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)

The modulation of HLA-DR and HLA-A, -B, and -C by human recombinant immune interferon (IFN-gamma) was studied on 10 malignant glioma cell lines established in our laboratory, on 8 clones or subclones derived from these lines, and on a fetal astrocyte cell line. Comparative studies were performed with recombinant leukocyte interferon (IFN-alpha). The results not only confirmed the selective activity of IFN-gamma on the modulation of HLA-DR expression, as opposed to that of IFN-alpha, but also demonstrated a marked heterogeneity in the response of glioma cell lines and their clones to the two types of IFN tested. For example, all 3 clones of an inducible cell line could be modulated to express HLA-DR, whereas only 2 of 5 clones derived from a noninducible line were modulated. This heterogeneity did not seem to be due to the absence of the receptor for IFN-gamma on the surface of these cells, since almost all of the cell lines or clones tested (17 of 19) responded to IFN-gamma by the induction or enhancement of the expression for either HLA-DR or HLA-A, -B, and -C (or both). The heterogeneity of induction was also demonstrated between clones derived from a glioma line that did not express HLA-DR after IFN-gamma treatment. The production of HLA-DR by one of the clones was abundant enough to be confirmed by immunoprecipitation and sodium dodecyl sulfate-polyacrylamide gel electrophoresis analysis.
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PMID:Heterogeneity of the induction of HLA-DR expression by human immune interferon on glioma cell lines and their clones. 308 Jun 35

Treatment of partly purified large granular lymphocytes (LGL) with either IFN-alpha or IFN-gamma for 2 hr augmented their NK cell activity. This augmentation was completely inhibited by the addition of 10 micrograms/ml of cycloheximide. In contrast, when the effects of IFN-gamma on the synthesis of specific proteins in these cells was directly studied by use of two-dimensional gel electrophoresis, we found that IFN-gamma was unable to induce any of the earlier detected, IFN-alpha/IFN-beta-inducible proteins within 18 hr of incubation. No additional, IFN-gamma-induced proteins were detected in either the partly purified LGL or purified T cells. In contrast, the effects of the two factors were comparable in the glioma cell line 251 MG. This shows i) that the effects of IFN-alpha and IFN-gamma are dependent on the responder cell type, ii) that there exists at least one mechanism that can augment NK cell activity that is not dependent on the increased synthesis of the IFN-alpha-inducible proteins, and iii) that either the nine IFN-alpha-inducible proteins are not involved in any leukocyte function that is augmentable by both IFN-alpha and IFN-gamma, or that the two factors exert their actions in leukocyte through different mechanisms.
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PMID:The augmentation of human natural killer cell activity by interferon-gamma is not associated with the induction of the interferon-alpha-inducible proteins. 308 47

Peripheral blood mononuclear cells (PBMC) of malignant glioma-bearing patients were stimulated in vitro with a glucomannan-protein antigen of Candida albicans (GMP) or Interleukin-2 (IL-2), then assayed for proliferation and production of Interferon gamma. PBMC of healthy, age and sex matched subjects were the controls. PBMC from glioma-bearing patients did not differ, as a whole, from PBMC of healthy donors in IL-2 or GMP-induced proliferation. However, they showed a definitely lesser ability to produce IFN. The results are discussed in the framework of the impairment of immune responses known to affect glioma-bearing patients.
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PMID:The response of peripheral blood mononuclear cells of glioma-bearing patients to stimulation with microbial antigen and IL-2: proliferation and IFN-gamma production. 314 74

Peripheral blood mononuclear cells (PBMC) of malignant glioma-bearing patients were stimulated in vitro with Interleukin-2 (IL-2) or a glucomannan-protein antigen of Candida albicans (GMP) then assayed for proliferation, production of IFN-gamma, and generation of cytotoxic effectors against either K562 tumor cell line or freshly-cultured allogenic glioma cells. PBMC of healthy, age and sex-matched subjects were the controls. PBMC of glioma-bearing patients did not differ, as a whole, from PBMC of healthy donors in IL-2 or GMP-induced proliferation. However, they showed a lesser ability to produce IFN as well as a substantial inability to generate cytotoxic effectors following GMP stimulation. PBMC of glioma patients were fully responsive to IL-2 in cytotoxicity generation, as were the PBMC from normal subjects. The results suggest that glioma patients may have a defective antigen-mediated activation of natural cytotoxic effectors. This hyporesponsiveness is not accompanied by depressed lymphoproliferation and does not apparently involve a reduced response to IL-2.
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PMID:Cell-mediated cytotoxicity in glioma-bearing patients: differential responses of peripheral blood mononuclear cells to stimulation with interleukin-2 and microbial antigen. 314 18

