Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0017638 (glioma)
 30,880 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The antigenic cell surface component NS-5 (nervous system antigen-5) is recognized by antiserum raised in C3H.SW/Sn mice against cerebellum of 4-day-old C57BL/6J mice. When analyzed in the cytotoxicity test the antiserum detects a cell surface antigen or set of antigens present not only an cerebellum but also other parts of the central nervous system, including retina, as well as on mature spermatozoa and to a lesser degree on kidney. All other non-neural tissues tested, liver, splee, thymocytes, muscle, testis, adrenal gland and epidermis do not express detectable amounts of the antigen. Among seven murine tumors of the nervous system, medulloepithelioma shows high levels of NS-5 expression, whereas neuroblastoma Cl300, glioma G26, glioblastome, ependymoblastoma, ependymoblastoma EPA and glioblastoma G26l do not carry detectable NS-5. All mouse strains tested (C57BL/6J, C3H.SW/Sn, C3H/HeDiSn, A/J, AKR/J, BALB/cJ and DBA/2) express similar levels of NS-5. The antigen is demonstrable not only on postnatal day 4 neural tissue, but also in lower amounts on adult nervous system. On embryonic day 9, the earliest stage tested, and at all subsequent stages during embryonic development, NS-K is already present in brain and spinal cord, but not in gut.
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PMID:Nervous system antigen-5, an antigenic cell surface component of neuroectodermal origin. 18 79

In this study, the role of exogenous fatty acids in the regulation of proteolipid protein (PLP) gene expression was investigated using the following model culture system: C6 glioma cells expressing the green-fluorescent protein (eGFP) driven by different segments of PLP promoter. Eicosapentanoic acid (EPA; 20:5 n-3), but not arachidonic acid (AA; 20:4 n-6), induced a significant increase in medium fluorescence intensity (MFI) determined by fluorescence-activated cell sorting (FACS). The induction of PLP promoter was time-dependent showing maximal activity between 24 and 48 h after EPA exposure. PLP promoter activation was dependent on fatty acid concentration, with maximum activation at 200 microM. Northern blot analysis confirmed the fluorescence data in C6 cells incubated with EPA. Furthermore, this treatment increased the adenylyl cyclase-cyclic AMP (cAMP) levels and the mitogen-activated protein kinase (MAPK) activation in C6 cells. PLP promoter activity was inhibited by pre-treatment with H89 (protein kinase A (PKA) inhibitor), but not with PD98059 (MAPK inhibitor), suggesting that EPA stimulates the expression of PLP via cAMP-mediated pathways.
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PMID:Stimulation of myelin proteolipid protein gene expression by eicosapentaenoic acid in C6 glioma cells. 1464 50

n-3 polyunsaturated fatty acids (PUFAs) have been described to have beneficial effects on brain development and in the prevention and treatment of brain damage. C6 glioma cells were incubated with 100 microM of either C20:4n-6 (ARA), or C20:5n-3 (EPA), or C22:6n-3 (DHA) for different time periods to assess whether these acids altered the cellular oxidative state. The ARA and EPA were promptly metabolised to C22:4n-6 and C22:5n-3, respectively, whereas DHA treatment simply increased the amount of DHA in the cells. Cell viability was not affected by ARA, while a cytotoxic effect was observed 72 h after n-3 PUFAs supplementation. The levels of reactive oxygen species and thiobarbituric acid-reactive substances were significantly higher in DHA-treated cells than in EPA- and ARA-treated groups. This modification in the oxidative cellular status was also highlighted by a significant increase in catalase activity and a decrease in glutathione content in DHA-supplemented cells. Glucose-6-phosphate dehydrogenase activity, an enzyme involved in redox regulation, and O2*- release were significantly increased both in EPA and DHA groups. The effect of DHA was more severe than that of EPA. No significant changes were observed in the ARA group with respect to untreated cells. These data show that EPA and DHA induce alterations in the oxidative status that could affect the glial function.
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PMID:Effect of arachidonic, eicosapentaenoic and docosahexaenoic acids on the oxidative status of C6 glioma cells. 1603 67

The San Jacinto River (SJR) waste pits that lie just under the 1-10 overpass in eastern Harris County east of Houston, Texas, USA, were created in the 1960s as dumping grounds for paper mill waste. The deposition of this waste led to accumulation of highly toxic polychlorinated dibenzo-p-dioxins and dibenzofurans (PCCDDs/PCDFs) over the course of several decades. After abandonment, the waste material eventually became submerged under the waters of the SJR, resulting in widespread environmental contamination that currently constitutes a significant health concern for eastern Harris County communities. The original waste pits were rediscovered in 2005, and the San Jacinto waste site is now a designated EPA superfund site. The objective of this review then is to discuss the history and current state of containment around the San Jacinto waste pits and analyze spatial and temporal trends in the PCDD/PCDF deposition through the SJR system from the data available. We will discuss the current exposure and health risks represented by the Superfund site and the SJR system itself, as well as the discovery of liver, kidney, brain (glioma), and retinoblastoma cancer clusters in eastern Harris County across multiple census tracts that border the Superfund site. We will also cover the two primary management options, containment versus removal of the waste from the Superfund and provide recommendations for increased monitoring of existing concentrations of polychlorinated waste in the SJR and its nearby associated communities.
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PMID:A review of the Texas, USA San Jacinto Superfund site and the deposition of polychlorinated dibenzo-p-dioxins and dibenzofurans in the San Jacinto River and Houston Ship Channel. 2766 60