The case of a 62-year old man diagnosed with radiation-induced meningioma (RIM) after treatment for astrocytoma with an unusually short latency period of 7 months is reported. The patient first presented with a 2-month history of memory decline. Magnetic resonance imaging (MRI) showed a tumour in the left parieto-temporal lobe. Gross total resection was performed and the tumour was confirmed to be an astrocytoma. The patient received cranial radiotherapy 2 weeks later, however 7 months after radiation treatment the patient presented with headache and vomiting. MRI showed massive meningeal enhancement in the left frontal lobe, which progressively enlarged. The patient's clinical condition deteriorated and a second craniotomy was performed with complete removal of the secondary tumour, which was shown to be a malignant meningioma. Immunohistochemical staining identified CD133-positive cells in both tumours. A rare fraction of brain tumour stem cells (BTSC) was isolated from the primary astrocytoma using a serum-free culture system, suggesting that BTSC may have been involved in the rapid emergence of RIM after resection and radiation of the primary astrocytoma.

Previously, we have reported that tumor necrosis factor receptor super-family member 6b (TNFRSF6B) is overexpressed in glioma tissues, as well as in the supernatant of cultured glioma cells. However, the function of TNFRSF6B in glioma remains unclarified. The aim of the study was to investigate the effect of anti-TNFRSF6B neutralization monoclonal antibody on the malignant phenotype of glioma cells in vitro. Three glioma cell lines U251MG, LN-308 and U87MG were treated with anti-TNFRSF6B antibody. Cell growth, cell cycle, apoptosis and relevant downstream signaling were detected further. We found that anti-TNFRSF6B antibody inhibited cell growth and induced apoptosis in time and dose-dependent manners in the glioma cells tested. Cell cycle was also arrested in G1/S-phase. Furthermore, anti-TNFRSF6B antibody downregulated the level of MMP-2, phospho-ERK1/2 and phospho-AKT. In conclusion, anti-TNFRSF6B treatment might be a critical targeted therapy strategy for gliomas due to its contribution to suppress cell growth and induce apoptosis. Key words: TNFRSF6B, glioma, proliferation, apoptosis, neutralization antibodyMalignant brain tumors are one of the most related causes of morbidity and mortality across a wide range of individuals [1]. Malignant gliomas, i.e., anaplastic astrocytoma and glioblastoma, are particularly aggressive [2]. They are the most frequent class of primary malignant brain tumors in China [3,4]. Many studies on this subject have produced advances in the understanding of glioma biology and pathogenesis and to the improvement of new agents for targeted molecular therapy [5]. However, the median survival of patients with newly diagnosed malignant glioma is only 12-14 months despite advanced therapeutic strategies. Thus, there is an urgent need to discover new biomarkers for the early detection and targeted molecular therapy. Tumor necrosis factor receptor super-family member 6b (TNFRSF6B, also termed as DcR3) locates on 20q13 [6-9] and we have previously reported the overexpression of TNFRSF6B mRNA and protein in sera or tissues of several human malignancies [10-13], including glioma [14]. We found that TNFRSF6B protein was significantly upregulated in glioma tissues, as well as in the supernatants of glioma cell lines and freshly primary cultured glioma cells. TNFRSF6B expression also had a positive correlation with tumor pathological grade. However, the exact role and pathomechanism of TNFRSF6B on the malignant phenotypes of glioma remains unclarified. Previously, our work showed that anti-TNFRSF6B neutralization monoclonal antibody could inhibit cell proliferation, reduce apoptosis and restrain migration ability in hepatocellular carcinoma HepG2 cells. Based on the overexpression of TNFRSF6B in glioma, we speculated that anti-TNFRSF6B neutralization monoclonal antibody could also affect the function of glioma cells. Therefore, in the present study, we treated glioma cells in vitro with anti-TNFRSF6B antibody and explored the effect of anti-TNFRSF6B antibody on the malignant phenotypes of glioma...