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

Oligodendroglioma represents a distinct type of diffuse glioma with a relatively favorable prognosis. Although an O2A-like glial progenitor cell of origin has been suggested, a neuronal-oligodendroglial progenitor cell is also of interest, particularly because variable degrees of neuronal marker expression have been reported in typical oligodendrogliomas. We present 2 female and 2 male patients (ages 34-54) with frontal lobe oligodendrogliomas containing a) morphologically distinct collections of small round cells with hyperchromatic nuclei, b) well-formed Homer Wright-like and perivascular rosettes, and c) demonstrable neuronal differentiation by immunohistochemistry and/or electron microscopy in the rosette-associated regions. Unlike extraventricular neurocytomas, these cases featured an infiltrative growth pattern and a classic oligodendroglioma immunophenotype in non-rosette bearing portions of each tumor. FISH analysis demonstrated chromosome 1p and 19q codeletions in 3 (75%) cases, both in regions with and without rosettes. Recurrences were common, although all patients are currently alive 4 months to 13 yr from initial diagnosis. Based on clinicopathologic and genetic features, we diagnosed these tumors as oligodendrogliomas with neurocytic differentiation. However, it is unclear whether they represent a) gliomas with divergent neuronal differentiation, b) a distinctive form of glioneuronal neoplasm, or c) a reflection of glioneuronal histogenesis in oligodendrogliomas in general. In any case, their occurrence suggests a histogenetic overlap between oligodendroglioma and extraventricular neurocytoma not previously recognized.
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PMID:Oligodendrogliomas with neurocytic differentiation. A report of 4 cases with diagnostic and histogenetic implications. 1243 Jul 11

We examined the mechanism of 17beta-estradiol (estrogen)-mediated inhibition of apoptosis in C6 (rat glioma) cells following exposure to hydrogen peroxide (H(2)O(2)). Cells were preincubated with 4 microM estrogen for 2 h and then exposed to 100 microM H(2)O(2) for 24 h. Exposure to H(2)O(2) caused significant increases in intracellular calcium (Ca(2+)), as determined by fura-2, which was attenuated by preincubation with estrogen. H(2)O(2) and ionomycin caused cell death in a dose-dependent manner, as measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay. Preincubation with estrogen restored viability in cells exposed to H(2)O(2) but not in cells exposed to ionomycin. Western blot analysis showed an increase in Bax/Bcl-2 ratio, calpain activity, and caspase-3 activity following treatment with H(2)O(2), and estrogen pretreatment decreased levels of all three. Cell morphology, as evaluated by Wright staining, indicated apoptosis in cells treated with H(2)O(2), and pretreatment with estrogen reduced apoptosis. Results from MTT and Wright staining were further supported by the terminal deoxyribonucleotidyl transferase (TdT)-mediated dUTP Nick End Labeling (TUNEL) assay. These results indicate a role for estrogen in preventing apoptosis in C6 glial cells exposed to H(2)O(2). Our results suggest that estrogen may have a protective role in minimizing glial cell apoptosis in neurological diseases such as demyelinating disease or central nervous system trauma.
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PMID:Estrogen attenuates oxidative stress-induced apoptosis in C6 glial cells. 1270 34