Identifying the mesenchymal molecular subtype of glioblastoma using quantitative volumetric analysis of anatomic magnetic resonance images

• Published in: Neuro-oncology (Charlottesville, Va.) Vol. 15; no. 5; pp. 626 - 634
• Main Authors: Naeini, Kourosh M, Pope, Whitney B, Cloughesy, Timothy F, Harris, Robert J, Lai, Albert, Eskin, Ascia, Chowdhury, Reshmi, Phillips, Heidi S, Nghiemphu, Phioanh L, Behbahanian, Yalda, Ellingson, Benjamin M
• Format: Journal Article
• Language: English
• Published: England Oxford University Press 01.05.2013
• Subjects: Biomarkers, Tumor - analysis; Brain Neoplasms - classification; Brain Neoplasms - drug therapy; Brain Neoplasms - pathology; Clinical Investigations; Clinical Trials, Phase II as Topic; Contrast Media; Follow-Up Studies; Glioblastoma - classification; Glioblastoma - drug therapy; Glioblastoma - pathology; Humans; Magnetic Resonance Imaging; Mesoderm - pathology; Necrosis; Prognosis; Retrospective Studies; Tumor Burden
• ISSN: 1522-8517; 1523-5866
• DOI: 10.1093/neuonc/not008

Subtypes of glioblastoma multiforme (GBM) based on genetic and molecular alterations are thought to cause alterations in anatomic MRI owing to downstream biological changes, such as edema production, blood-brain barrier breakdown, and necrosis. The purpose of the current study was to identify a potential relationship between imaging features and the mesenchymal (MES) GBM subtype, which has the worst patient prognosis. MRIs from 46 patients with histologically confirmed GBM were retrospectively analyzed. The volume of contrast enhancement, regions of central necrosis, and hyperintensity of T2/fluid attenuated inversion recovery (FLAIR) were measured. Additionally, the ratio of T2/FLAIR hyperintense volume to the volume of contrast enhancement and necrosis was calculated. The volume of contrast enhancement, volume of central necrosis, combined volume of contrast enhancement and central necrosis, and the ratio of T2/FLAIR to contrast enhancement and necrosis were significantly different in MES compared with non-MES GBM (Mann-Whitney, P < .05). Receiver-operator characteristics indicated that these 4 metrics were all significant predictors of the MES phenotype. The volume ratio of T2 hyperintensity to contrast enhancement and central necrosis was significantly lower in MES vs non-MES GBM (P < .0001), was a significant predictor of the MES phenotype (area under the curve = 0.93, P < .001), and could be used to stratify short- and long-term overall survival (log-rank, P = .0064 using cutoff of 3.0). These trends were also present when excluding isocitrate dehydrogenase 1 mutant tumors and incorporating covariates such as age and KPS score. Results suggest that volume ratio may be a simple, cost-effective, and noninvasive biomarker for quickly identifying MES GBM.