Abstract

Malignant glioma is a brain tumor with a very high mortality rate resulting from the specific morphology of its infiltrative growth and poor early detection rates. The causes of one of its very specific types, i.e., post-traumatic glioma, have been discussed for many years, with some studies providing evidence for mechanisms where the reaction to an injury may in some cases lead to the onset of carcinogenesis in the brain. In this review of the available literature, we discuss the consequences of breaking the blood–brain barrier and consequences of the influx of immune-system cells to the site of injury. We also analyze the influence of inflammatory mediators on the expression of genes controlling the process of apoptosis and the effect of chemical mutagenic factors on glial cells in the brain. We present the results of experimental studies indicating a relationship between injury and glioma development. However, epidemiological studies on post-traumatic glioma, of which only a few confirm the conclusions of experimental research, indicate that any potential relationship between injury and glioma, if any, is indirect.

Highlights

  • One of the most serious brain tumors is the central-nervous-system glioma

  • Macrophages flowing to the site of the traumatically interrupted blood–brain barrier are activated to monocytes and secrete interleukin 6 (IL-6), a compound which is secreted by T and B lymphocytes, endothelial cells, and in the brain mainly produced by astrocytes and glial cells

  • Due to the well-known ability of Reactive Oxygen Species (ROS) to induce mutations that fundamentally change the functions of microglia, intensive proliferation of eosinophils induced by substances secreted by other cells of the immune system may contribute to the development of a cancer-transformed cell line

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Summary

Introduction

One of the most serious brain tumors is the central-nervous-system glioma. Characterized by high morphological and genetic complexity, it is formed as a result of neoplastic transformation of glial cells. The first guidelines in this field were proposed as early as the pre-computed tomography (CT) era by Zulch in 1965, and by Manuelidis in 1972—both described in the study by Zhou [7] Those researchers identified the following criteria for post-traumatic glioma: (1) The patient should be in good health before being injured; (2) damage must be serious enough to cause brain injury and a secondary repair process; (3) tumor and injury location must be the same; (4) both the tumor and traumatic brain environment should be confirmed histopathologically; (5) the interval between injury and the onset of the tumor should be more than a year—the later the onset, the greater the cause–effect relationship; (6) the trauma should arise from an external force; (7) bleeding, scars, and secondary edema must be characterized as being induced by the tumor, not the injury; (8) tumor tissue should be a direct continuity of the traumatic scar, and be in its vicinity or separated by a healthy zone [7]. The study was approved by the Local Ethical Committee at the Pomeranian Medical University in Szczecin, Poland (approval No KB-0012/96/14; Szczecin, Poland, 24.11.2014)

Brain Injury and Repair Processes
The Role of IL-6 Secreted by Macrophages
Inflow of Stem Cells
The Role of Microglia Cells
Interruption of the Blood–Brain Barrier
Strategy for Further Study and at the Clinical Approach
Findings
10. Conclusions
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