Tumor Habitats Based on Multiparametric MRI Distinguish Atypical Glioblastoma From Primary Central Nervous System...

Atypical glioblastoma (GBM) (minimal or no necrosis on MRI) and primary central nervous system lymphoma (PCNSL) are difficult to distinguish on MRI; whether tumor habitat can more accurately distinguish atypical GBM from PCNSL remains uncertain.

To evaluate the diagnostic performance with tumor habitats, apparent diffusion coefficient (ADC), and edema index (EI) to distinguish atypical GBM from PCNSL.

Retrospective.

One hundred twenty-five patients (63 male and 62 female) diagnosed with atypical GBM or PCNSL were included.

1.5 T and 3.0 T, Axial ADC and T1 contrast-enhanced spin-echo inversion recovery sequence (T1-CE).

The tumor habitat was derived using T1-CE and ADC sequences. Based on this tumor habitat, EI and relative ADC (rADC), we constructed a model.

Logistic regression; Akaike Information Criterion; Receiver operating characteristic (ROC) curves, calibration curves, and Decision Curve Analysis.

Three tumor habitats were identified: high-enhancement cellular habitat (Habitat 1), low-enhancement cellular habitat (Habitat 2), and nonviable tissue habitat (Habitat 3). The voxel fraction of the three tumor habitats in atypical GBM and PCNSL groups shows statistically significant differences. The EI of patients in the PCNSL group was significantly higher than that of the patients in atypical GBM. A model was established incorporating the parameters Habitat 2, Habitat 3, EI, and rADCmean. The model exhibits excellent discriminative ability in the training set (AUC = 0.851, 95% CI: 0.781-0.921) and validation set (AUC = 0.807, 95% CI: 0.724-0.889). Histopathological evaluation showed that vasculogenic mimicry (VM) levels were significantly higher in the PCNSL group. Multiple linear regression analysis showed a significant correlation between habitat voxel fraction and VM levels.

A model built based on tumor habitat, EI, and rADCmean can differentiate atypical GBM from PCNSL preoperatively. The differences in VM levels are one of the pathological mechanisms underlying the variations in tumor habitats between atypical GBM and PCNSL.

3.