Kerem Ozturk1, Esra Soylu1, Zuzan Cayci2. 1. Department of Radiology, University of Minnesota, Minneapolis, MN, 55455, USA. 2. Department of Radiology, University of Minnesota, Minneapolis, MN, 55455, USA. Electronic address: cayci001@umn.edu.
Abstract
PURPOSE: We aimed to differentiate primary central nervous system lymphoma (PCNSL) from atypical glioblastoma (GB) and distinguish major genomic subtypes between these tumors using susceptibility-weighted imaging (SWI) along with diffusion-weighted imaging (DWI). METHODS: Thirty-one immuno-competent patients with PCNSL stratified by BCL2 and MYC rearrangement, and 57 patients with atypical GB (no visible necrosis) grouped according to isocitrate dehydrogenase-1 (IDH1) mutation status underwent 3.0-Tesla MRI before treatment in this retrospective study. Region of interest analysis with apparent diffusion coefficient (ADC) and SWI signal intensity values of the tumors were normalized by dividing those of contralateral white matter. The independent-samples t-test and Kruskal-Wallis test were utilized to compare parameters. The diagnostic ability of each parameter and their optimal combination was evaluated by logistic regression analysis and receiver operating characteristic. RESULTS: PCNSL with rearrangement of both MYC and BCL2 (n = 7) [mean relative (r) ADCmean:0.87 ± 0.06, rADCmin:0.72 ± 0.08] demonstrated significantly lower rADCmean, and rADCmin compared to other PCNSLs (n = 24) (rADCmean:1.19 ± 0.18, rADCmin:1.03 ± 0.17;p < 0.001) and GBs (p < 0.001). GB without IDH1 mutation (n = 44) (mean rSWI value:0.95 ± 0.15) demonstrated significantly lower rSWI value compared to GB with IDH1 mutation (n = 13) (rSWI value:1.13 ± 0.09;p < 0.001) and PCNSL (p < 0.001). The incorporation of rADCmean and rSWI parameters distinguished GB with IDH1 mutation [Area under the curve (AUC):0.985] with sensitivity and specificity of 94.3 and 100 % respectively; and PCNSL with rearrangement of both MYC and BCL2 (AUC:0.982) with sensitivity and specificity of 100 % and 95.4 %, respectively. CONCLUSıONS: Combined analysis of SWI and DWI could differentiate atypical GB from PCNSL and distinguish major genomic subtypes between these tumors.
PURPOSE: We aimed to differentiate primary central nervous system lymphoma (PCNSL) from atypical glioblastoma (GB) and distinguish major genomic subtypes between these tumors using susceptibility-weighted imaging (SWI) along with diffusion-weighted imaging (DWI). METHODS: Thirty-one immuno-competent patients with PCNSL stratified by BCL2 and MYC rearrangement, and 57 patients with atypical GB (no visible necrosis) grouped according to isocitrate dehydrogenase-1 (IDH1) mutation status underwent 3.0-Tesla MRI before treatment in this retrospective study. Region of interest analysis with apparent diffusion coefficient (ADC) and SWI signal intensity values of the tumors were normalized by dividing those of contralateral white matter. The independent-samples t-test and Kruskal-Wallis test were utilized to compare parameters. The diagnostic ability of each parameter and their optimal combination was evaluated by logistic regression analysis and receiver operating characteristic. RESULTS: PCNSL with rearrangement of both MYC and BCL2 (n = 7) [mean relative (r) ADCmean:0.87 ± 0.06, rADCmin:0.72 ± 0.08] demonstrated significantly lower rADCmean, and rADCmin compared to other PCNSLs (n = 24) (rADCmean:1.19 ± 0.18, rADCmin:1.03 ± 0.17;p < 0.001) and GBs (p < 0.001). GB without IDH1 mutation (n = 44) (mean rSWI value:0.95 ± 0.15) demonstrated significantly lower rSWI value compared to GB with IDH1 mutation (n = 13) (rSWI value:1.13 ± 0.09;p < 0.001) and PCNSL (p < 0.001). The incorporation of rADCmean and rSWI parameters distinguished GB with IDH1 mutation [Area under the curve (AUC):0.985] with sensitivity and specificity of 94.3 and 100 % respectively; and PCNSL with rearrangement of both MYC and BCL2 (AUC:0.982) with sensitivity and specificity of 100 % and 95.4 %, respectively. CONCLUSıONS: Combined analysis of SWI and DWI could differentiate atypical GB from PCNSL and distinguish major genomic subtypes between these tumors.