Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027819 (neuroblastoma)
 27,800 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two clonal immortalized neurons designated CL8c4.7 and CL8a5.2 were established by somatic cell fusion between a hypoxanthine phosphoribosyltransferase-(HPRT-) deficient neuroblastoma N18TG2 and newborn mouse cerebellar/brain stem neurons. In the serum-containing medium without extra differentiating agents, both clones exhibited a morphology of differentiated neurons. They contained high levels of glutamate but no gamma-aminobutyric acid (GABA). The CL8a5.2 clone synthesized choline acetyltransferase and serotonin. In immunocytochemical studies, both clones expressed 200 kD neurofilament protein, neuron-specific enolase, microtubule-associated protein 2 (MAP2), tau protein, neuronal cell adhesion molecule (N-CAM), HNK-1, Thy-1.2, saxitoxin-binding sodium channel protein, and glutamate. Synaptophysin immunoreactivity was identified in the neuritic terminals of CL8c4.7 cells. Most of these antigens were barely detectable on N18TG2 cells. Electrophysiologically, both clones generated action potentials in response to electrical stimuli. The hybrid clones that express characteristics of differentiated neurons derived from the cerebellar and brain stem regions might be invaluable for the study of the molecular basis of neuronal differentiation and degeneration in these regions.
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PMID:Establishment of mouse-immortalized hybrid clones expressing characteristics of differentiated neurons derived from the cerebellar and brain stem regions. 135 6

During the course of studies of anti-Thy-1-mediated T-cell activation, we found that anti-Thy-1 monoclonal antibodies (mAb) could induce strong homotypic aggregation of murine T-lineage cells. We demonstrated that anti-Thy-1 mAb-mediated T-cell aggregation started at 10 min and reached maximum level 1 hr after addition of antibody. It was temperature dependent, requiring metabolic energy and cytoskeletal integrity similar to that mediated by phorbol myristate acetate (PMA). But the striking difference between anti-Thy-1 mAb-mediated cell aggregation and PMA-mediated cell aggregation was that the latter but not the former was blocked by anti-LFA-1 mAb. This indicates that, unlike treatment with PMA, anti-CD2 mAb or anti-CD3 mAb, anti-Thy-1 mAb treatment of T lymphocytes does not induce LFA-1 activation for cell adhesion. Murine neuroblastoma cells were not induced to aggregate by anti-Thy-1 mAb treatment, although murine T lymphoma cells were aggregated by anti-Thy-1 mAb. The T-lineage cell specificity of anti-Thy-1-mediated aggregation was further shown by the Thy-1 gene transfection into non-Thy-1 expressing cell lines. Thy-1.1 gene transfected mastocytoma cells were not aggregated by anti-Thy-1.1 antibody.
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PMID:Homotypic aggregation of murine T lymphocytes induced by anti-Thy-1 monoclonal antibodies. 167 86

Solid tumour cells were shown to express VLA-beta and Thy-1 antigens. For identification of these molecules two monoclonal antibodies, K-20 and ICO-10, characterised in detail previously, were used. Four groups of solid tumours have been identified according to their immunophenotype: VLA-beta+ and Thy-1-; VLA-beta+ and Thy-1+; VLA-beta- and Thy-1+; VLA-beta- and Thy-1-. To a certain extent these groups have been shown to reflect tumour histogenesis: tumours of epithelial origin never expressed an ICO-10+, K20-phenotype while soft tissue sarcomas and neuroblastoma cells never expressed the beta-chain of VLA molecular complexes.
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PMID:K20 and ICO-10 monoclonal antibodies (gp120/200; Thy-1): immunophenotyping of human solid tumours. 196 60

