Purpose: To determine if apparent diffusion coefficient (ADC) histogram analysis can stratify progression-free survival in patients with recurrent glioblastoma multiforme (GBM) prior to bevacizumab...

To determine whether enhancement at multiphasic multidetector computed tomography (CT) can help differentiate clear cell renal cell carcinoma (RCC) from oncocytoma, papillary RCC, and chromophobe RCC. With institutional review board approval for this HIPAA-compliant retrospective study, the pathology database was queried to derive a cohort of 298 cases of RCC and oncocytoma with preoperative multiphasic multidetector CT with as many as four phases (unenhanced, corticomedullary, nephrographic, and excretory). A total of 170 clear cell RCCs, 57 papillary RCCs, 49 oncocytomas, and 22 chromophobe RCCs were evaluated for multiphasic enhancement and compared by using t tests. Cutoff analysis was performed to determine optimal threshold levels to discriminate among the four groups. Mean enhancement of clear cell RCCs and oncocytomas peaked in the corticomedullary phase; mean enhancement of papillary and chromophobe RCCs peaked in the nephrographic phase. Enhancement of clear cell RCCs was greater than that of oncocytomas in the corticomedullary (125 HU vs 106 HU, P = .045) and excretory (80 HU vs 67 HU, P = .034) phases. Enhancement of clear cell RCCs was greater than that of papillary RCCs in the corticomedullary (125 HU vs 54 HU, P < .001), nephrographic (103 HU vs 64 HU, P < .001), and excretory (80 HU vs 54 HU, P < .001) phases. Enhancement of clear cell RCCs was greater than that of chromophobe RCCs in the corticomedullary (125 HU vs 74 HU, P < .001) and excretory (80 HU vs 60 HU, P = .008) phases. Thresholding of enhancement helped to discriminate clear cell RCC from oncocytoma, papillary RCC, and chromophobe RCC with accuracies of 77% (83 of 108 cases), 85% (101 of 119 cases), and 84% (81 of 97 cases). Enhancement at multiphasic multidetector CT, if prospectively validated, may assist in the discrimination of clear cell RCC from oncocytoma, papillary RCC, and chromophobe RCC.

BACKGROUND AND PURPOSE: Currently it is difficult to predict tumor response to anti-angiogenic therapy in individual patients. Our aim was to determine if ADC histogram analysis can stratify progression-free and overall survival in patients with newly diagnosed GBM treated “up-front” (ie, before tumor recurrence) with bevacizumab. MATERIALS AND METHODS: Up-front bevacizumab-treated and control patients (n = 59 and 62, respectively) with newly diagnosed GBM were analyzed by using an ADC histogram approach based on enhancing tumor. Progression-free and overall survival was determined by using Cox proportional HRs and the Kaplan-Meier method with logrank and Wilcoxon tests. RESULTS: For up-front bevacizumab-treated patients, lower ADC_L was associated with significantly longer progression-free survival (median, 459 days for ADC_L < 1200 versus 315 days for ADC_L ≥ 1200 10⁻⁶mm²/s; P = .008, logrank test) and trended with longer overall survival (581 versus 429 days, P = .055). ADC values did not stratify progression-free or overall survival for patients in the control group (P = .92 and P = .22, respectively). Tumors with MGMT promoter methylation had lower ADC_L values than unmethylated tumors (mean, 1071 versus 1183 10⁻⁶mm²/s; P = .01, 2-group t test). CONCLUSIONS: Pretreatment ADC histogram analysis can stratify progression-free survival in bevacizumab-treated patients with newly diagnosed GBM. Lower ADC is associated with tumor MGMT promoter methylation, which may, in part, account for the favorable outcome associated with low ADC_L tumors.

The purpose of this study was to differentiate clear cell renal cell carcinoma (RCC) from other solid renal masses on four-phase MDCT. Our study cohort included all pathologically proven solid renal masses that underwent pretreatment four-phase MDCT at our institution from 2001 to 2012. Both retrospective qualitative analysis (blinded dual-radiologist evaluation of morphologic features: enhancement pattern, lesion contour, neovascularity, and calcification) and quantitative analysis (mean absolute and relative attenuation and changes in attenuation across phases) were performed. ANOVA with post-hoc analysis, Pearson chi-square tests, and ROC analysis were used. One hundred fifty-six consecutive patients (99 men, 57 women) with a mean age of 62.7 years (range, 26-91 years) had 165 solid renal masses (median size, 3.0 cm): 86 clear cell RCCs, 36 papillary RCCs, 10 chromophobe RCCs, 23 oncocytomas, and 10 lipid-poor angiomyolipomas. Kappa for interradiologist agreement regarding morphologic features was 0.33-0.76. There were significant associations between histologic subtype and enhancement pattern (p < 0.001), lesion contour (p < 0.014), and neovascularity (p < 0.001). Clear cell RCC had the highest mean relative corticomedullary attenuation (p < 0.02). Clear cell RCC had greater deenhancement than oncocytoma (p < 0.001); deenhancement less than 50 HU or relative corticomedullary attenuation greater than 0% differentiated clear cell RCC from oncocytoma with a positive predictive value of 90%. Lipid-poor angiomyolipoma had the highest mean absolute unenhanced attenuation (p < 0.01); absolute unenhanced attenuation greater than 45 HU and relative corticomedullary attenuation less than 10% differentiated lipid-poor angiomyolipoma from clear cell RCC with a negative predictive value of 97%. Four-phase MDCT renal attenuation profiles enable differentiation of clear cell RCC from other solid renal cortical masses, most notably papillary RCC and lipid-poor angiomyolipoma.

Bevacizumab is thought to normalize tumor vasculature and restore the blood–brain barrier, decreasing enhancement and peritumoral edema. Conventional measurements of tumor response rely upon dimensions of enhancing tumor. After bevacizumab treatment, glioblastomas are more prone to progress as nonenhancing tumor. The RANO (Response Assessment in Neuro-Oncology) criteria for glioma response use fluid-attenuated inversion recovery (FLAIR)/T2 hyperintensity as a surrogate for nonenhancing tumor; however, nonenhancing tumor can be difficult to differentiate from other causes of FLAIR/T2 hyperintensity (eg, radiation-induced gliosis). Due to these difficulties, recent efforts have been directed toward identifying new biomarkers that either predict treatment response or accurately measure response of both enhancing and nonenhancing tumor shortly after treatment initiation. This will allow for earlier treatment decisions, saving patients from the adverse effects of ineffective therapies while allowing them to try alternative therapies sooner. An active area of research is the use of physiologic imaging, which can potentially detect treatment effects before changes in tumor size are evident.