Abstract
Gliomas are the most common primary and aggressive intracranial tumors, represent 80% of malignant brain tumors, and despite the fact that are relatively rare tumors are responsible for significant mortality and morbidity. Glioblastoma multiforme (GBM) or diffuse astrocytoma, WHO grade IV, is the most common and aggressive primary central nervous system malignancy, represents 45% of all gliomas, shows an average incidence of 3.19/100,000 individuals, its median age of diagnosis is 64 years, and the median survival is 15 months as the 5-year relative survival is 5%. Previous studies have investigated the possible role of genetic and environmental factors in GBM pathogenesis; however, the majority of GBM cases were sporadic and certain risk factors have not been detected. GBM is divided into primary and secondary subtypes which develop through different genetic pathways, affect patients at different ages, and have differences in clinical outcomes, as show a great morphological and genetic heterogeneity. The role of traumatic brain injury (TBI) in GBM formation has been investigated in many previous reports which have hypothesized that TBI may predispose to gliomagenesis; however, the outcomes were highly controversial. Some of those researches have proposed a supposed pathogenesis model that involves a post-traumatic inflammation, stem and progenitor cell transformation, and gliomagenesis. Other similar studies have involved transcription factors associated with TBI such as p53, hypoxia-inducible factor-1a (HIF-1a), and c-Myc. On the other hand, the possibility of a pre-existing tumor rather than a trauma-induced tumor is very possible in such cases.
Highlights
Gliomas are primary brain tumors, and classified according to their supposed origin cell, as astrocytic tumors, oligodendrogliomas, ependymomas, and mixed gliomas [1]
The present review aims to present an overview of the current knowledge regarding the pathogenesis of glioblastoma multiforme (GBM) mainly focusing on the possible role of previous traumatic brain injuries and its association with GBM development, according to the international literature’’
With regard to the possible pathogenic mechanisms they proposed that the inflammatory reaction which is activated after traumatic brain injury (TBI) is related to the oncogenic transformation of neural stem cells (NSCs) and progenitor cells that migrate chemotactically to the injured region in response to inflammation [60]
Summary
Gliomas are primary brain tumors, and classified according to their supposed origin cell, as astrocytic tumors (astrocytoma, anaplastic astrocytoma, and glioblastoma), oligodendrogliomas, ependymomas, and mixed gliomas [1]. A multicenter case-control study in a group [33] of 801 children showed that the odds ratio of developing a primary brain tumor after previous TBI was 1.4 and was remained after adjusting for age, gender, and location Another finding was that multiple brain injuries may be much more likely to cause a primary tumor than a single injury and was recorded that the severity of the injury is possible to be associated with the risk of developing a brain tumor. Other investigators have suggested more pathologic criteria for the diagnosis of a post-traumatic glioma, such as a computed tomography (CT) or magnetic resonance imaging (MRI) immediately after the TBI that displays evidence of brain injury but no tumor and histopathological confirmation [52]
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