Abstract
Platelets play an important part in the progression and pathological angiogenesis of brain glioma because of the different granules content and release of microvesicles that are the source of numerous mediators and bioactive substances, which probably provides a "strategy" for the tumour survival. The objective of study was exploring the effect of platelet-released secretion products of patients with brain glioma on the experimental model of tumour growth in vitro. For this purpose, the cells of glioma C6 were cultured for 72 hours under the addition of modified media containing platelet-released secretion products or conditioned media of peripheral blood cells of patients with glioma as well as persons of the comparison group without rough somatic pathology. In control glioma C6 cultures in standard conditions cell clusters were formed by the type of "spheroids", from which radial cell migration occurred, a tense cellular or reticular growth zone was formed, and tumour cells preserved their ability to mitotic division. Under the influence of platelet-released secretion products of patients with glioma, differently directed effects on cell mitotic activity and the number of cell clusters in glioma C6 cultures were detected depending on the degree of tumour malignancy: stimulating effect under the influence of platelet factors of patients with high-malignancy glioma (G4) and inhibitory effect – due to the influence of platelet factors of patients with differentiated glioma (G2). In contrast to the thrombocyte-released factors, the conditioned media of a common pool of peripheral blood cells of patients with G4 glioma suppressed the mitotic activity of tumour cells and did not affect the number of cell clusters. No changes in glioma C6 cultures were revealed after the influence of platelet-released secretion products of persons of the comparison group. The obtained data confirm the important role of platelets in the pathogenesis of brain glioma, pointing to the fundamental difference in the spectrum of biologically active molecules that are released by platelets of patients depending on the degree of tumour malignancy and are able to regulate the cell cycle and proliferative activity of the glioma tumour cells, which may have application as a diagnostic marker as well as predictive marker of response to antitumour therapy.
Highlights
Despite careful studies of the causes and mechanisms of the glial tumour progression around the world, today no significant clinical progress in their treatment has been achieved due to the invasive spread and multiresistance to adjuvant therapy methods
In parallel experiments, the conditioned media of peripheral blood cells (CMPBC) of patients were added to C6 glioma cell cultures
After 72 hours of cultivation in control cultures a significant increase in the growth and stratification of cellular microaggregates was observed, with predominance of tumour cells of the astrocytic structure of the unipolar, triangular, rhomboid, polygonal form with elongated processes that formed reticular structure (Fig. 1b, c)
Summary
Despite careful studies of the causes and mechanisms of the glial tumour progression around the world, today no significant clinical progress in their treatment has been achieved due to the invasive spread and multiresistance to adjuvant therapy methods. The current incidence of malignant variants of primary brain tumours in Ukraine, by the last National Cancer Registry data, is 5.2 per 100 thousand of population, and mortality – 3.8 (Fedorenko et al, 2019). Among the primary tumours of the central nervous system, malignant forms of glioma predominate. The combination of surgery, radiation and chemotherapy is a gold standard in the complex treatment of these tumours, but does not provide the desired efficacy. In this context, the active search for alternative methods of treatment of this type of CNS pathology continues. Other actively developing directions are adoptive immunotherapy with effector immune cells (T-, NK-cells) and different approaches to increasing their functionality: immunological checkpoint blockade with monoclonal antibodies; bispecific antibodies against both tumour antigens and immune cells; genetically engineered cells with chimeric antigen receptors (CARs); systemic administration of cytokines or priming immune cells to strengthen tumour killing and homing function (Poggi & Giuliany, 2016; Veluchamy et al, 2017; Matosevic, 2018)
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