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)

The interferon (IFN)-induced enzyme 2',5'-oligoadenylate (2-5A) synthetase has been implicated in the development of antiviral activity in human and animal cells. However, its role in IFN-mediated growth inhibition remains unclear. To elucidate the function of 2-5A synthetase, we have stably introduced a human 2-5A synthetase cDNA into a human glioblastoma cell line (T98G). Constitutive expression of the cDNA in these cells is associated with increased levels of resistance to infection by encephalomyocarditis virus. One transfected subclone, which expresses elevated levels of 2-5A synthetase enzyme activity, also shows a reduced rate of cellular proliferation.
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PMID:Constitutive expression of a 2',5'-oligoadenylate synthetase cDNA results in increased antiviral activity and growth suppression. 248 99

Human beta-interferon (IFN) induced an antiviral state in two fetal brain and six glioma cell lines. The growth-inhibitory effect of IFN was most pronounced on three glioblastoma lines and least on fetal brain and oligodendroglioma cells; IFN growth inhibition of one schwannoma and one anaplastic cell line was intermediate between the two other groups. Thus, the growth-inhibitory effect of IFN generally correlated with the degree of anaplasia of the tissue from which the cells were derived. IFN (1000 units/ml) had to be present for 24 to 48 hr to have a significant inhibitory effect on growth of glioblastoma (12-18) cells. However, growth inhibition of 12-18 cells exposed to IFN for 3 days persisted for 3 weeks. Both sialic acid-N-acetylgalactosamine ganglioside and a mixture of normal human brain gangliosides (50 microM) inhibited growth of fetal brain (CHII) but not glioblastoma 12-18 cells. However, preincubation of cells with either sialic acid-N-acetylgalactosamine or a mixture of gangliosides did not augment the growth-inhibitory effects of IFN on either CHII or 12-18. These results indicate that gangliosides and IFN may be operating through different mechanisms to cause growth inhibition.
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PMID:Effects of interferon and gangliosides on growth of cultured human glioma and fetal brain cells. 257 69

In order to clarify the mechanism of action of recombinant human leucocyte interferon, the effect of local injection of it to the human malignant gliomas (one oligodendroglioma, the other glioblastoma) transplanted into nude mice were evaluated. The volume of the tumors were calculated as 1/2 (short diameter [cm])2 x (long diameter[cm]). And the ratio of tumor volume (T)/original size (C) were calculated in terms of experimental day. Among the groups of control (vehicle of IFN injected), 1 million units of IFN locally injected group, 3 million units injected group, and 9 million units injected group, the effects of the treatment were statistically evaluated in terms of T/C. At the end of the experiment, each animal was injected 4 mg of BrdU intraperitoneally, and the labeling indices of the tumor tissue were measured and compared among the groups above mentioned. Local injection of IFN to the tumor was effective even at the dose of 1 million units every other day for 16 days for glioblastoma and 50 days for oligodendroglioma. The labeling index of the treated groups was significantly reduced when compared to that of control group in both tumors. And the experiment was performed to evaluate the variation of NK activity and ADCC activity of mouse spleen cells among the experimental groups. For the oligodendroglioma, NK activities were significantly increased in the 9 million units of IFN injected group when compared to those of control group. For glioblastoma, there was no definite variation of NK and ADCC activities among the groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The effect of local injection of interferon against human malignant glioma transplanted into nude mice and the mechanism of its effect]. 259 May 60

