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)

Immunophenotype (IP) analysis of 14 childhood glial tumors was performed with a library of 16 monoclonal antibodies (MAbs) using biotin-streptavidin-alkaline phosphatase immunohistochemical detection technique. Presence of glial or neuronal differentiated cells within the tumors was evaluated with MAbs against cell-lineage-specific markers: high-, medium- and low-molecular-weight neurofilament protein (NFP) and glial fibrillary acidic protein (GFAP). Intense expression of GFAP was demonstrated in 14/14 astrocytomas. The three NFs were detected in 10-50% of the cells in 6/14 cases. The pan-neuro-ectodermal antigen defined by MAb UJ 13/A was present in 7/14 astrocytomas on more than 10% of the cells. Thy-1 was expressed in 14/14 tumors on more than 50% of their cells. The GQ ganglioside antigen detected by MAB A2B5, was found in 12/14 tumors. Shared antigens exist among morphologically benign and malignant glial tumor cells and leukocytes detectable with the following four MAbs: Thy-1, PI 153/3, UJ 308 and anti-HLe, common leukocyte antigen (CLA). CLA-expressing cells were demonstrated in 8/12 astrocytomas, and in 4/12 cases more than 90% of the cells were positive. We have shown that cells within childhood astrocytomas can express neuronal IP. The most common expressed phenotype for glial tumors was: GFAP+, Thy-1+, A2B5+, UJ 167.11+, UJ 223.8+, NF (H,M)+, UJ 13/A+, UJ 127.11-, and NF (L)-.
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PMID:Immunophenotyping of childhood astrocytomas with a library of monoclonal antibodies. 216 98

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

The growth of PC12 cells on a collagen substratum or on monolayers of several non-neuronal cell types was studied by measuring nerve growth factor (NGF)-dependent increases in the expression of a 150 X 10(3) (Mr) neurofilament protein subunit and the membrane glycoprotein Thy-1. Both responses were found to be greatly suppressed in cultures of fibroblasts as compared to the C2 and G8-1 muscle cell lines and the C6 glioma cell line. This suppression was associated with an inhibition of NGF-dependent neuritic outgrowth from PC12 cells grown on fibroblast monolayers. There was no evidence that fibroblasts secrete soluble molecules that directly inhibit these responses or neutralize NGF. In addition, there was no difference in the neurofilament protein response from PC12 cells that had been treated with NGF prior to coculture, and the now primed PC12 cells readily extended axons over fibroblast monolayers. These data demonstrate that cell-cell and/or cell-matrix interactions can modulate biochemical responses to NGF and suggest that responsiveness of neuronal cells to environmental cues is not immutable. Control of the latter may be at the level of expression of receptor molecules for cell-surface- or matrix-associated macromolecules and a similar mechanism operating during development could play a role in growth cone guidance.
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PMID:Cell-cell interactions modulate the responsiveness of PC12 cells to nerve growth factor. 350 97

Neuroblastoma (NB) arises from primitive sympathetic neuroblasts in the adrenal gland or the sympathetic ganglion. NB in situ, sometimes observed in the adrenal glands of autopsied infants, is considered to be a premalignant lesion that may develop into NB. Little is understood about the morphological and biochemical changes that accompany this malignant progression. In this study, a unique monoclonal antibody, KP-NAC8, raised against a human NB cell line is described. This binds to NB cells but not to fetal neuroblasts. The antibody recognizes a Mr 200,000 surface protein on NB cells. KP-NAC8 binds to 15 of 17 human NB cell lines and all 26 fresh NB samples either from tumor tissues or from marrow aspirates involved with tumor. The antibody was found to cross-react with some other tumor cell lines, namely, Ewing's sarcoma (1 of 2), melanoma (1 of 4), lung cancer (3 of 3), and leukemia (2 of 14) cell lines. However, KP-NAC8 did not bind to any rhabdomyosarcoma (0 of 4), Wilms' tumor (0 of 4), retinoblastoma (0 of 2), glioma (0 of 4), and gastric cancer (0 of 2) cell lines examined. Among fetal tissues, KP-NAC8 did not react with normal neuroblasts in the adrenal glands of 5 fetuses. In a further study, the membrane phenotype of fetal adrenal neuroblasts was analyzed by a panel of 12 monoclonal antibodies including KP-NAC8. A comparison of the binding of the same panel of antibodies to fresh NB revealed that antibodies UJ13A, UJ127:11, PI153/3, anti-Thy-1, A2B5, BA-1, BA-2, HSAN1.2, and Leu-7 bound to both fetal adrenal neuroblasts and NB cells. Monoclonal antibodies OKIa-1 and J5 did not bind to either tissues. The only antibody that could distinguish fetal adrenal neuroblasts from NB cells was KP-NAC8. KP-NAC8 may, therefore, define a differentiation-related antigen that may prove helpful in understanding the biological nature of NB and NB in situ.
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PMID:Cell surface membrane antigen present on neuroblastoma cells but not fetal neuroblasts recognized by a monoclonal antibody (KP-NAC8). 356 10

