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)

Type beta transforming growth factor (beta-TGF) is a potent regulator of cell growth and differentiation. The human glioblastoma cell line, T-MGI, was growth inhibited by beta-TGF under anchorage independent conditions. The antiproliferative effect of beta-TGF was potentiated to nearly total arrest by low doses of retinoic acid (RA) or tumor necrosis factor (TNF), while epidermal growth factor, platelet-derived growth factor, interleukin-2, and gamma interferon did not have this potentiating effect. The potentiation of the beta-TGF effect by RA and TNF could not be explained by modulation of the epidermal growth factor receptor, the beta-TGF receptor, or the TNF receptor. beta-TGF alone and in combination with RA or TNF were further tested on primary cultures from freshly resected human glioma biopsies (n = 13). There was great individual variation in sensitivity to beta-TGF, RA, or TNF. The astrocytoma and oligodendroglioma cells were inhibited to various degrees by beta-TGF or TNF, while most of the glioblastomas were not sensitive to these agents. Most of the biopsies were stimulated by RA. RA or TNF did not potentiate the growth inhibitory effect of beta-TGF on biopsy cells. We therefore think it unlikely that beta-TGF in combination with RA or TNF will be effective agents in the treatment of gliomas.
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PMID:Effects of type beta transforming growth factor in combination with retinoic acid or tumor necrosis factor on proliferation of a human glioblastoma cell line and clonogenic cells from freshly resected human brain tumors. 316 58

Growth of cultured human glioblastoma cells was profoundly inhibited by concentrated lymphokines prepared from mitogen-activated blood mononuclear cells of normal donors. Cloning efficiency of glioma cells and their absolute number were decreased as well. Partially purified leukoregulin, free of lymphotoxin, tumor necrosis factor and gamma-interferon, similarly suppressed DNA synthesis and clonogenicity. The decrease in absolute numbers of tumor target cells indicated that leukoregulin was directly cytolytic as well as cytostatic for human glioblastoma cells. Our data indicate that leukoregulin is at least one of the factors produced by activated lymphocytes which inhibits the proliferation of human glioblastoma in vitro.
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PMID:Leukoregulin inhibits the growth of human glioblastoma in vitro. 376 Jan 59

Colony growth in soft agar was used to identify human tumors that were sensitive to the direct antiproliferative effects of mismatched dsRNA (Ampligen). The results suggest that different human solid malignancies vary significantly in their sensitivity to Ampligen. Tumors with 50% or more of their surgical specimens showing sensitivity included carcinoid, glioblastoma, and carcinomas of the kidney, and lung. Resistant tumors (less than 15% sensitivity) included sarcomas and colo-rectal carcinomas. Overall, 42% of the tumor specimens studied showed a 50% or greater reduction in tumor cell colony formation after a single initial treatment with Ampligen (250 micrograms/ml). Interestingly, one patient's tumor which was de novo sensitive to interferon (IFN), but emerged as IFN-resistant following IFN therapy, remained sensitive to Ampligen. Thus, a clonogenic assay may prove useful in identifying human tumors and individuals for clinical trials with Ampligen, including patients resistant to IFN.
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PMID:Antiproliferative effect of mismatched double-stranded RNA on fresh human tumor cells analyzed in a clonogenic assay. 377 78

In a patient with glioblastoma treated with interferon (IFN-alpha) for a long period of time, a high titer of IFN-neutralizing antibody was detected in the serum during and after IFN therapy. Computerized tomography findings and neurological symptoms in this patient were unchanged during IFN therapy. General malaise, fever, anorexia, nausea, and decrease of leukocytes, platelets, erythrocytes, hemoglobin, and hematocrit were recognized transiently as side effects of IFN administration. These side effects were not serious and resolved spontaneously without discontinuation of therapy. The appearance of IFN-neutralizing antibody is clinically important because the antibody probably neutralizes the effect of systemically administered IFN before it reaches the site of action.
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PMID:High titer of interferon (IFN)-neutralizing antibody in a patient with glioblastoma treated with IFN-alpha. Case report. 608 59

