This study provides Class II evidence that vitamin E supplementation significantly reduces the relative risk of developing signs or symptoms of neurotoxicity (relative risk = 0.14) (95% confidence interval = 0.02-1.00, p < 0.05).

Purpose:Two clinical-molecular glioblastoma subtypes have been described: ''primary'' glioblastomas arise de novo in older patients and often overexpress epidermal growth factor receptor (EGFR); ''secondary'' glioblastomas progress from lower-grade tumors in younger patients and commonly have TP53 mutations. EGFR overexpression correlates in experimental gliomas with increased angiogenesis, edema, and invasion. No radiographic predictors of molecular glioblastoma subtype are known. Experimental Design: We retrospectively reviewed 75 glioblastomas, classified as TP53 -mutated (n = 11), EGFR-amplified (n = 31), or neither (non-TP53/non-EGFR; n = 33). Four variables were derived from preoperative magnetic resonance imaging: (a) T2/T1, the ratio of T2-bright volume to enclosed T1-enhancing volume; (b) percentage of tumor volume that was necrosis; and (c and d) T1 and T2 border sharpness coefficients (BSC), the rates of change in grayscale intensity of adjacent 0.02-cm 2 voxels traversing the anterior, posterior, and lateral borders onT1-enhanced and T2 images. Results and Conclusions: Mean T2/T1 was 4.7 for EGFR-amplified glioblastomas, greater than that of TP53 -mutated glioblastomas (2.3) or non-TP53 /non-EGFR glioblastomas (2.6; P < 0.00005). All four tumors with T2/T1 > 7.2 were EGFR-amplified; 0 of 15 with T2/T1 < 4.7 underwent gross total resection. The meanT2 BSC of EGFR-amplified glioblastomas was 33.7, less sharp (P < 0.0000005) than TP53 -mutated (72.2) and non-TP53/non-EGFR glioblastomas (81.2). All 15 glioblastomas withT2 BSC < 30.8 were EGFR-amplified. Percentage necrosis and T1BSC did not differ between glioblastoma subtypes. The increased T2/T1ratio and decreased T2 BSC in EGFR-overexpressing tumors are the first radiographic distinctions described between glioblastoma molecular subtypes.These findings may reflect increased angiogenesis, edema, and/or invasion in EGFR-overexpressing tumors.

Brain metastases occur in about 25% of patients who die of cancer. The most common sources of brain metastases in adults are lung, breast, kidney, colorectal cancer and melanoma. The chemokine/receptor system CXCL12/CXCR4 plays a key role in multiple biological functions; among these, homing of neoplastic cells from the primary site to the target and metastasis progression. Recently, an alternative CXCL12 receptor CXCR7 has been discovered. The aim of our study was to investigate the expression of CXCL12 and its receptors CXCR4 and CXCR7 by immunohistochemistry in 56 patients with metastatic brain disease from different non-CNS primary tumors and evaluate their prognostic relevance as well as that of other patient/treatment-related features on patient survival. CXCL12 showed an expression in tumor cells and in tumor vessels; CXCR7 was expressed by tumor and endothelial cells (both within the tumor and in the adjacent brain tissue), while CXCR4 showed a positivity in all samples with a nuclear pattern. Among the investigated immunohistochemical parameters, only CXCL12 expression in tumor endothelial cells showed a statistically significant correlation with shorter survival (p = 0.04 log-rank), perhaps identifying more aggressive tumors. Thus, this is the first study evaluating at the same time the expression of CXCL12 and its two receptors in a cohort of brain metastases.

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