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OBJECTIVEThe (pro)renin receptor (PRR) plays an essential role in the early development of the central nervous system by activating the Wnt/β-catenin signaling pathway. The authors investigated the potential role of the PRR in the pathogenesis of glioma.METHODSThe authors performed immunohistochemical analysis to detect both the PRR and isocitrate dehydrogenase 1 with mutations involving arginine 132 (IDH1R132H) in paraffin sections of 31 gliomas. Expression of the PRR and Wnt pathway components in cultured human glioma cell lines (U251MG, U87MG, and T98G) was measured using Western blotting. The effects of PRR short interfering RNA (siRNA) on glioma cell proliferation (WST-1 assay and direct cell counting) and apoptosis (flow cytometry and the caspase-3 assay) were also examined.RESULTSPRR expression was significantly higher in glioblastoma than in normal tissue or in lower grade glioma, regardless of IDH1R132H mutation. PRR expression was also higher in human glioblastoma cell lines than in human astrocytes. PRR expression showed a significant positive correlation with the Ki-67 labeling index, while it had a significant negative correlation with the survival time of glioma patients. Treatment with PRR siRNA significantly reduced expression of Wnt2, activated β-catenin, and cyclin D1 by human glioblastoma cell lines, and it reduced the proliferative capacity of these cell lines and induced apoptosis.CONCLUSIONSThis is the first evidence that the PRR has an important role in development of glioma by aberrant activation of the Wnt/β-catenin signaling pathway. This receptor may be both a prognostic marker and a therapeutic target for glioma.

The authors report on a case of concurrent herpes simplex encephalitis (HSE) and malignant glioma. The co-occurrence of HSE and malignant glioma is very rare, but it can occur during glioma treatment. Both radiotherapy and chemoradiation with temozolomide can induce viral reactivation, leading to HSE relapse. Careful observation for HSE is necessary when administering chemoradiation to patients with a history of HSE. Antiviral therapy for HSE must be initiated immediately, and the chemoradiation for glioma should be stopped; however, it is not clear what antitumor therapy is optimal when HSE co-occurs during the treatment of glioma.

✓ The authors describe a case of de novo formation and rupture of an aneurysm located at the junction of the left internal carotid artery and the superior hypophyseal artery in a middle-aged woman 2 months after another aneurysm, located on the anterior communicating artery, had been clipped. This case is rare because of the short interval between the last angiographic study performed at the first operation and the diagnosis of the de novo aneurysm; in this case the interval was only 47 days, compared with other cases in the literature in which the intervals were 3 to 34 years. Aneurysms can enlarge considerably in 2 to 4 weeks and can rupture at or soon after their formation. This case provides insight into aneurysm formation and rupture.

✓ A 33-year-old woman with Turcot syndrome harbored a brain tumor and colon cancer and had a familial history of this syndrome. On histological examination, the brain tumor was found to have large and diffusely scattered ganglion cells within a diffuse background of astrocytic cells in a fibrillary matrix. The tumor was diagnosed as a ganglioglioma. No germline mutation in the adenomatous polyposis coli gene was detected using a protein truncation assay. These findings indicate that this patient had brain tumor—polyposis syndrome Type 1 of Turcot syndrome. This is the first report of a ganglioglioma related to Turcot syndrome.

Object. This study was conducted to evaluate the effects of grafting encapsulated basic fibroblast growth factor (bFGF)—secreting cells in rat brains subjected to ischemic injury. Methods. Two cell lines were used for encapsulated grafting in this experiment, namely, a bFGF-secreting cell line established by genetic manipulation of baby hamster kidney (BHK) cells, and a naive BHK cell line. Forty-seven Sprague—Dawley rats were used in this experiment. The animals were divided into the following three groups: those receiving grafts of encapsulated bFGF-secreting cells (BHK-bFGF group); those with grafts of encapsulated naive BHK cells (naive BHK group); and those with no grafts (control group). The authors implanted encapsulated cells into the right striatum of host rats in the BHK-bFGF and naive BHK groups. Six days after grafting, the host and control animals underwent permanent right middle cerebral artery occlusion (MCAO) with an intraluminal suture procedure. The infarct volume was evaluated using 2,3,5-triphenyltetrazolium chloride staining and computerized image analysis 24 hours after MCAO. Fragmentations of DNA in the host brains were analyzed using terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling 12 hours after MCAO. The authors found that the infarct volume in the BHK-bFGF group was reduced by approximately 30% compared with that in the naive BHK and control groups. In the ischemic penumbral area, the number of apoptotic cells in the BHK-bFGF group was significantly decreased compared with that in the other groups. Conclusions. The grafting of encapsulated BHK bFGF-secreting cells protected the brain from ischemic injury. Encapsulation and grafting of genetically engineered cells such as bFGF-secreting cells is thus thought to be a useful method for protection against cerebral ischemia.

ma underwent subtotal resection of the tumor on August 16, 1988. A second subtotal resection for a recurrent tumor in the right parasagittal region was performed on January 22, 1991. Postoperative external-beam radiotherapy (50 Gy in 25 fractions for 36 days) was then administered using a linear accelerator, and the patient was discharged on April 20, 1991 with no neurological deficits. On April 3, 1995, the patient was admitted to a neighborhood hospital because of dyspnea and high fever; 1 month previously he had presented at the same hospital with right-sided hemiparesis and Gerstmann’s syndrome. Magnetic resonance (MR) imaging obtained at that institution revealed a mass in the left parietooccipital lobe and a small lesion in the right paraventricular white matter (Fig. 1 upper left). He was treated for pneumonia, but no specific treatment was given for the brain lesion because of his poor condition. Although the patient’s general condition improved, his neurological signs and symptoms persisted, and he was transferred to our hospital for further treatment on July 17, 1995. Magnetic resonance imaging on admission revealed enlargement of the original lesion compared with its size as seen on initial examination (Fig. 1 upper right). Based on computerized tomography–guided stereotactic biopsy, the patient was started on a course of intravenously administered dexamethasone (8 mg/day) on July 22, 1995; this was tapered for 6 months. The patient’s neurological symptoms markedly improved after treatment was initiated. Magnetic resonance images obtained every 5 months after initiation of dexamethasone treatment revealed a persistent reduction in the enhanced lesions, which correlated with an improvement in clinical symptoms (Fig. 1 lower left and right). The biopsy specimen yielded a diagnosis of delayed radiation necrosis (DRN) (Fig. 2). There are few reports of DRN on MR imaging, and no report of symptomatic multifocal necrosis on serial MR imaging.1–3 Serial MR imaging demonstrated clinical features of DRN and also monitored the response to dexamethasone in this case. Nonresective treatment after diagnosis using stereotactic biopsy was considered an option for management of DRN following radiotherapy of a benign brain tumor.