Growth of cell-free subacute sclerosing panencephalitis (SSPE) virus was compared with that of measles virus in three human neural cell lines; neuroblastoma, oligodendroglioma, and glioblastoma. The Edmonston strain of measles virus replicated in these neural cells as efficiently as in Vero cells. In contrast, the growth of the Mantooth strain of SSPE virus was suppressed moderately in neuroblastoma cells and markedly in oligodendroglioma and glioblastoma cells in spite of the induction of apparent cytopathic effects in these cells. Virus adsorption, defective interfering particles, interferon, and temperature sensitivity were not responsible for this low yield of SSPE virus in neural cell lines. Synthesis of viral proteins of SSPE virus was slower than that of measles virus in oligodendroglioma and glioblastoma cells. These results suggest that the slow rate of synthesis of viral proteins may be relevant to the low yield of SSPE virus in neural cells.
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PMID:Growth of measles and subacute sclerosing panencephalitis viruses in human neural cell lines. 608 91

Three types of interferon preparation (alpha, beta and gamma) have been used in the treatment of tumours in vivo. At the time of writing no information is available on IFN-gamma treatment of tumour patients. Treatments with IFN-alpha and IFN-beta have been undertaken at many clinical centres. Both types of preparation can exert side effects. Both types have also been able to cause regression of certain tumours in individual patients. At our hospital, IFN-alpha has been given to tumour patients over the last decade. Antitumour effects have been registered on patients with juvenile laryngeal papillomatosis, Hodgkin's disease, myelomatosis, ovarian carcinoma, hypernephroma and glioblastoma. Further study is needed on how therapy with IFN should best be undertaken and also how such treatment compares with other treatments of various tumour diseases. IFN therapy should also be combined with other such treatments.
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PMID:Interferon therapy in neoplastic diseases. 618 85

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

This report presents the results of a phase I trial of the value of human leucocyte interferon-alpha in the treatment of glioblastoma. Twelve patients entered the trial. In one case we believe that the patient benefitted from the interferon treatment. CT scans of patients on interferon did not reveal the true extent of the tumorous tissue.
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PMID:The effect of systemic human interferon-alpha administration to patients with glioblastoma multiforme. 630 69

Human peripheral blood mononuclear cells from normal donors obtained by separation on a Percoll gradient were incubated with free or liposome-entrapped lymphokines produced from concanavalin A-stimulated lymphocytes and then were tested for cytotoxic activity against tumor cells. The treated monocytes lysed tumorigenic melanoma and glioblastoma target cells, but had no effect on three types of nontumorigenic target cells. The activation of monocytes to become tumoricidal was caused by macrophage-activating factor (MAF) and not by contamination with endotoxins, concanavalin A, or interferon. The endocytosis of liposomes containing MAF, but not of those containing control supernatants, led to the activation of cytotoxic properties in the monocytes. Activation by liposome-encapsulated MAF was very efficient and required less than 1/800th of the amount of free MAF necessary to achieve the same levels of cytotoxicity. Thus, the encapsulation of mitogen-induced MAF in liposomes could provide an effective approach for the activation of blood monocytes in situ.
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PMID:Tumoricidal activity of human monocytes activated in vitro by free and liposome-encapsulated human lymphokines. 634 87

Phase I and phase II clinical studies of interferon (IFN) were conducted in malignant brain tumours (47 cases of glioblastoma, medulloblastoma and others) using three preparations of the drug. The drug was administered daily in doses 3.0 - 9.0 X 10(6) I.U. locally or intravenously (beta-type) or intramuscularly (alpha-type). The administration was continued as many days as possible, eight weeks being the shortest period. The efficacy of the therapy was assessed mainly by the CT findings (computed volume of the tumour). As for efficacy against glioblastomas, the highest effectiveness rate (40%) was obtained with Human Fibroblast IFN (HFIF) (beta-type) (Toray) (one case of complete remission and seven cases of partial remission out of 20 cases) as compared to Human Lymphoblastoid IFN (HLBI) (alpha a-type) (Wellcome) (one case of partial remission out of three cases) and recombinant IFN (rIFN-alpha A) (alpha-type) (Roche) (two cases of partial remission out of nine cases). The high rate of responsiveness of HFIF seems to be largely attributable to the local, rather than systemic, administration of the drug. Our pharmacokinetic study revealed that, by means of intrathecal administration a much higher IFN titre was detected in the cerebrospinal fluid, while by intravenous or intramuscular route, the IFN titre in the CSF was undetectably low. The generally lower incidence of side-effects with HFIF compared to other preparations was also largely ascribable to the route of administration. IFN therapy in combination with radiotherapy and/or chemotherapy should also be investigated.
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PMID:Clinical effect of interferon in malignant brain tumours. 637 11


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