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 surface antigenic characteristics of human glial brain tumor (HGBT) cells were studied by complement-dependent cytotoxic antibody assays and indirect membrane immunofluorescence. Eight permanent, well-characterized cell lines derived from human gliomas were used for analysis with antisera raised by hyperimmunization of nonhuman primates (Macaca fascicularis) with glioblastoma multiforme tissue or established HGBT cells lines. Exhaustive absorption of these antisera to remove predominantly antispecies activity rendered HLA nonreactive "preabsorbed" antisera, which reacted with a large panel of gliomatous and nongliomatous human tumor cells; 1 carcinoma, 2 sarcomas, 2 melanomas, 1 neuroblastoma, and 8 HGBT cell lines. Four lymphoblastoid lines and 2 carcinomas were unreactive. After further absorption with a human osteogenic sarcoma cell line, the antisera demonstrated significant levels of reactivity for 8 tested HGBT cell lines and no longer reacted with the nongliomatous cultured tumor cells lines. Therefore, extensive absorption of nonhuman primate anti-human glioma sera removed all activity for the nongliomatous cell lines tested, but it left significant reactivity against a glial tumor cell line-associated antigen(s) present on all 8 human glioma cell lines tested.
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PMID:Surface antigenic characteristics of human glial brain tumor cells. 7 98

HLA typing of 80 glioma patients was determined and the antigen frequencies were compared with 176 normal controls. Increased phenotypic frequencies of Bw35 and DRw1 were observed, but when P values were corrected by the number of antigens tested (35), the results were no longer significant.
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PMID:HLA and glioma. 70 70

Sera from patients with various types of central nervous system tumors display antibodies reactive in serologic assays with cells and extracts derived from human brain neoplasms. Soluble antigens extracted and purified from surgical specimens of human meningiomas (MSA) were used to test for precipitating antibodies in sera from patients with various histologic types of brain tumors, non-neural solid tumors and from normal donors. Blind studies by immunodiffusion (ID) showed that 63% (15/24) of meningioma patients, 53% (9/17) of glioma patients and 17% (5/29) of patients with various other brain neoplasms had antibodies that reacted with two of three meningioma-associated antigens. Sera from normal donors and patients with non-neural solid neoplasms reacted to a limited extent (7/118) with another of these tumor-associated antigens. Cross-reaction and absorption studies revealed that the three meningioma-associated antigens were detecting different antibodies. None of the antigens was related to HLA antigens or to the human non-neurotropic viruses used in our assays.
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PMID:Human meningioma antigens. 80 46

An extensive panel of monoclonal antibodies (MAb) and monospecific antisera reactive against neuroectodermal-, neuronal-, glial-, and lymphoid-associated antigens, extracellular matrix, HLA, and cell-surface receptors was used to characterize the phenotype of four continuous, karyotypically distinct medulloblastoma cell lines and transplantable xenografts. All four cell lines demonstrated significant reactivity with anti-neuroectodermal-associated MAb. No apparent pattern of reactivity with anti-lymphoid MAb was seen; notably, there was a uniform absence of detectable Thy-1. Review of the complete antibody reactivity profile revealed a dichotomy between lines TE-671 and Daoy and lines D283 Med and D341 Med, which have been previously shown to express neurofilament protein in culture and xenografts, and to exhibit neuroblastic morphological features in biopsy and xenograft tissue sections. TE-671 and Daoy reacted with the MAb directed against tenascin, epidermal growth factor (EGF) receptor, HLA-A,B epitopes, beta 2-microglobulin and 5/8 of the glioma-associated antigens, but did not react with the anti-neurofilament protein (NFP) MAb. D283 Med and D341 Med expressed NFP but did not react with MAb against tenascin, EGF receptor, HLA-A,B epitopes, beta 2-microglobulin or 6/8 and 7/8 (respectively) of the glioma-associated antigens. The observed phenotypic differences provide a conceptual framework for investigating basic differences in the biological behavior of medulloblastoma. Moreover, the subdivisions can be evaluated for prospective value in tissue diagnosis, cerebrospinal fluid cytology and antibody-mediated imaging and therapy.
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PMID:Phenotypic analysis of four human medulloblastoma cell lines and transplantable xenografts. 253 15

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

We have investigated the phenotype of seven human glioma cell lines established in vitro from primary tumour explants. Indirect immunofluorescence and flow cytofluorimetry revealed a heterogeneous distribution of surface GE 2 and CG 12 Tumour Associated Antigens (TAA). In one group of cell lines TAA were detected both at the cell surface and in the cytosol, whereas in a second group of glioma cell lines TAA were found only in the cytosol. We have also investigated the sensitivity of glioma-derived cell lines to antibody-toxin and ligand-toxin conjugates (Immunotoxins). Monoclonal antibodies anti GE 2 antigen linked to ricin toxin A subunit (RTA) showed poor cytotoxicity, which increased about 50 fold when the whole toxin was linked to anti GE 2 monoclonals. Treatment with human recombinant interferon gamma (IFN-gamma) greatly augmented the percentage of HLA-DR+ cells and the amount of HLA-DR antigens per cell. IFN-gamma treatment resulted in a net increase of sensitivity to anti HLA-DR Immunotoxins (IT). Human diferric transferrin linked to RTA exhibited a potent cytotoxic effect against human glioma-derived cells when used in the presence of the lysosomotropic carboxylic ionophore monensin.
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PMID:Human glioma cell lines: tumour associated antigens distribution and sensitivity to antibody-toxin or ligand-toxin conjugates. A preliminary report. 326 95

