Extraventricular neurocytomas (EVNs) are rare neoplasms with many similar morphologic features compared with central neurocytomas. EVNs have been reported in a variety of locations and mainly occur within the cerebral hemispheres. These lesions display wide variability in morphologic features, cellularity, and proliferation rates. In addition, given their aggressive biological nature and tendencies to affect eloquent areas, EVNs are associated with a poorer prognosis. The epidemiology of these rare tumors is not definitively known, and effective treatment strategies have not been developed. This article reviews these tumors, including their epidemiology, clinical presentation, locations, radiological findings, treatment options, and prognosis.
The question of whether and how race plays a role in TBI is controversial. At a single, diverse center, we found that mortality is associated with race, age, and Injury Severity Score. Future clinical studies will benefit from detailed genotypic and phenotypic data and should balance larger sample sizes with ethnic diversity.
Transcription factors that induce epithelial-mesenchymal transition (EMT) promote invasion, chemoresistance and a stem-cell phenotype in epithelial tumors, but their roles in central nervous system tumors are not well-understood. We hypothesized these transcription factors have a functional impact in grades II–III gliomas. Using the National Cancer Institute (NCI) Repository for Molecular Brain Neoplasia Data (REMBRANDT) and the Cancer Genome Atlas (TCGA) Lower-Grade Glioma (LGG) data, we determined the impact of EMT-promoting transcription factors (EMT-TFs) on overall survival in grades II–III gliomas, compared their expression across common genetic subtypes and subsequently validated these findings in a set of 31 tumors using quantitative real-time polymerase chain reaction (PCR) and immunohistochemishy. Increased expression of the gene coding for the transcriptional repressor Zinc Finger E box-binding Homeobox 1 (ZEB1) was associated with a significant increase in overall survival (OS) on Kaplan–Meier analysis. Genetic subtype analysis revealed that ZEB1 expression was relatively increased in IDH1/2-mutant gliomas, and IDH1/2-mutant gliomas expressed significantly lower levels of many ZEB1 transcriptional targets. Similarly, IDH1/2-mutant tumors expressed significantly higher levels of targets of microRNA 200C (MIR200C), a key regulator of ZEB1. In a validation study, ZEB1 mRNA was significantly increased in IDH1-mutant grades II–III gliomas, and ZEB1 protein expression was more pronounced in these tumors. Our findings demonstrate a novel relationship between IDH1/2 mutations and expression of ZEB1 and its transcriptional targets. Therapy targeting ZEB1-associated pathways may represent a novel therapeutic avenue for this class of tumors.
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