Subventricular zone contacting glioblastoma: tumor size, molecular biological factors and patient survival.

BACKGROUND

Several studies show that subventricular zone (SVZ) contact of glioblastoma at diagnosis is a negative prognosticator of survival. In this report, we study glioblastoma patient survival, molecular biological and MRI-based volumetric findings according to SVZ contact.

PATIENTS AND METHODS

We conducted a retrospective study of adult patients diagnosed with supratentorial glioblastoma and uniformly treated with temozolomide-based chemoradiotherapy after surgery. The patient cohort was dichotomized according to tumor contact with the SVZ at diagnosis as determined on preoperative MR imaging. Tumor volume was measured using semi-automated segmentation technique. MGMT-gene promoter methylation and IDH mutation status were determined on stored tumor tissue. Kaplan-Meier survival curves were constructed. Cox regression analysis was used to adjust for known confounding factors of glioblastoma patient survival.

RESULTS

A total of 214 patients were included in the study of whom 68% belonged to the SVZ group. Median tumor volume was significantly larger in the SVZ group (33,8 mL vs 15,6 mL;  < .001). MGMT-unmethylated glioblastoma was more frequent in the SVZ group (61.4% vs 44.9%;  = .028). The overall survival and progression-free survival were 12.2 months and 5.9 months for the SVZ patient group but 16.9 months and 10.3 months for the SVZ group (log-rank  = .016 and .007 respectively). In multivariate Cox survival analysis, SVZ contact proved a negative prognostic parameter, independent from age, KPS, extent of resection, MGMT-methylation and IDH mutation status.

CONCLUSIONS

This study confirms SVZ contact at diagnosis as an independent negative prognostic factor for glioblastoma patient survival. SVZ glioblastoma had larger tumor size and a larger proportion of unmethylated tumors than SVZ glioblastoma. Further research is needed to establish whether the observed differences are solely explained by a different molecular profile of SVZ glioblastoma or by interaction of glioblastoma with the unique SVZ microenvironment.