HLA was studied in 35 patients with gliomas (20 anaplastic gliomas, 11 astrocytomas, 2 ependymomas, 2 oligodendrogliomas) and 38 volunteers who served as controls, by using the microdroplet lymphocyte cytotoxicity test. Phenotype frequency (PF), gene frequency (GF) and relative risk (RR) of each HLA antigen were studied statistically with the chi 2-test, where corrected P (CP) less than 0.05 was considered significant. Concerning HLA-B antigens, either Bw 61 or Bw 62 was found in 45.7% of the patients and the both in 14.3%. HLA-Bw 61 had a tendency to increase in the patients (PF = 0.46, GF = 0.27, RR = 7.16, chi 2 = 9.64, P less than 0.002, CP less than 0.064). Contrary to HLA-B antigens, HLA-DRw 6 was absent in the patient (chi 2 = 8.3379, P less than 0.004, CP less than 0.04). No relation between HLA and histological types was found. HLA has its genetic locus on the short brachium of the 6th chromosome and complement C2, C4, properdin, etc are considered to link HLA. Immunoregulatory genes (Ir genes), immunosuppressive genes (Is genes), disease susceptibility genes and disease resistant genes are also considered to link HLA, especially HLA-B, D loci. Although diseases are multifactorial, according to our report, the incidence of HLA-Bw 61 is higher, while that of HLA-DRw 6 is lower in patients with glioma. These phenomena seem very interesting considering the previous evidence that HLA has a close relation between disease susceptibility and immunological competence.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Investigation of HLA in patients with glioma]. 346 15

Serial serological studies were carried out on 19 of 20 patients with malignant gliomas who were actively immunized with one of two human glioma tissue culture cell lines (D-54MG or U-251MG). Most patients mounted a significant serum reaction to histocompatibility antigens (HLA's), as well as an antibody response to fetal bovine serum (FBS) which was added to the glioma-cell inoculum. These two sources of antibody accounted for greater than 90% of the antibody induced by these inoculations. Two patients continued to have significant amounts of binding antibody to the original immunizing cell line following exhaustive absorptions of FBS and these two had all remaining significant antibody removed by further absorption of the serum against the 2-T osteogenic sarcoma tissue culture cell line known to possess antigens cross-reactive with human gliomas. One single patient continued to show significant antibody binding to the original glioma cell line following absorption against FBS, human platelets, and the 2-T cell line, and therefore seems to have produced glioma-distinctive antibodies in response to immunization. The antibody preparation from this patient was also cytotoxic against the original glioma cell line, as well as another recently cultured human glioblastoma cell line. The significance of these serological studies is discussed as it relates to immunological responses patients with gliomas may make to active immunization.
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PMID:Immunobiology of primary intracranial tumors. Part 8: Serological responses to active immunization of patients with anaplastic gliomas. 660 66

The reactivity of a mAb (M16) raised against a small cell lung carcinoma line is described. M16 identifies a surface antigen expressed on cells of neuroectodermal origin following activation, as well as neoplastic transformation. M16 antigen expression is increased on retinoblastoma and neuroblastoma cell lines upon 'in vitro' stimulation and it is induced 'in vivo' on glial cells activated following brain injury. Furthermore, glial tumors show levels of M16 molecule expression increasing with the degree of malignancy, and in a retinoblastoma cell line, the expression of M16 was inversely related to the level of HLA-Class I and N-CAM antigens. The M16 antigen may represent a marker of both activation and neoplastic progression for neuroectodermal cells.
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PMID:Biochemical characterization and membrane expression of an antigen shared by activated and neoplastic cells of neuroectodermal origin. 770 33

Many immune responses are controlled by genes of the major histocompatibility complex (MHC). In humans these include the loci encoding the HLA-A, -B, -C, -DR, -DQ, and -DP antigens, and many diseases have been linked with these. However, little information is available about any connection between malignant tumors and HLA. In this study the possible association of HLA-A, -B, -C and -DR specificities with susceptibilities to malignant glioma was investigated in 42 patients with malignant glioma and 42 controls with non-glial intracranial tumors using the Terasaki-NIH standard method. The data were also compared with those of the 11th International HLA Workshop. The result showed that a high frequency of HLA-24(9) was observed in patients with intracranial malignant gliomas, which was not common in other, non-glial patient groups. In animals the MHC acts in defense against virally induced tumors, but until now there has been no evidence that they do so in human gliomas. Our discovery of its association with an HLA antigen is important for understanding the immunogenetic basis of susceptibility to glioma.
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PMID:Association of malignant glioma with the human leukocyte antigen, HLA-A24(9). 783


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