CD150 (IPO3/SLAM) belongs to the SLAM family of receptors and serves as a major entry receptor for measles virus. CD150 is expressed on normal and malignant cells of the immune system. However, little is known about its expression outside the hematopoietic system, especially tumors of the central nervous system (CNS). Although CD150 was not found in different regions of normal brain tissues, our immunohistochemical study revealed its expression in 77.6% of human CNS tumors, including glioblastoma, anaplastic astrocytoma, diffuse astrocytoma, ependymoma, and others. CD150 was detected in the cytoplasm, but not on the cell surface of glioma cell lines, and it was colocalized with the endoplasmic reticulum and Golgi complex markers. In addition to the full length mRNA of the mCD150 splice isoform, in glioma cells we found a highly expressed novel CD150 transcript (nCD150), containing an 83 bp insert. The insert is derived from a previously unrecognized exon designated Cyt-new, which is located 510 bp downstream of the transmembrane region exon, and is a specific feature of primate SLAMF1. Both mCD150 and nCD150 cDNA variants did not contain any mutations and had the leader sequence. The nCD150 transcript was also detected in normal and malignant B lymphocytes, primary T cells, dendritic cells and macrophages; however, in glioma cells nCD150 was found to be the predominant CD150 isoform. Similarly to mCD150, cell surface expression of nCD150 allows wild type measles virus entry to the cell. Our data indicate that CD150 expression in CNS tumors can be considered a new diagnostic marker and potential target for novel therapeutic approaches.

Eukaryotic elongation factor 1 (eEF1) mediates the binding of aminoacyl-tRNA to the ribosome in GTP-dependent manner. eEF1 consists of four subunits: eEF1A, eEF1Ba, eEF1Bb and eEF1Bg. eEF1A has two different isoforms: eEF1A1 is present throughout development and is ubiquitously expressed with the exception of adult muscle, while eEF1A2 is developmentally regulated and expressed only in muscle cells and neurons. Expression of eEF1A1, eEF1A2, eEF1Ba, eEF1Bb and eEF1Bg genes was analyzed by Northern blot hybridization of a panel of brain tumor and normal brain tissue RNAs. Totally 23 glioblastoma and 10 normal brain samples were investigated. In gliomas, no meaningful difference in the mRNA content for the eEF1A1, eEF1Ba and eEF1Bg subunits as compared to normal brain tissues was found. However, we have observed approximately 2-fold decrease in the eEF1Bb mRNA expression in human gliomas as compared to normal human brain by Northern blot analysis. Besides, we have shown reduced level of the eEF1A2 mRNA expression in glioblastoma as compared to normal human glia.

The aim of the work was to study the impact of fetal rat brain cell supernatant (FRBCS) on the expression of transforming growth factor β1 (TGF-β1) and p53 in C6 cells of rat glioma in vitro. Materials and Methods: FRBCS was obtained from suspensions of fetal rat brain cells on the 14th (E14) day of gestation. C6 glioma cells were cultured for 48 h in the presence of FRBCS or FRBCS + anti-TGF-β1 monoclonal antibody. Immunocytochemical staining for TGF-β1 and p53 was performed. Results: The proportion of TGF-β1-immunopositive tumor cells in C6 glioma cultures was statistically significantly higher than in the control cell cultures of normal fetal rat brain. FRBCS reduced the proportion of TGF-β1-immunopositive tumor cells and increased the proportion of p53-immunopositive cells in C6 glioma cultures. In cells cultured with FRBCS + anti-TGF-β1 monoclonal antibody, the above effects of FRBCS were abrogated. Conclusion: The obtained results suggest that TGF-β1 seems to be responsible for decrease in TGF-β1 expression and increase in p53 expression in C6 glioma cells treated with FRBCS.

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Aim. To investigate protein level of all subunits of the eukaryotic elongation translation factor eEF1H (eEF1A, eEF1Bα, eEF1Bβand eEF1Bγ) in glial tumors of human brain in comparison with normal brain. Methods. The eEF1H components content has been investigated in human glioblastoma clinical samples by Western blot analysis. Results. To determine the eEF1Bα, eEF1Bβ and eEF1Bγ content, the polyclonal antibodies against all eEF1H subunits were obtained. The tendency of the eEF1Bγ protein level to increase in glioblastomas was observed. There were no significant differences in the eEF1A, eEF1Bα and eEF1Bβ protein contents. Conclusions. In the previous report we analysed the expression of all eEF1H subunits in human glial brain tumor on the mRNA level. This study showed that eEF1Bγ was overexpressed while no significant changes in other eEF1H subunits were observed. It suggests a possible function of eEFBg which is cancer-related and is not connected with the functioning of eEF1H complex in translation