Antibodies to the differentation antigen Thy-1 were linked via a dextran-hydrazide bridge to adriamycin. These monoclonal antibodies, which were previously prepared against first-trimester human fetal cells, reacted with several human brain tissue tumors such as neuroblastoma, glioma, and leiomyosarcoma through a common differentiation antigen, Thy-1. The conjugates were tested in vitro for their cytotoxic effects on a neuroblastoma cell line LA-N-I. The conjugate maintained its full drug and antibody activities. Moreover, the specific conjugate exhibited a higher efficacy in inhibition of RNA synthesis and was more cytotoxic than the nonspecific Ig-drug conjugate. Fluorescent microscopy showed that the specific conjugate was able to penetrate the cell membrane. Both the specific antibody and the drug were also observed to accumulate in the cell nucleus. Flow microfluorometric analysis of cellular DNA traverse showed that the specific antibody-drug conjugate caused a higher accumulation of neuroblastoma cells in stage G2 of the cell cycle than did the free drug, perhaps indicating a more efficient prevention of the progression of cells through mitosis.
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PMID:A conjugate of adriamycin and monoclonal antibodies to Thy-1 antigen inhibits human neuroblastoma cells in vitro. 614 73

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

We have investigated the antigenic heterogeneity of human glioma cells and its correlation with other parameters of tumor cell heterogeneity (karyotype, 2':3' cyclic nucleotide 3'-phosphohydrolase expression, in vitro morphology) using the established human glioma cell line D-54 MG and eight single-cell-derived clones. The panel of antibodies used included 3 previously described heterologous sera raised against human gliomas and lamb oligodendroglia and 10 monoclonal antibodies with demonstrated reactivity for tumors of neuroectodermal origin, human fetal tissue, or human Thy-1. Antigen expression was determined by cell surface radioimmunoassay and peroxidase-antiperoxidase immunohistology. The use of a monoclonal antibody panel composed of ten reagents of varied specificity resulted in the demonstration of highly variable and complex antigenic patterns on the cell surfaces of cloned subpopulations of the human glioma cell line D-54 MG. Only one antigen, human Thy-1, was present on the parent line and all clones; the remaining nine antigens exhibited a distribution unrelated to other predictive parameters of genotypic or phenotypic heterogeneity such as karyotype, 2':3' cyclic nucleotide 3'-phosphohydrolase expression, or in vitro morphology. With the exception of clones 3 and 4, which shared a common antigen profile but exhibited distinctly different in vitro morphological patterns, the detected antigenic profile of each clone was distinct, with the proportion of expressed antigens ranging from 2 of 10 (clone 2) to 10 of 10 (clone 1). The demonstration of distinct, selectively maintained cell subpopulations within a human glioma cell line has direct implications for immunotherapeutic designs.
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PMID:Demonstration of complex antigenic heterogeneity in a human glioma cell line and eight derived clones by specific monoclonal antibodies. 630 81

