, cyclines and cycline-dependent proteinkinases), proteins of transduction (e.g. Ras-cascade factors of growth (e.g., PDGF) and their receptors, as well as factors inhibiting the development of a cellular cycle and activating the cascades of the apoptotic elimination of the cell. At that, the defects of loci related to the system of the regulation of progression of a cellular cycle result in the hyperexpression of promoters of mitotical activity or in appearance of new persistent pathological forms of promitotical factors with functional overactivity. While the damages of genes of the apoptotic system in the context of oncogenesis take the character of prolapse.
Presently, the information has appeared which allows to suppose that primary genetic damages take place in cells with an active expression of the apparatus of regulation of a cellular cycle, that is in mitotically active cells. The overactivity of the mitotical apparatus of the cell results in its division and the genetic information is saved in tissue, while apoptotic overactivity results in the elimination of the cell and all deviations of the cellular genome. But here specialized progenitors of tissue, tissue stem cells can for a long time be in the state between apoptosis and mitosis that opens the possibility of a gradual degeneration of genetic loci of both the mitotical and apoptotic systems with the possibility of transmission of appearing defects to subsequent cellular generations.
An important condition of transition of a proliferating cell from the rank of that possessing mitotic overactivity to the rank of those possessing uncontrolled mitotical activity is a gradual accumulation of some mutational changes in the genome of the cellular line. Thus, the development of an astrocytic glioma and its regeneration into a malignant form - glioblastoma - is accompanied by the accumulation of mutational changes in the genome of tumour cells. It has been presently established that mutations in chromosomes 1,6, 9p, l0q, lip, 13q, 14, 17p, 18, 19q, 22q are the key moment of the origin and progression of the main types of brain tumours.
The mutational regeneration of genetic loci can take place for diverse reasons. It should be noted that some of them can have a direct damaging influence on the genome of brain cells. Another group is made by factors which indirectly increase the transcription loading on the indicated genes or reduce the activity of the system of genetic reparation. In sum, a combination of some negative factors against the background of an innate predisposition which can acquire its expression in different genetic deviations, results in the disturbance of the integrity of the genetic information of a mitotically active cell which is a primary event on the way of oncogenic regeneration. The deregulation of the system of genetic transcription, reparation and replication, inevitably arising here, increases the vulnerability of the genome of the cell clone that increases the probability of the origin of subsequent mutational events.
Among the unfavorable in that respect factors it is necessary to single out ionizing radiation, electromagnetic field, pesticides and other factors of a chemical contamination of the environment.
Important is a transmitter of oncogenic viruses which can provoke or facilitate progression of the described processes. To such it is necessary to refer Epstein-Bar's viruses, papillomas of the man (types 16 and 18), HIV and others.
Harmful habits, as well as a "dietary" factor, have for a long time been referred to the group of "classic" factors increasing the risk of appearing of oncologic diseases. In that respect brain tumours are not an exception.
Presently, the influence of a survived CCT on the possible development of brain tumours it is necessary to consider to a large extent as hypothetical, because the corresponding temporal combination of the both pathologies of the brain occurs extremely rarely and belongs to the rank of casual findings.
Taking into account a large predisposition of representatives of different sexes to the origin of certain variants of brain tumours (e.g. meningiomas occur more frequently in women), it is expedient to regard the influence of sexual hormones in progression and, possibly, in the increase of the probability of display or even appearance of primary tumour foci.
Finally, the presence in the closest relatives of tumours of the nervous system or such diseases as, for example, reklinkhgauzen's disease, increases the risk of the appearance of brain tumours.