The specimen was small in quantity but nonetheless, revealed the typical features of PTPR, which were tumor cells with vacuolated cytoplasm forming a pseudopapillary architecture. The PCI-32765 supplier tumor cells were diffusely immunoreactive for vimentin, INI-1 and c-Kit, focally immunoreactive for neuronal specific enolase (NSE) and S100 protein but

negative for cytokeratin, epithelial membrane antigen (EMA), synaptophysin and GFAP. Ultrastructurally, the tumor cells revealed variably-sized cytoplasmic vacuoles, intermediate filaments and villous cytoplasmic membrane. With these features, a diagnosis of PTPR was rendered. The lesions at the pineal gland and bilateral IAC were irradiated through gamma knife radiosurgery and a decrease in size of the lesions was noted on follow-up MRI. However, soon after, other lesions were also noted to develop along the adjacent sites. The case presented is proof that PTPR can disseminate to other sites distant from the original lesion. This case was a c-kit expressing PTPR, which might represent the more primitive nature of this tumor. Ultrastructural examination is useful to differentiate PTPR from other tumors of the pineal gland in addition to immunohistochemistry. “
“Atypical teratoid/rhabdoid tumors (AT/RT) are aggressive embryonal tumors having a poor prognosis and are associated with mutations in the tumor suppressor gene hSNF5/SMARCB1/INI1. Differential diagnosis includes choroid plexus

carcinoma which has occasionally been attributed as showing an inactivation of INI1/SMARCB1 nuclear staining in immunohistochemistry. However, these findings CHIR-99021 mw have been challenged by others. We therefore examined eight AT/RTs from six patients by immunohistochemistry for membranous expression of the inward rectifier potassium channel Kir7.1, which was in the central nervous system so far considered specific for choroid plexus IMP dehydrogenase tumors and normal choroid plexus epithelium. Two AT/RT cases exhibited membranous staining of Kir7.1, indicating a plexus epithelial differentiation of these tumors. The implications of these results on tumor diagnosis are discussed. “
“Insufficient oligodendroglial

differentiation of oligodendroglial progenitor cells (OPCs) is suggested to be responsible for remyelination failure and astroglial scar formation in Theiler’s murine encephalomyelitis (TME). The aim of the present study is to identify molecular key regulators of OPC differentiation in TME, and to dissect their mechanism of action in vitro. TME virus (TMEV) infected SJL/J-mice were evaluated by rotarod analysis, histopathology, immunohistology, and gene expression microarray analysis. The STAT3 pathway was activated using meteorin and inhibited using STAT3 inhibitor VII in the glial progenitor cell line BO-1 and in primary rat OPCs in vitro. As expected, immunohistology demonstrated progressively decreasing myelin basic protein-positive white matter in TME.