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

The effects of adult thymectomy in C 57 BL/6 mice on in vivo and in vitro responses to syngeneic methylcholanthrene-induced glioma (203-glioma) were investigated in order to analyse the role of T cell subpopulation in relation to the antitumor immunity. The tumor growth in adult mice thymectomized 3 weeks before subcutaneous inoculation of tumor cells was significantly suppressed. On the other hand, in mice thymectomized 7 or 10 weeks before tumor cell inoculation, the tumor growth was enhanced resulting in shorter mean survival time. The cytotoxic activity of the regional lymph node T cells in the former mice was increased from the beginning after tumor cell inoculation with peak observed on day 14 and maintained for about 4 weeks, while it was extremely decreased in the latter mice. The marked enhancement of cytotoxic activity in the former mice is probably due to a reduced proportion of short-lived T lymphocyte population after adult thymectomy. In contrast, the low level of cytotoxic activity in the latter mice may be due to a gradual reduction of long-lived T lymphocyte population in addition to short-lived T lymphocyte population after adult thymectomy. The cytotoxic activity was specific for 203-glioma cells and almost completely eliminated with anti-Thy-1 monoclonal antibody and complement. The surface markers of these killer T cells were checked with the results that in normal mice Lyt-1-.2.3+ and Lyt-1+.2.3+ cells participate in cytotoxic reaction. In mice thymectomized 3-10 weeks before tumor cell inoculation, however, Lyt-1+.2.3+ killer T cells were not detected suggesting strongly that the progenitors of Lyt-1+.2.3+ killer T cells are short-lived cells in contrast to those of Lyt-1-.2.3+ killer T cells which survive more than 10 weeks after adult thymectomy. The tumor growth was also significantly suppressed by the intravenous adoptive transfer of sensitized lymphocytes obtained from mice thymectomized 3 weeks before tumor cell inoculation. This effect of tumor suppression was disappeared by the pretreatment of infused lymphocytes with anti-Thy-1 monoclonal antibody and complement. These evidences may suggest that in tumor bearing mice short-lived suppressor T cells or their precursors exist and regulate the growth and differentiation of killer T cells and that adult thymectomy affects immunoregulation, possibly by altering the generation of suppressor T cells.
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PMID:[Effects of adult thymectomy on the growth of 203-glioma in mice--analysis of T cell subpopulation in tumor immunology]. 698 37

Changes of natural killer activity (NK activity) by local 60Co irradiation in intracranial tumor-bearing mice were studied by the method of 51Cr release assay. Local irradiation was administered 10 days after intracranial transplantation of 203-Glioma which had been originally induced by 20-methylcholanthrene in C 57 BL mice. Irradiation suppressed the growth of tumor and prolonged the mean survival time. The 50% survival time of untreated mice was about 2.5 weeks but that of mice treated by a single dose of 1000 rad and 1500 rad of irradiation was about 4.5 weeks and 6.5 weeks respectively. NK activity of spleen cells in these mice was serially examined. NK activity was gradually increased in mice treated by local irradiation, while it was gradually decreased in mice without treatment. On the other hand, NK activity remained unchanged in non-tumor-bearing control mice. Mice treated with 1000 rad and 1500 rad of irradiation showed 44.0% and 47.6% of % specific 51Cr release respectively 11 days after irradiation while normal mice showed 18.0%. The increased NK activity after local irradiation suggested that local irradiation might have enhanced the immunological defence mechanism against the tumor in the tumor-bearing hosts. Some characteristics of effector cells in this assay system were examined. The cytotoxicity of spleen cells was removed by the treatment of anti-BAT serum and complement but was not removed by the treatment of anti-Thy-1. 2 serum and complement. Since NK activity reflects the immunological resistance to tumors to some extent, it is felt important to clarify the significance of changes of NK activity in patients with brain tumors in relation to various treatments including surgery, radiotherapy, chemotherapy and immunotherapy in the next step.
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PMID:[Changes of natural killer activity following local 60Co irradiation in intracranial tumor-bearing mice (author's transl)]. 709 76


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