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)

This publication describes a new model to investigate the influence of tumor necrosis factor-alpha (TNF-alpha) on a three-dimensional glial cell aggregate under defined, standardized, reproducible conditions using the glioma cell line A 172. The cells are initially grown as normal monolayer culture until they reach a cell density of up to 1 x 10(6). Subsequently they are grown as spheroids by the liquid overlay technique. Spheroids grown in this way were divided into ten groups of more than 50 cell aggregates. Three groups were coincubated with free TNF-alpha in increasing dosages (100 ng/ml, 200 ng/ml and 1000 ng/ml); three groups were incubated with empty liposomes (0.2 mg/ml, 0.4 mg/ml and 2 mg/ml); three groups received liposomes which had been loaded with TNF-alpha, and one group, which received no treatment, served as control. The diameter of the spheroids ranged from 80 microns to 350 microns. There was no significant difference in growth between the 3 groups treated with 'free' TNF-alpha. Comparing spheroids treated with TNF-alpha with those which had been coincubated with empty liposomes, there was a significant difference (p < 0.001) in growth, which correlated with the amount of liposomes. Similarly, free TNF-alpha had a significantly (P < 0.001) stronger growth-inhibiting effect as compared to liposomes loaded with TNF-alpha. Comparing the groups treated with liposomes only to those treated with liposomes loaded with TNF-alpha, the latter exhibited a more marked (although not significantly) growth-inhibiting effect. The preliminary conclusion is that the major growth-inhibiting effect seems to be mediated by the liposomes.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Response of multicellular tumor spheroids to liposomes containing TNF-alpha. 796 82

Prostaglandin H synthase (PHS) is a key enzyme in the synthesis of prostaglandins (PGs). Recently, enhanced expression of PHS-2 in brain tumors and the correlation between the PHS-2 level and the histopathological grade of glioma has been reported. Furthermore, in vitro inhibition of glioma cell growth by a specific PHS-2 inhibitor, NS398, has been demonstrated. It has also been shown that prostaglandin E2 (PGE2) contributes to colon carcinogenesis by binding to the prostaglandin E receptor subtype EP1. We therefore evaluated the effects of NS398 and two EP1 antagonists, SC51089 and AH6809, on glioma cell lines. To evaluate mechanisms of NS398's action, two glioma cell lines, a PHS-2-positive cell line (KMG4) and a PHS-2-deficient cell line (A 172), were used. NS398 inhibited both the anchorage-dependent and -independent growth of glioma cell lines regardless of PHS-2 expression, suggesting that some PHS-2-independent mechanisms underlie the antineoplastic effect of NS398. However, the antineoplastic effect was attenuated by the addition of PGE2, which is one of the main products of PHS, suggesting the predominant mechanism is PHS-dependent. The EP1 antagonists, SC51089 and AH6809, inhibited the growth of glioma cell lines in vitro. Furthermore, NS398 or SC51089 slowed tumor growth in vivo, which was assessed using KMG4 tumor xenografts on SCID mice. PHS-2 inhibitors and EP1 antagonists might be useful in the prevention and/or treatment of glioma.
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PMID:Inhibition of human glioma cell growth by a PHS-2 inhibitor, NS398, and a prostaglandin E receptor subtype EP1-selective antagonist, SC51089. 1501 58

Despite progresses in surgery and treatments of malignant gliomas, prognosis of these tumors remains poor, with a median life expectancy of 12 months in glioblastomas. Chemotherapy (mostly with nitrosoureas) has been demonstrated to prolong overall survival, but the entity of this improvement is slight and disease recurrence/progression is the rule, stressing the need for multimodality treatment. In this work we investigated the effect of association of temozolomide (TMZ), an orally bioavailable alkylating agent, with three chemotherapeutic drugs, liposomal doxorubicin (DOXO), cis-platinum (CDDP). and topotecan (TP), on cell growth of A 172, U373, U138, U87, and SW1783 (all human glioma cell lines). Results indicate a synergistic effect (CI < 1) of TMZ in association with liposomal DOXO and CDDP on cell growth inhibition in most of the studied cell lines (A172, U373, U138, U87). Synergistic effect also has been obtained after treatment of A 172 and U373 with TMZ and TP in association. In conclusion, our results confirm the potential effect of association of chemotherapic drugs with different mechanisms of action in the treatment of gliomas.
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PMID:Effect of association of temozolomide with other chemotherapic agents on cell growth inhibition in glioma cell lines. 1530 23

Macrocyclic bisbibenzyls, a class of characteristic components derived from liverworts, are attracting more and more attention because of their wide range of biological significance, including anti-bacterial, anti-fungus, anti-oxidation and cytotoxicity. Herein, we investigated the pro-apoptotic effect of marchantin C on human glioma A 172 cells. The results demonstrated that marchantin C conferred dose-dependent inhibitory effects onto cell growth, viability and colony formation ability of A 172 cells. Morphological observation and DNA laddering assay showed that marchantin C-treated A172 cells displayed outstanding apoptosis characteristics, such as nuclear fragmentation, the appearance of membrane-enclosed apoptotic bodies and DNA laddering fragment. Moreover, flow cytometric detection of phosphatidylserine externalization indicated that marchantin C-induced apoptosis occurred in a dose-dependent manner. RT-PCR and western blot assay further substantiated that marchantin C, as a promising pro-apoptotic agent, had strong effects to induce A172 cell apoptosis, suggesting that the action was achieved through up-regulating Bax and down-regulating Bcl-2.
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PMID:Marchantin C, a macrocyclic bisbibenzyl, induces apoptosis of human glioma A172 cells. 1821 58