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)

The human glioma cell line U-251 MG, with a well-characterized defect in growth control, was sensitive to the antiproliferative effects of human (fibroblast) interferon (IFN). IFN inhibited exponentially growing cells by increasing the number of cells in the S stage of the cell cycle. At the same time the number of cells in Go/G1 diminished. The rate of thymidine incorporation was decreased during the first cell cycle, with no prolongation of S. However, in synchronized cultures, the wave of cells with a S-phase content did not decrease over a time period several hours longer than the length of S measured by pulse labelling. Thus we conclude that, at a sufficient dose, the cells were unable to accomplish cell division as they prematurely stopped synthesizing DNA.
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PMID:Block of glioma cell line in S by interferon. 616 66

The influence of interferon (IFN) on the growth rate and on the radiation sensitivity of 2 human tumour cell lines was investigated. The 2 glioma cell lines (U-118 MG and U-251 MG) were continuously exposed to IFN (100 U/ml) in the culture medium. Irradiation (3 Gy) was performed either on the first day of IF treatment or on day 14 of IFN treatment. The growth delay induced by the treatments was analysed. The results indicated that IFN had an anti-proliferative effect on the 2 cell lines. However, this effect declined during the treatment and after 2 to 3 weeks of continuous IFN treatment, both cell lines had re-established their original growth rate. IFN did not seem to affect the sensitivity of the cells to radiation. Only an additive effect could be observed.
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PMID:Effects of interferon on growth rate and radiation sensitivity of cultured, human glioma cells. 618 24

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

Mouse interferon (IFN) induced in L 929 cells by Newcastle disease virus was examined for its effect on the growth of mouse brain tumor cell line. In this study, we used subcutaneously transplanted 203 Glioma model, which had been originally induced by methylcholanthrene in C 57 BL mice. After subcutaneous transplantation, intraperitoneal administration of IFN was started by following schedule; 5 X 10(3) IU twice a week, 5 X 10(4) IU twice a week, 2.5 X 10(5) IU twice a week, 5 X 10(3) IU every day and 2.5 X 10(4) IU every day. In all groups treated by IFN intraperitoneally, no inhibition of the tumor growth was seen. On the other hand, natural killer (NK) activity was augmented by IFN treatment. Therefore, we considered that augmentation of NK activity was not directly correlated with the antitumor effect of IFN. Then, local administration was examined. After subcutaneous tumor was recognized, 2.5 X 10(4) IU of IFN was injected intratumorally every day. About 20 days later, the tumor decreased its size less than that treated by local injection of saline. It was suggested that the local administration of IFN might be better than the systemic administration.
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PMID:[Effect of interferon on mouse glioma]. 619 81

The anti-tumour effect of mouse interferon (IFN) on an intracranially transplanted 203-glioma in C 57BL mice and the natural killer (NK) activity of spleen cells were studied. As a clinical trial, five patients with glioblastomas were treated with human fibroblast IFN and the anti-tumour effect of IFN and the NK activity of peripheral blood lymphocytes were also studied. The NK activity increased after the beginning of IFN therapy but there was no remarkable anti-tumour effect of IFN in both mouse and human studies. There was no marked correlation between the increased NK activity and the anti-tumour effect of IFN in this study.
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PMID:Single agent therapy of interferon for brain tumours: correlation between natural killer activity and clinical course. 620 58

In the first part of this paper, various chemotherapies were performed against oligodendrogliomas subcutaneously transplanted in to nude mice. Vincristine (VCR), adriamycin, and 1000 rads irradiation were effective against this tumors. Concerning these two drugs, dose response effect was observed. And the effect of 1 mg/kg injection of VCR roughly corresponded to that of five weekly injections of 0.2 mg/kg. In the second part of this experiment, single or combined effects of VCR and immunotherapeutic agents including OK-432 (OK), PSK, and recombinant leucocytic interferon (IFN) were examined. Two glioma lines including oligodendroglioma and glioblastoma were used. Following results were obtained from this experiment: 1) Effect of OK and VCR against oligodendrogliomas were as follows: control less than OK local injection (Local) less than OK intraperitoneal injection (IP); VCR; OK (IP X 2) less than VCR + OK(IP) less than VCR + OK (IP X 2). Effects of OK and VCR were expressed in order of their effects against glioblastomas: control less than VCR less than OK (IP); OK(IP X 2); OK(Local) less than VCR + OK (IP); VCR + OK (IP X 2). Effects of PSK and VCR against glioblastomas were as follows: control; PSK (Local) less than VCR less than VCR + PSK (Local) less than VCR + PSK (IP). Effects of IFN and VCR against oligodendrogliomas were as follows: control; IFN (IP) less than VCR less than IFN (Local) less than VCR + IFN (IP); VCR + IFN (Local). Effects of IFN and VCR against glioblastomas were as follows: control less than IFN (IP) less than VCR; IFN (Local); VCR + IFN (IP).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Immunochemotherapy of human gliomas transplanted into nude mice]. 623 39