Freshly isolated cells of murine thymuses and in vitro cultured murine neuroblastoma cells were seeded into microplates, treated with either phorbol myristate acetate (PMA) or dibutyryl-cyclic adenosine monophosphate (DBcAMP), and then processed for enzyme immunoassay to analyze with G4 monoclonal antibody the expression of Thy-1.2 antigen epitope. Pretreatment of thymic cells with PMA resulted in little, if any, decrease of Thy-1 expression, while treatment of these cells with DBcAMP caused a significant down-modulation of the epitope. DBcAMP did not affect binding of another murine IgG antibody to the thymic cells. Modulation of the epitope on thymic cells caused by DBcAMP was dose-dependent with maximal effect seen at the drug concentration of 10(-4) M. However, at various doses of DBcAMP (10(-6) to 10(-3) M) we were unable to detect any significant shift of Thy-1 expression on neuroblastoma cells. Though mechanisms of the above phenomena need further elucidation, we conclude that cellular ELISA may provide a useful alternative to more commonly used cytofluorimetric studies for the analysis of immune cell-surface antigen expression and its pharmacological and physiological modulation.
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PMID:Second messenger-induced modulation of Thy-1 antigen expression: an ELISA study using murine thymic and neuroblastoma cells. 197 51

Hybrid cell lines derived from neonatal rat dorsal root ganglia neurons fused with the mouse neuroblastoma N18Tg2 exhibit sensory neuron-like properties not displayed by the parental neuroblastoma. These properties include an inward (depolarizing) current with a conductance increase in response to activation of a bradykinin receptor, an inward (depolarizing) current with a conductance increase in response to the sensory excitotoxin capsaicin, the expression of sensory neuropeptides (substance P, CGRP and somatostatin), the expression of phosphatidylinositol-anchored molecules including adhesion molecules of the immunoglobulin superfamily that can be regulated in serum-free culture by nerve growth factor (N-CAM, F-3 and Thy-1), and low permissivity to herpes simplex virus infection. These lines thus provide appropriate models for the study of mechanisms involved in nociceptor activation and the regulation of expression of sensory-neuron specific markers including neuropeptides.
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PMID:Novel cell lines display properties of nociceptive sensory neurons. 197 43

ICO - 10 (Thy-1 antigen) and K 20 (gp 120/200) monoclonal antibodies proved suitable for immunophenotyping solid tumors. The following typical antigen combinations were identified with regard to reaction with those antibodies: ICO - 10+ K 20- (neuroblastoma, malignant schwannoma, neurosarcoma and soft tissue sarcomas); K 20+ ICO - 10- (cancer of the tongue and esophagus, adenoma of the adrenal cortex, adenocarcinoma of the stomach, hepatoblastoma and nephroblastoma); ICO - 10+ K 20+ (immature teratoma and cervical and esophageal leiomyoma) and ICO - 10+ K 20- (malignant fibrous histiocytoma).
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PMID:[ICO-10 (Thy-1) and K-20 (gp 120/200) monoclonal antibodies in immunophenotyping of solid tumors in man]. 233 Jun 81

A monoclonal antibody (mAb) (T-199) of IgG1 isotype was raised against medulloblastoma by immunizations of mice with the medulloblastoma cell line TE-671. Studies of the specificity of mAb T-199 on cell lines as well as fresh frozen sections of normal and malignant tissues revealed the antigen in high amounts on the cell surface of neuroectodermally derived tumors such as medulloblastoma, neuroblastoma, retinoblastoma, and astrocytoma. Some melanomas and a subgroup of rhabdomyosarcomas also expressed the antigen. In contrast, mesenchymal tumors, osteosarcomas, and Ewing's sarcomas did not bear the T-199 antigen. Reactivity of T-199 with normal tissues has not been found with few exceptions; in certain areas of the brain, especially in the cerebellum and part of the hypothalamus, in the adrenal glands, and in the pancreatic islet cells small amounts of antigen were detectable. Natural killer cells could also be demonstrated to express the T-199 antigen similar to the NKH-1 antigen. However, despite some striking similarities, the antigens or antigen epitopes recognized by mAbs T-199 and NKH-1 are not identical. Therefore, mAb T-199 seems to detect a unique differentiation antigen on neuroectodermal tumors, coexpressed in low amounts on normal neuroectodermally derived cells and natural killer cells. The pattern of reactivity and the biochemical properties of the T-199 antigen are different from other cell surface markers for neuroectodermal cells coexpressed on natural killer cells or T-cells (HNK-1, NKH-1, or Thy-1). Biochemical analysis of the T-199 antigen showed that it is a heat-labile protein.
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PMID:Monoclonal antibody T-199 directed against human medulloblastoma: characterization of a new antigenic system expressed on neuroectodermal tumors and natural killer cells. 274 22

