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Major vault protein (MVP) is a vesicular drug transporter and may participate in multidrug resistance (MDR). The aim of this study was to determine the expression and cellular localization of MVP in refractory frontal lobe epilepsy (FLE). We detected MVP expression in tissue samples from the refractory frontal cortex of 30 patients who had been surgically treated for refractory epilepsy. We compared these tissues with twelve histologically normal frontal lobe samples from controls. In the control group, the expression of MVP was faint in the cortex. The expression of MVP protein increased dramatically in the refractory epilepsy group; MVP immunoreactivity (IR) was observed in the cytoplasm of neurons. Thus, MVP protein was increased in the frontal cortex of patients with refractory epilepsy. Further research is necessary to determine whether or not MVP plays a role in the mechanisms underlying drug resistance in refractory FLE., (Copyright © 2011 Elsevier B.V. All rights reserved.)

Urokinase-type plasminogen activator receptor (uPAR) is a glycosyl phosphatidylinositol-anchored protein involved in cell adhesion, proliferation, differentiation, migration, invasion, and tissue repair and remodeling. Our aim was to investigate uPAR expression in the frontal cortex of patients with intractable frontal lobe epilepsy and to explore the possible role of uPAR in intractable epilepsy. Tissue samples were obtained from the frontal cortex of 25 patients who had undergone surgery for intractable epilepsy and 15 histologically normal frontal cortex tissues from patients with orbital frontal lobe severe contusion (the control group). The frontal cortex expression of uPAR was studied by Western blot and immnohistochemistry. Double immunofluorescence was used to determine the expression of uPAR in astrocytes, microglia, and neurons. The normal frontal cortex uPAR protein level was shown to be low. In the brain tissue of patients with intractable epilepsy, the expression of uPAR protein increased dramatically. Based on the results of double immunofluorescence, many uPAR-positive cells are colocalized with the cell soma of NeuN-positive neurons, whereas only a few GFAP- and CD11b-positive cells colocalized with uPAR staining. These findings provide new information pertaining to the epileptogenesis of intractable epilepsy and suggest that increased expression of uPAR in human brain may be associated with human intractable epilepsy.

Objective A case of secondary gliosarcoma transformed from lower grade glioma was analyzed. The clinicopathological features, molecular pathological features and prognosis of secondary gliosarcoma were discussed with relevant literatures. Methods and Results A 42-year-old female patient was admitted to our hospital. CT showed occupying lesion in left frontal lobe. The first surgery was performed and the initial pathological diagnosis was oligodendroglioma (WHO II grade). Nineteen months after the first surgery, the tumor recurred, and the second surgery and chemotherapy were performed. The post-operative pathological diagnosis was glioblastoma (WHO IV grade). Twenty-two months after the second surgery, the tumor recurred again. Then the third surgery was performed and the pathological diagnosis was gliosarcoma (WHO IV grade). Radiotherapy and chemotherapy were given after operation. The patient died 14 months after the third surgery. Conclusions According to the 2016 WHO classification, gliosarcoma, classified as a subtype of glioblastoma, was a WHO grade IV tumor. As of now, the treatment paradigms for gliosarcoma were similar to that of gliosarcoma, including maximal safe resection, post - operative radiotherapy and concurrent and adjuvant chemotherapy. IDH1 mutation and MGMT promoter methylation had certain predictive value for the prognosis. [ABSTRACT FROM AUTHOR]