Com par i son of gene ex pres sion pro files in hu man nor mal brain and glioblastoma us ing SAGE da ta base revealed 129 genes with 5-fold dif fer ence of ex pres sion level in glioblastoma (P£0.05), 85 of them were down-reg u lated. The num ber of genes with 5-fold down-reg u lated ex pres sion is less in the dif fuse and anaplastic astrocytomas. Five-fold de crease of the ex pres sion in the dif fuse astrocytoma and nearly the same ex pres sion lev els in the anaplastic astrocytoma and glioblastoma were re vealed for 9 genes only. For over whelm ing ma jor ity of in ac ti vated genes in the low-grade astrocytoma the ex pres sion level de creased pro gres sively in the sub se quent stages of ma lig nant pro gres sion of astrocytoma. Ex pres sion lev els of some genes were very low or un de tect able in glioblastoma, the most ag gres sive brain tu mour. The de creased expres sion of se lected genes in glioblastoma was con firmed by North ern anal y sis and RT-PCR. Some genes, de scribed in this work, may en code the tu mour suppressors and their de creased ex pres sion may play an impor tant role in ini ti a tion and pro gres sion of hu man glioma.

Background Ischemic stroke is a major cause of death among patients with systemic hypertension. The narrowing of the brain vascular lumen increases the incidence of stroke and the formation of hyalinosis lesion is an irreversible process that occurs in the late stage of the disease and contributes to the vascular narrowing and stroke. Understanding pathologic mechanisms of brain vascular hyalinosis, thus, should contribute to the development of new therapeutic agents that inhibits and/or reverse the formation of hyalinosis, thereby reducing the incidence of ischemic stroke. Despite the clinical importance of this lesion, properties of brain vascular hyalinosis have not been well investigated. Thus, the present study performed detailed histological examinations of the hyalinosis lesions of postmortem brain vascular tissues of human patients who died of ischemic stroke due to systemic hypertension. Methods & Results Hematoxylin and eosin staining, as well as periodic acid‐Schiff staining, showed the presence of vascular hyalinosis in patient brain tissues. In these lesions, the protein organization of the extracellular matrix was changed, the number and size of smooth muscle cells were altered, and plasma proteins, such as apolipoprotein E and fibrin, infiltrated into the vessel wall. Signs of oxidative stress and lipid peroxidation were also found. These changes are pronounced at the loci of the infiltration of the vessel walls by ApoE. We found increased number of vasa vasorum in adventitia of the small arteries. The formation and deposition of hyaline occur both from the side of the lumen of the artery and from the side of the vase vasorum. Transmission electron microscopy showed that with the development of hyalinosis, the number of smooth muscle cells that undergo atrophy. The deposition of proteins in the arterial wall is also associated with the degree of damage to endothelial cells in the lumen of the vessel and in the vasa vasorum. Conclusions These results demonstrate that, at the beginning of the development of hyalinosis, smooth muscle cells and vasa vasorum are increased. This process seem to involve oxidative stress, which damages endothelial cells both in the lumen of the arteries and in the vasorum vase and contributes to the infiltration of blood plasma proteins into the vascular wall. The resulting hyalinosis decreases the lumen of the arteries and increases the incidence of stroke. Support or Funding Information Supported by NIH

Introduction. The current approach to oligoastrocytoma (OA) treatment includes surgery taking into account the anatomical and physiological accessibility using various radio-and chemotherapy protocols. Nevertheless, it should be recognized that influence of OA histological structure on the surgery of these tumors has not conclusively established.Objective. To improve diagnostic and surgical tactics in oligoastrocytoma by comparing determined clinical-histological patterns. Materials and methods.Retrospective clinical-morphological comparison and analysis of treatment results in 163 patients with OA were performed taking into account histological structure. OAII (WHO) was diagnosed in 32 patients (19.6 %), 131 patients (80.4 %) developed OAIII (WHO). Results. In 52 OA cases (32 %) oligodendroglial component (oOA) prevailed, in 48 OA cases (29 %) astrocytic component (aOA) prevailed, in 63 OA cases (39 %) there was relatively equal cells distribution of both components (оаОА). The surgical treatment of 163 patients included the following: gross total removal, 60 patients (31.4 %); subtotal removal, 98 patients (60.2 %); and partial removal, 4 patients (2.4 %). A total of 106 (65.0 %) patients presented with Karnofsky Performance Status Scale (KPS) ≥ 80. One hundred and fifty-three patients (93.9 %) experienced postsurgery KPS ≥ 80. There was no perioperative death. All 163 patients received radiation therapy and 87 patients (53.4 %) received chemotherapy as well. A significant difference (p< 0.05) in overall survival (OS) was found between surgery results of OA histological groups. Clinical and MRI/CT findings significantly correlated with histological types of OA as well as results of treatment: the overall survival in patients with oOA was 100.5 ± 4.6 months, aOA -48.2 ± 4.5 months, oaOA -76.6 ± 4.9 months, averaging 49.9 ± 2.4 months. Conclusions.Diagnosing, surgery, and survival of OA are determined by the uniqueness of the histological structure of these tumors, the interaction of their components, topography and expansion direction. The key to successful results is a differential approach to planning diagnostic tactics, method of removal and management in late post-op period.