We studied the effects of cytokines on cultured microvascular endothelial cells derived from gerbil brain. Microvascular endothelial cells were derived from the endothelial cells of gerbil brain. First, effects of tumor necrosis factor (TNF) or [3H] thymidine up-take by the endothelial cells and human smooth muscle cells were studied. After 4 days exposure to TNF, 50 microCi/ml of [3H] thymidine were added to these cells. [3H] thymidine up-take by the endothelial cells were suppressed by adding TNF dose-dependently. Especially, [3H] thymidine up-take by endothelial cells cultured with 1000 U/ml TNF for 4 days were 25 to 62% of the control values. These cells exposed to 1000 U/ml TNF, furthermore, became spindlelike in appearance and over up each other. But, TNF had no effect on human smooth muscle cells. Second, instead of TNF, interferon-gamma (gamma IFN) were studied in the same way. But, [3H] thymidine up-take by the endothelial cells were not effected by adding gamma IFN. Third, the supernatant of the cultured glioma cells were studied in the same way. The supernatants of 6 glioma cells in 8 cases showed TNF like activity to the endothelial cells of gerbil brain. These supernatants, that is, suppressed [3H] thymidine up-take by the endothelial cells over 50%. These suppression were, furthermore, released by adding 50 microliter anti-TNF antibodies. So, we found the cytotoxic effects of TNF on the endothelial cells of gerbil brain. The supernatants of glioma cells, also, showed TNF like activity to the endothelial cells.
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PMID:[Effects of cytokines on cultured microvascular endothelial cells derived from gerbil brain]. 315 Feb 87

A study was made on the antitumor effect of recombinant murine interferon-beta (rMuIFN-beta) against virus-induced mouse malignant glioma. In in vitro experiments, a dose-dependent and a time-dependent manner were observed for 24 h in the antiproliferative activity of rMuIFN-beta. In in vitro experiments, the growth of subcutaneously transplanted gliomas in mice treated with intraperitoneal administration of rMuIFN-beta was inhibited slightly, whereas, with intratumoral administration, it was inhibited more effectively. In immunological studies, natural killer (NK) cell and cytotoxic T-lymphocyte activities of spleen cells were enhanced with intraperitoneal administration of rMuIFN-beta. The analysis of IFN-induced change in a subpopulation of peripheral blood lymphocytes revealed a decrease of Thy.1,2-positive cells and an increase in the ratio of Lyt.1/Lyt.2-positive cells. But these immunological effects of rMuIFN-beta declined on the 7th day with daily administration. Such hyporeactivity may be noteworthy for the clinical application of IFN.
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PMID:Antitumor effect of recombinant murine interferon-beta against mouse malignant glioma. 349 13

The antineoplastic effects and mechanism of IFN-alpha with a newly designed fluorescent isothiocyanate-labelled IFN-alpha were studied on three established glioma-cell lines and cultured cells of clinical brain tumors. Viability, cell cycle and cells showing positive reaction with fluorescent isothiocyanate-labelled IFN were analyzed by flow cytometry. U373MG glioma cells in contact with 10(4) IU/ml of IFN for 24 hours had a dose dependency, decreased viability, S-phase block in the cell cycle and high rate of positive reaction with fluorescent isothiocyanate-labelled IFN. Two surgical cases, except for one case, showed similar results and other cell lines or meningiomas were not affected by IFN. As the antineoplastic effects of IFN-alpha correlated with the rate of occurrence of positive cells with fluorescent isothiocyanate-labelled IFN, sensitive tumor cells may have a respective specific receptor for IFN-alpha, and, therefore, fluorescent isothiocyanate-labelled IFN-alpha might be of clinical value with regard to the problem of the receptor as well as sensitivity test.
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PMID:[Antineoplastic effects and mechanism of action of IFN-alpha on brain tumors with use of fluorescent isothiocyanate-labelled IFN]. 372 91

The authors report a case of anaplastic oligodendroglioma, in which multiple bone metastases developed about 6 years after the first craniotomy. A 32-year-old woman was admitted because of an apathetic state. CT scan and angiography suggested right frontal glioma. On August 15, 1977, a right frontal lobectomy was performed and histological sections showed anaplastic oligodendroglioma. Postoperative course was uneventful and she was discharged after chemoradiotherapy. In January, 1982, CT scan suggested recurrence of the right frontal tumor. On February 8, 1982, the second craniotomy was performed and this time, local radiation therapy by the afterloading technique (192Ir seed assembly) was given after the operation. In March, 1983, she began to complain of low back pains and multiple bone metastases were found by bone X-Ps and scintigrams. Biopsy of bone metastases was performed and at the same time, the whole body was surveyed for malignant tumors. But no primary cancer other than the right frontal brain tumor was found. In spite of therapy such as IFN, her condition gradually deteriorated and she died in December, 1983. Histological bone biopsy sections showed anaplastic oligodendroglioma much like the histology of the first operation. As the progress of curative means has increased, so has also the number of long-time survivors of malignant brain tumors. And in proportion to the increase in long-time survivors, cases of extracranial metastases may also increase. The etiology, diagnosis and therapy of extracranial metastases from the literature was also studied.
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PMID:[Diffuse bone marrow metastasis of an anaplastic oligodendroglioma]. 405 67

