Search results for "oligodendroglioma"

Neural antigens in oligodendrogliomas and dysembryoplastic neuroepithelial tumors

1997

Oligodendrogliomas and dysembryoplastic neuroepithelial tumors (DNT) are frequently associated with epilepsies and share the presence of oligodendroglia-like cells with small round nuclei and optically empty perinuclear halos. The two entities may be difficult to discriminate in small surgical specimens and the origin and differentiation of the oligodendroglia-like cells has been controversial. To better characterize and distinguish the two entities we examined 25 oligodendrogliomas and 16 DNT immunohistochemically for the presence of the proliferation-associated Ki-67 antigen and the following neural antigens: the alpha 1 subunit of the GABAA receptor (GABAR), N-methyl-D-aspartate receptor…

Membrane vesicles shed by oligodendroglioma cells induce neuronal apoptosis.

2006

In order to investigate the mechanism by which oligodendrogliomas cause neuronal damage, media conditioned by G26/24 oligodendroglioma cells, were fractionated into shed vesicles and vesicle-free supernatants, and added to primary cultures of rat fetal cortical neurons. After one night treatment with vesicles, a reproducible, dose-dependent, inhibitory effect on neurite outgrowth was already induced and, after 48-72 h of incubation, neuronal apoptosis was evident. Vesicle-free supernatants and vesicles shed by NIH-3T3 cells had no inhibitory effects on neurons. Western blot analyses showed that treated neurons expressed a decreased amount of neurofilament (NF), growth-associated protein (GA…

TMIC-49. POTASSIUM CHANNEL KIR4.1 AND GLUTAMINE SYNTHETASE ARE DYSREGULATED IN GLIOMA

2017

The potassium channel KIR4.1 (KCNJ10) and the glutamate catalyzing enzyme glutamine synthetase (GS) are highly expressed in glial cells of the central nervous system. Both glial proteins play important roles in the maintenance of neuronal activity and neurotransmission. Dysfunction of both proteins can result in altered neuronal excitability and may lead to excitotoxicity. We analyzed 35 snap frozen tissue blocks (glioblastoma [GBM], n=22; low grade astrocytoma (LGA), n=8; oligodendroglioma (OG), n=3; oligoastrocytoma, n=2). All glioma samples had a matching tissue specimen from both the tumor core and the adjacent normal-appearing infiltration zone. Molecular subtyping (MGMT, IDH1/2, 1p/19…

Oligodendroglioma cells synthesize the differentiation-specific linker histone H1˚ and release it into the extracellular environment through shed ves…

2013

Chromatin remodelling can be involved in some of the epigenetic modifications found in tumor cells. One of the mechanisms at the basis of chromatin dynamics is likely to be synthesis and incorporation of replacement histone variants, such as the H1° linker histone. Regulation of the expression of this protein can thus be critical in tumorigenesis. In developing brain, H1° expression is mainly regulated at the post-transcriptional level and RNA-binding proteins (RBPs) are involved. In the past, attention mainly focused on the whole brain or isolated neurons and little information is available on H1° expression in other brain cells. Even less is known relating to tumor glial cells. In this st…

Oligodendroglioma cells shed microvesicles which contain TRAIL as well as molecular chaperones and induce cell death in astrocytes.

2011

Microvesicles (MVs) shed from G26/24 oligodendroglioma cells were previously reported to cause a reproducible, dose-dependent, inhibitory effect on neurite outgrowth, and eventually neuronal apoptosis, when added to primary cultures of rat cortical neurons. These effects were reduced but not abolished by functional monoclonal antibodies against Fas-L. In order to investigate whether MVs contain other factors able to induce cell death, we tested them for TRAIL and found clear evidence of its presence in the vesicles. This finding suggests the possibility that Fas-L and TRAIL cooperate in inducing brain cell death. Aimed at understanding the route through which the vesicles deliver their mess…

Melanoma cells release extracellular vesicles which contain H1° RNA and RNA-binding proteins

2015

G26/24 oligodendroglioma cells produce EVs that contain pro-apoptotic proteins, such as FasL and TRAIL, able to induce neuronal- [1] and astrocytic- [2] death. Cancer cells release EVs [3] through which transferring proteins, such as extracellular matrix remodelling proteases [4], and H1°, a differentiation-specific histone [5]. By releasing H1°, cells could escape differentiation cues [5]. To verify the role of EVs in releasing specific proteins and mRNAs, in this study we used A375 melanoma cells. EVs were purified from cell culture media as previously reported [1, 2]. T1 RNase-protection assays were performed on total cell lysates and EVs, as described elsewhere [6]. RNA-binding proteins…

Cell death and oxidative stress in gliomas.

1999

In gliomas, apoptosis and necrosis are determined by a number of promoting and inhibiting factors including oxidative cell stress mediated by nitric oxide synthases (NOS) and reduced by superoxide dismutases. Therefore, in 46 gliomas (including astrocytomas, oligodendrogliomas, oligo-astrocytomas, and glioblastomas), the relationship of apoptosis and necrosis and the expression of apoptosis-promoting (p53, bax, Fas, Fas-L) and inhibiting (bcl-2) factors as well as of different isoforms of NOS (NOSb, NOSe, NOSi) and manganese superoxide dismutase (MnSOD) were studied. Apoptosis was measured in situ by the TUNEL method while expression profiles of apoptosis-related and oxidative stress-associ…

COMPOSITION AND EFFECTS OF EXTRACELLULAR VESICLES SHED BY OLIGODENDROGLIOMA CELLS

2011

Microvesicles shed by oligodendroglioma cells and rheumatoid synovial fibroblasts contain aggrecanase activity

2012

Membrane microvesicle shedding is an active process and occurs in viable cells with no signs of apoptosis or necrosis. We report here that microvesicles shed by oligodendroglioma cells contain an ‘aggrecanase’ activity, cleaving aggrecan at sites previously identified as targets for adamalysin metalloproteinases with disintegrin and thrombospondin domains (ADAMTSs). Degradation was inhibited by EDTA, the metalloproteinase inhibitor GM6001 and by tissue inhibitor of metalloproteinases (TIMP)-3, but not by TIMP-1 or TIMP-2. This inhibitor profile indicates that the shed microvesicles contain aggrecanolytic ADAMTS(s) or related TIMP-3-sensitive metalloproteinase(s). The oligodendroglioma cells…

Strategies in Glioma-Surgery

2011

1.1 Epidemiology and classification of gliomas Malignant glioma is one of the most feared diseases in the industrialized nations. About 77% of all malignant tumors within the central nervous system are gliomas. There are about 18.000 newly diagnosed cases annually within the USA (9/100.000 inhabitants per year) and the disease causes about 13.000 deaths each year. Statistically this is a higher loss of life-time than all other tumor-entities together (Schwartzbaum et al., 2006). About 45-50% of these gliomas are histologically classified as gliobalstoma multiforme (GBM) the most aggressive type of glioma which is classified as WHO grade IV (following the classification of Kleihues et al., 2…