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ABSTRACT: Objectives
Isocitrate dehydrogenase (IDH1/2) mutations and O6-alkylguanine DNA methyltransferase (MGMT) promoter methylations are acknowledged survival predictors in patients with glioblastoma (GB). Moreover, tumor growth patterns like multifocality and subventricular zone (SVZ) involvement seem to be associated with poorer outcomes. Here, we wanted to evaluate the influence of the SVZ involvement and the multifocal tumor growth on the extent of surgical resection and its correlation with overall survival (OS) and molecular characteristics of patients with GB.Methods
Adult patients with primary GB who underwent surgery at our department between 2012 and 2014 were included. Preoperative magnetic resonance imaging findings were analyzed with regard to tumor location, presence of multifocality and SVZ involvement. The extent of surgical resection as well as clinical and molecular parameters was collected from electronic patient records. Univariate and multivariate analyses were performed.Results
Two hundred eight patients were retrospectively analyzed, comprising 90 (43.3%) female individuals with a mean age of 62.9 (±12.26) years and OS of 10.2 months (±8.9). Unifocal tumor location was a predictor for better OS with a mean of 11.4 (±9.4) months (vs. 8.0 [±7.4] months, p=0.008). Affection of the SVZ was also associated with lower surgical resection rates (p<0.001). SVZ involvement revealed with 7.8 (±7.0) months a significant worse OS [vs. 13.9 (±10.1) months, p<0.001]. All six IDH1/2 wildtype tumors showed an unifocal location (p=0.066). MGMT promoter methylation was not associated with multifocal tumor growth (p=0.649) or SVZ involvement (p=0.348). Multivariate analysis confirmed independent association between the SVZ involvement and OS (p=0.001).Conclusion
The involvement of the SVZ appears to have an influence on a lower resection rate of GB. This negative impact of SVZ on GB outcome might be related to lesser extent of resection, higher rates of multifocality and greater surgical morbidity but not inevitably to IDH1/2 mutation and MGMT promoter methylation status.
SUBMITTER: Ahmadipour Y
PROVIDER: S-EPMC8668024 | biostudies-literature |
REPOSITORIES: biostudies-literature