The effects of IFN (interferon) on the activation and differentiation of syngeneic murine malignant glioma-specific killer T cell were investigated in C57BL/6 adult mice in order to clarify the potential usefulness for anti-tumor local immunotherapy. It was confirmed that the specific killer T cell against 20-methylcholanthrene-induced 203-glioma was generated in mice after intracranial and subcutaneous inoculation of the tumor cells. The cytotoxic activities of splenic cells obtained from intracranial and subcutaneous tumor-bearing mice were assessed on MLTC (mixed lymphocyte-tumor cell culture) for 18 hours by microcytotoxicity assay modified Takasugi and Klein's method. The addition of IFN to MLTC resulted in a similar 1.5- to 2.0-fold increase of generated cytotoxic activities. Prior treatment of sensitized splenic cells with IFN resulted in an enhancement of the specific cytotoxic activity for the target tumor cells. IFN enhanced cytotoxic activities in MLTC only in the first 3 hours. These cytotoxic activities were eliminated by the treatment of sensitized lymphocytes with anti-Thy-1 antibody and complement before adding IFN. Therefore, it was found that IFN was able to enhance killer T cell activity of sensitized lymphocytes. Normal lymphocytes did not exhibit any cytotoxic activity even after the treatment with IFN. On the other hand, IFN had a cytostatic effect on the growth of 203-glioma cells. This effect of IFN on 203-glioma cells was not observed when IFN was removed from the suspension (by washing 203-glioma cells).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Effects of interferons on syngeneic murine malignant glioma-specific killer T cell]. 619 74

The immunoregulatory effects of TCGF (T-cell growth factor) on the generation and growth of syngeneic murine malignant glioma (20-methylcholanthrene-induced 203-glioma)-specific killer T-cell were investigated in C57BL/6 adult mice in order to clarify the immunopotential usefulness for anti-tumor local adoptive immunotherapy against malignant brain tumor. TCGF was prepared and assayed. Briefly, 5 x 10(6) ml mouse spleen cells were cultured with 2 microgram/ml concanavalin A in RPMI-1640 medium supplemented with 2% fetal calf serum for 24 hours. Culture supernatants were concentrated by ammonium sulphate precipitation (55 to 80% saturation) and purified by gel filtration (Sephadex G-100, a molecular weight from 30 to 36,000 daltons) and ion exchange chromatography (DEAE-cellulose, elution with 0.15 M in NaCl at ph 7.4). The purified TCGF had no IFN activity. Assays for TCGF was performed for quantitative analysis using 203-glioma-specific killer T cell clone (G-CTLL), which was obtained by limiting dilution method (0.3 cells/well in 96 well microtiter plate) and maintained for over 6 months in the presence of TCGF. Titer (U/ml) of TCGF was defined as the quantity of TCGF required to obtain one-half of the maximal stimulation of G-CTLL proliferation assay. It was confirmed that the specific killer T-cell against 203-glioma was generated in mice after intracranial as well as subcutaneous inoculation of the tumor cells. The killer T-cell activity of spleen cells, however, began to be severely impaired 2 weeks after intracranial inoculation concurrently with the increased intracranial pressure due to developing the tumor growth. Sensitized lymphocytes obtained from intracranial and subcutaneous tumor-bearing mice were assessed for CTL (cytotoxic T-lymphocyte) activity in MLTC (mixed lymphocyte-tumor cell culture) for 18 hours by microcytotoxicity assay. The specific cytotoxicity against 203-glioma cells was enhanced when sensitized lymphocytes from intracranial and subcutaneous tumor-bearing mice were pre-cultured with optimal TCGF (20 U/ml) for over 5 days. After the treatment of sensitized lymphocytes with anti-Thy-1 monoclonal antibody and complement, however, the specific cytotoxicity of sensitized lymphocytes was eliminated almost completely. Therefore, it was thought that TCGF possesses immunoregulatory effects of enhancement of killer T-cell activity. On the contrary, TCGF had no influence on normal T lymphocytes and the growth of 203-glioma cells in vitro.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Effects of TCGF (T-cell growth factor) on experimental malignant glioma-specific killer T-cell]. 660 19


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