Significance and role of morphological mechanisms of growth of glial tumors in clinical practice

It is known that the clinical course of glial tumors often shows similarities with inflammatory diseases of the brain, which made it possible to distinguish a special inflammatory type of gliomas. Chronic processes associated with the persistence of an infectious etiological factor proceed as a productive inflammation, while the etiological factor itself causes a proliferative cellular response.
AIM OF THE STUDY: biopsies of 1424 glial tumors contaminated with hSV (glioblastomas (748), anaplastic astrocytomas (103), astrocytomas (248), oligodendrogliomas (126), anaplastic oligodendrogliomas (25), mixed gliomas (60), anaplastic mixed gliomas (15), ependymomas (85), anaplastic ependymomas (14)).
The control groups consisted of tumors that did not express antibodiEs to hSV, in which intranuclear inclusions characteristic of hSV were not detected.
Staining with hematoxylin-eosin was carried out in an automatic staining apparatus according to the generally accepted histological method. To detect hSV in tumors, an immunohistochemical study was used with antibodies to the antigen of hSV type I and II. Proliferative activity (Ki-67) was determined. Vessels were counted (CD 34). To identify inflammatory infiltration, an IhC study was performed with a set of monoclonal antibodies CD 45 (total leukocyte factor), CD 8 (T-lymphocytes). The IhC assay with p53 and bcl-2 was used to study apoptosis. To study the aggressiveness of tumor growth, the epidermal growth factor receptor (EGFR) was studied.
RESULTS. It was found that glioblastomas occurring against the background of chronic inflammation have a median difference in the expression of bcl-2 and p53 in the vascular endothelium equal to 7.9 %. With an exacerbation of a chronic inflammatory process — 8.7 %. For anaplastic astrocytomas, the difference in chronic inflammation was 7.9 %, with its exacerbation — 8.2 %, for anaplastic oligodendrogliomas — 6.9 % and 7.1 %, for anaplastic oligoastrocytomas — 7.4 and 8.1 %, for anaplastic ependymomas — 7.2 % and 7.8 %, respectively. The difference between the expression of bcl-2 and p53 in tumor cells during chronic inflammation and its exacerbation for glioblastomas was 1.4 % and 1.5 %, for anaplastic astrocytomas — 0.73 % and 0.8 %, for anaplastic oligodendrogliomas — 0.7 % and 0.8 %, for anaplastic oligoastrocytomas — 0.7 % and 0.8 %, for anaplastic ependymomas — 0.6 % and 0.7 %. The difference in the expression of anti-apoptotic (bcl-2) and apoptotic (p53) factors for endothelial cells is significantly greater than for tumor cells (p<0.01), which determines the primacy of vessel growth. When comparing each of the groups of high-grade glial tumors with the control group, the amount of Ki-67 expression in endothelial cells was increased by an average of 3 times in each of the groups. This was manifested by a significant increase in the number of vessels in the «hot spot», accompanied by an acceleration of tumor growth.
The correlation analysis between the amount of expression of antibodies to hSV and EGFR in high-grade glial tumors showed that there is a positive correlation between the amount of expression of antibodies to hSV and EGFR.
Glial tumors of low malignancy progress due to an increase in the cell population, with a twofold increase in which the appearance of a proliferating vessel is fixed, which increases the degree of aggressiveness of tumor growth.
CONCLUSION. The main growth mechanism of high-grade glial tumors is that the difference in the expression of antiapoptotic (bcl-2) and apoptotic (p53) factors for endothelial cells is significantly greater than for tumor cells (p<0.01), which determines the primacy of vessel growth. The main growth mechanism of low-grade glial tumors is characterized by an increase in their cell population. With an increase in the number of cells by 2 times, a proliferating vessel is formed, which increases the degree of aggressiveness of the tumor process. The aggressiveness of the disease depends on the presence of signs of exacerbation of inflammation caused by contamination of glial tumors with hSV, since EGFR activation is directly related to a high degree of tumor malignancy, aneuploidy, and a proliferative index. When planning the volume of surgical intervention during operations to remove glial tumors, the removal of the maximum number of proliferating vessels in the peritumorous zone should be taken into account as a cause provoking the onset of relapse, which will significantly increase the radicalness of the surgical intervention without reducing the quality of life of the patient.

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