The nature of the refractoriness of C6 rat glioma cells to herpes simplex virus type 2 (HSV-2) was examined. Infection of C6 cells with HSV-2 results in low virus yields, not exceeding the input virus. Although virus growth studies suggested a restricted cycle of virus replication, synthesis of HSV-2 DNA and HSV-2-specific antigens could not be detected. In addition, HSV-2 yields in C6 cells were unaffected by interferon, cycloheximide, tunicamycin, actinomycin D and cytosine arabinoside. However, trypsin, but not EDTA, treatment of infected C6 cells at 4 hours postinfection (p.i.) reduced maximal HSV-2 yields at 24 hours p.i. by 61 percent. These data: 1) indicate that HSV-2 fails to replicate in C6 cells and is prohibited from directing the synthesis of virus macromolecules; and 2) suggests that the increment of HSV-2 yields observed during the synthesis phase of the virus growth cycle represents re-envelopment and egress of a portion of the input virus.
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PMID:Abortive infection of neural cells by herpes simplex virus type 2. 629 39

The purposes of the current study were: (1) to investigate the immunoregulatory effects of T-cell growth factor (TCGF) on the activation and differentiation of syngeneic cytotoxic T lymphocyte (CTL) populations generated against a 20-methylcholanthrene-induced ependymoblastoma, 203-glioma, in C57BL/6 mice; and (2) to determine whether the glioma-specific CTL clone (G-CTLL) could be established by TCGF, and whether the in vivo efficacy of the cloned cells could be rendered more effective in adoptive therapy. It was found that TCGF largely allows the CTL populations to proliferate and thus can activate the depressed cytotoxic activity in tumour-bearing mice. Two lines of G-CTLL were successfully obtained by the limiting dilution technique. The G-CTLL retained a TCGF-dependent proliferative growth and a marked cytotoxic activity with target specificity for over 18 months, characterized by a surface phenotype of Lyt-1-.2.3+, Lyt-2 antibody blocking of cytotoxicity and the production of immune interferon in response to mitogen and tumour antigen. In the Winn assay and the adoptive transfer assay, the therapeutic effects were detected in intracranially inoculated tumours in mice. The in vivo efficacy was dependent on the dose of G-CTLL and on the time of the intravenous administration, although the transfer was inversely ineffective in conditions of increased intracranial pressure. The mechanism responsible for the in vivo effect was probably due to the adoptive immunity and/or the tumour-specific interferon production of G-CTLL.
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PMID:Specific adoptive immunotherapy of malignant glioma with long-term cytotoxic T lymphocyte line expanded in T-cell growth factor. Experimental study and future prospects. 661 23

Beta-type human fibroblast interferon inhibited the multiplication of human glioma cells in a dose-dependent manner. The inhibitory effects were thought to be due to suppression of the cells entering the S-phase. After interferon treatment with 5 X 10(3) IU/ml for ten days, the mean cell volume, the soluble protein, and the glial fibrillary acidic protein increased to 970%, 190%, and 380% that of the controls, respectively. The interferon-treated cells changed shape and resembled mature astrocytes. It is presumed that beta-type human fibroblast interferon inhibits DNA synthesis of cultured glial cells and subsequently induces specific differentiated proteins and morphologic alteration.
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PMID:Interferon effects on multiplication, cytoplasmic protein and GFAP content, and morphology in human glioma cells. 667 8

We investigated the effects of local administration of interferon (IFN) on 13 patients with recurrent brain tumors. Histologic diagnoses were glioblastoma (eight patients), medulloblastoma (one), ependymoma (one), ependymoblastoma (one), pontine glioma (one), and astrocytoma (one). When tumor recurrence was evident local administration of IFN was started through an Ommaya reservoir, which was placed during repeat craniotomy. No tumor regressions were seen in the patients given weekly injections of IFN; however, in two of six patients given daily injections, a decrease of tumor volume and augmentation of natural killer activity were seen.
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PMID:Local administration of interferon for malignant brain tumors. 668 76


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