Implications of Cellular Immaturity in Necrosis and Microvascularization in Glioblastomas IDH-Wild-Type

Abstract

Necrosis and increased microvascular density in glioblastoma IDH-wild-type are the consequence of both hypoxia and cellular immaturity. Our study aimed to identify the main clinical-imaging and morphogenetic risk factors associated with tumor necrosis and microvascular in the prognosis of patient survival. We performed a retrospective study (10 years) in which we identified 39 cases. We used IDH1, Ki-67 and Nestin immunomarkers, as well as CDKN2A by FISH. The data were analyzed using SPSS Statistics. The clinical characterization identified only age over 50 years as a risk factor (HR = 3.127). The presence of the tumor residue, as well as the absence of any therapeutic element from the trimodal treatment, were predictive factors of mortality (HR = 1.024, respectively HR = 7.460). Cellular immaturity quantified by Nestin was associated with reduced overall survival (p = 0.007). Increased microvascular density was associated with an increased proliferative index (p = 0.009) as well as alterations of the CDKN2A gene (p < 0.001). CDKN2A deletions and cellular immaturity were associated with an increased percentage of necrosis (p < 0.001, respectively, p = 0.017). The main risk factors involved in the unfavorable prognosis are moderate and increased Nestin immunointensity, as well as the association of increased microvascular density with age over 50 years. Necrosis was not a risk factor.