A cooperative clinical trial of human fibroblast interferon (BM532) (HuIFN-beta with a specific activity of greater than 1 X 10(7) IU/mg protein; Toray Industries, Inc.) in the treatment of malignant brain tumors was conducted by the neurosurgical departments of 34 medical institutions. The patients admitted to the study had measurable lesions with an established histopathologic diagnosis, and desirably, a favorable performance status. The interferon therapy was instituted after a minimum 4-week interval following termination or completion of previous therapy so that the effect of interferon alone was able to assess. HuIFN-beta was administered either locally (intrathecally or intratumorally) or intravenously in doses of 1 X to 6 X 10(6)IU/body, daily for a period of 8 weeks or longer as a rule. Evaluation of the clinical responses was based primarily upon the findings of CT scans and conformed to Koyama-Saito's criteria. There were a total of 65 patients, 49 males and 16 females, whose clinical responses were amenable to assessment in the study. They were 64 cases of gliomas (neuroectodermal tumors other than glioblastoma) and one case of germinoma. The treatment was effective in 26.2% of all cases and 26.6% of the glioma cases. The efficacy rate was 24.5% (12/49) in the cases administered intravenously at dose of 1 X to 6 X 10(6)IU/body of HuIFN-beta. The efficacy did not vary appreciably with the route of administration of interferon. The response rates for new cases and recurrent cases did not show any significant differences. Side effects occurred in 61.1% of the patients with transient fever being the most common.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Clinical effect of human fibroblast interferon (BM532) on malignant brain tumors--with special reference to gliomas]. 267 Dec 5

In the present study we have evaluated the effect of recombinant human fibroblast, IFN-beta ser, and immune, IFN-gamma, interferon, alone and in combination, on the proliferation of fifteen early passage human glioblastoma cell cultures. Explant cultures were established from glioblastoma tumor tissue obtained at the time of surgery. After sufficient outgrowth, cultures were dispersed with trypsin/versene and maintained as independent cell lines. IFN-beta ser induced a greater than or equal to 50% reduction in the 7 day growth of 6 of the 15 cultures. The majority of cultures, 9 of 15, displayed less than or equal to 50% growth suppression in comparison with control cultures after 7 days exposure to 2000 Units/ml of IFN-beta ser. When treated with 2000 Units/ml of IFN-gamma, only 1 of the 15 glioblastoma cultures exhibited a greater than or equal to 50% reduction in growth. In contrast, when treated with the combination of IFN-beta ser plus IFN-gamma, 1000 Units/ml of each interferon preparation, 12 of 15 cultures were inhibited by greater than or equal to 50% after 7 days growth. The combination of interferons was effective in suppressing glioblastoma growth both in cultures displaying relative sensitivity and those exhibiting innate resistance to either or both types of interferon when employed alone. One glioblastoma culture, G-7, was studied through 45 passages and displayed the same sensitivity at different passages to growth inhibition when exposed to IFN-beta ser, IFN-gamma or both interferons. Based on previous clinical studies indicating that IFN-beta or IFN-gamma when administered alone to patients do not generally alter the clinical progression of malignant gliomas, the present results suggest that the combination of IFN-beta plus IFN-gamma may prove more effective than either agent alone in the clinical treatment of patients with glioblastoma multiforme.
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PMID:Enhanced in vitro growth suppression of human glioblastoma cultures treated with the combination of recombinant fibroblast and immune interferons. 283 97

Human gamma type interferon (IFN) preparations were obtained through phytohemagglutinin stimulation of leukocytes from the peripheral blood. Biological value of these preparations varied between 160 u and 800 u/ml, depending on leukocyte incubation medium, culture system and inductor conservation. The rising of the antiviral activity through association between gamma (3 u) and alpha (27 u) interferons was revealed by the virus quantity reduction (in this case the vesicular stomatitis virus was used) during a 24-hour multiplication cycle. The protection ensured by the mixture of the two types of interferon was about ten times higher than the additive effect of the two preparations. Study of the antiproliferative activity of a gamma interferon preparation was conducted on two human cell lines of tumoral origin (T-10 from a glioblastoma, and HEp-2) and revealed the difficulties to quantify precisely this property of the crude gamma interferon preparations.
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PMID:[Gamma interferon induced in human leukocytes by phytohemagglutinin: its production and biological characteristics]. 284 34

