Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017636 (glioblastoma)
18,345 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Expression of the two types of tumor necrosis factor (TNF) receptor, p55 and p75, in 12 human glioblastoma cell lines was studied. Reverse-transcription polymerase chain reaction detected messenger ribonucleic acid (mRNA) transcripts of p55 TNF receptor in all 12 cell lines tested, but p75 TNF receptor mRNA in only four cell lines. Flow cytometric analysis with anti-p55 and anti-p75 TNF receptor monoclonal antibodies demonstrated both p55 and p75 proteins in these four cell lines, but the level of expression of p75 molecule was very low. Correlation of p55 and p75 TNF receptor expression with TNF-induced growth suppression and production of bioactive molecules (interleukin-6, interleukin-8, manganase-superoxide dismutase, prostaglandin E2) showed that p55 TNF receptor mediates these TNF actions, but none of the responses were influenced by the presence of the p75 TNF receptor, which apparently has no specific role.
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PMID:p55 and p75 tumor necrosis factor receptor expression on human glioblastoma cells. 756 86

Although tumor necrosis factor-alpha (TNF) has been applied to early clinical trials for patients with malignant glioma, majority of human glioma cells has been reported to be resistant to TNF cytocidal effect in vitro. This study investigated antiproliferative effect of the TNF associated with induction of differentiation and expression of two distinct TNF receptors on human glioblastoma cell lines. The expression of p55 and p75 TNF receptors on 12 human glioblastoma cell lines was assessed by polymerase chain reaction and flow cytometry. p55 TNF receptor was detected in all cell lines, and only 4 cell lines concomitantly expressed p75 TNF receptor. Twelve human glioblastoma cell lines were treated with low-dose TNF, up to 256 U/ml for 7 days. TNF did not exhibit its cytocidal effect, but showed antiproliferative effects with inhibition of DNA synthesis in majority of cell lines tested. Flow cytometry with the bromodeoxyuridine-propidium iodide dual staining technique demonstrated that this antiproliferative effect of TNF was attributed to accumulation of glioblastoma cells in G0/G1 phase, suppressing the proliferative pathway. Furthermore the TNF stimulation increased glial fibrillary acidic protein and production of bioactive molecules including interleukin(IL)-6, IL-8, granulocyte-macrophage colony stimulating factor, prostaglandin E2 and manganous superoxide dismutase. In conclusion, human glioblastoma cells had p55 TNF receptor as a functional receptor and well responded to low-dose TNF stimulation, but not susceptible TNF cytocydal effect. The effect of TNF on glioblastoma cells appeared to modulate cell differentiation. TNF may be utilized as an agent for a differentiation therapy for human glioblastomas.
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PMID:[Antiproliferative effect of tumor necrosis factor-alpha on human glioblastoma cells]. 777 79