The growth inhibitory effects of the combination of beta-interferon (beta-IFN) and conventional anticancer drugs such as adriamycin (ADM) and ACNU were evaluated in nude mice receiving subcutaneous transplants of human glioblastoma. Next, the anticancer and radiation sensitizing effects of beta-IFN on human glioblastoma was also evaluated in nude mice model. After three weeks of combined treatment, tumour reduction rates (treated/control values) were evaluated by the Battelle's method. In conclusion, the growth inhibitory effect of IFN was most enhanced when IFN was administered following radiotherapy. Furthermore, the combined effect was enhanced in proportion to the dose of radiation.
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PMID:Interactions of human fibroblast interferon with chemotherapeutic agents and radiation against human gliomas in nude mice. 287 8

Purified human natural tumor necrosis factor (n-TNF) was prepared by stimulating human leukemic B cell line (BALL-1) with Sendai virus. The colony formations of all of 18 human cancer-derived abnormal cell lines were suppressed by 10(1)-10(6) U/ml of n-TNF, while n-TNF was nontoxic to all human normal fibroblast cells. This in vitro inhibition of cell growth was reversible. In breast adenocarcinoma MCF7 cells treated with n-TNF a specific decrease of DNA synthesis was observed, and DNA histograms showed a block at G1 in the cell cycle. In vivo studies revealed that n-TNF suppressed the tumor growth of murine Meth A sarcoma, human renal adenocarcinoma (ACHN), malignant melanoma (SK-MEL-28) and glioblastoma (U-373 MG). Isobologram analysis showed that n-TNF synergistically inhibited cell growth in combination with human natural interferon (IFN)-a. In vivo synergism of n-TNF and IFN-a was also found in the U-373 MG tumor model implanted into nude mice.
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PMID:The inhibition of neoplastic cell proliferation with human natural tumor necrosis factor. 303 Sep 86

Antiproliferative and antiviral activities of a type alpha human leukocytic interferon on several heteroploidic cell lines: HeLa, HEp-2, and T-10, a cell line of malignant origin (glioblastoma) were investigated, as compared to subcultures of human embryo fibroblasts. The tumor cell multiplication rate decreased proportionally to the amount of interferon in the culture medium. The highest interferon concentration used in our experiments (1,000 mu/ml) induced a decrease of the normal cell multiplication rate (human embryo fibroblasts). The same amount of interferon had a cytotoxic effect against the T-10 cells, but this phenomenon is reversible if the interferon is excluded after 24 h from the culture medium. There was no quantitative relation between the magnitude of the antiviral and of the cytotoxic effects of the type alpha human interferon on the tested cellular substrates.
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PMID:[Anti-proliferative and antiviral effects of human alpha-interferon on tumor cells]. 303 26

Transforming growth factor-beta (TGF-beta) is known to have a potent inhibitory influence on several immune functions. It has recently been demonstrated that TGF-beta 2 is identical to the glioblastoma-derived T cell suppressor factor (G-TsF). In the present study, human malignant glioma cell lines were incubated with various concentrations of TGF-beta 2. An optimal concentration of 1 ng/ml TGF-beta 2 produced a partial but significant decrease of HLA-DR (class II) surface antigen expression on glioma cells expressing this antigen, as well as decreased levels of HLA-DR-specific mRNA. The surface expression of other HLA-related molecules, such as HLA-ABC (class I) and beta 2-microglobulin, was not influenced by TGF-beta 2. The suppressive effect of TGF-beta 2 on HLA-DR expression, both at the surface antigenic and cytoplasmic mRNA levels, could be completely overcome by adding relatively high concentrations (500 U/ml) of interferon (IFN)-gamma to the culture system. However, TGF-beta 2 inhibited the enhancement of HLA-DR surface expression produced by low concentrations of IFN-gamma on some cells which initially did not express these antigens. These results show that TGF-beta 2 can act as a regulator of HLA-DR antigen expression on human glioma cells.
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PMID:Transforming growth factor-beta 2 down-regulates HLA-DR antigen expression on human malignant glioma cells. 314 81


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