In normal development the neural crest gives rise to sympathetic neuroblasts, sensory and autonomic ganglia, as well as Schwann cells. One tumor arising from this tissue is the neuroblastoma (NB), a malignancy of the adrenergic component of the sympathetic nervous system. Recent histological studies have shown that neuroblastomas can present with a schwannian cell component, rich in S100 protein. We have investigated the differentiation of NB cell lines, GOTO and RT-LN-1, into a schwannian cell phenotype using bromodeoxyuridine (BrdU). This agent induced morphological changes in these cell lines. Flat-epithelial cells were identified in the GOTO cell line and both flat-epithelial and neuronal phenotypes were found in the RT-LN-1 cell line. S100 protein (beta-Subunit) was induced in both cell lines after 18-25 days of BrdU treatment as determined by enzyme-linked immunoassay. In addition increase in the beta-subunit of S100 protein was identified in BrdU-treated flat-epithelial cells by indirect immunofluorescence using a monoclonal antibody specific for the beta-subunit of the protein. Cyclic nucleotide phosphodiesterase activity significantly increased in both BrdU-treated NB cell lines, as compared with nontreated cells. However no significant increase of glial fibrillary acidic protein in BrdU-treated cells was found either by enzyme-linked immunoassay or indirect immunofluorescence using a monoclonal antibody to glial fibrillary acidic protein. Thus, cells with Schwann cell characteristics can clearly be identified in the neuroblastoma cell lines after BrdU treatment. Fluorescence-activated cell sorting analysis revealed no quantitative changes in cell membrane antigens recognized by monoclonal antibodies UJ-13A (neuroectodermal associated antigen) and anti-Thy-1 (Thy-1) on BrdU treatment. In contrast, UJ-127-11 (neuroectodermal associated) decreased, and W6/32 and BB7.7 (HLA-ABC) and BBM.1 (beta 2-microglobulin) markedly increased in both BrdU-treated cell lines. No induction of L243 (HLA-DR), B7/21 (HLA-DP), and Genox 3.55 (HLA-DQ) was noted. The increased HLA-ABC (HLA class I) antigen may enable BrdU-treated NB cells to be recognized by cytotoxic T-cells. This may be related to the pathological evidence that NB patients whose tumors are rich in S100 protein have a better prognosis. Further studies on the potential of differentiation agents to induce a phenotypic change, that is associated with an improved prognosis for NB patients, are required.
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PMID:Schwannian cell differentiation of human neuroblastoma cell lines in vitro induced by bromodeoxyuridine. 283 49

The expression of eight serologically and biochemically distinct human cell surface antigens defined by monoclonal antibodies was examined on a panel of rodent-human somatic cell hybrids. Cosegregation was observed for human chromosome 11, and surface expression of all eight antigens was studied. Serological analysis of hybrids containing defined segments of human chromosome 11 permitted the regional assignment of genes controlling antigens JF23 (90 kD glycoprotein), G344 (25 kD), T43 (85 kD), A124, and NP13 to chromosome 11pter-q13, and of genes controlling Q14 (130 kD), MC139 (35 kD), and K117 (25 kD) to chromosome 11q13-qter. K117, the putative human Thy-1 antigen, was expressed at high levels in chromosome 11-containing hybrids constructed with mouse neuroblastoma cells, but showed little or no expression in hybrids constructed with mouse L cells. A similar pattern of expression in hybrids was found for MC139, an antigen shared by neuroectoderm-derived cells and normal and malignant T lymphocytes. T43 is a marker of malignant tumors (but not benign tumors) derived from a number of T43- epithelia, and the regional assignment of the T43 locus on chromosome 11 raises questions about its possible involvement in the specific rearrangements of this chromosome seen in human malignancies.
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PMID:Role of human chromosome 11 in determining surface antigenic phenotype of normal and malignant cells. Somatic cell genetic analysis of eight antigens, including putative human Thy-1. 286 25

Thy-1 is a cell surface differentiation marker which shows distinct patterns of tissue-specific expression in different species. In man, the Thy-1 antigen is encoded by chromosome 11. We have examined the regulatory signals determining human Thy-1 expression through serologic analysis of rodent-human somatic cell hybrids retaining human chromosome 11 in which the fusion partners belong to distinct differentiation lineages. Cell surface expression of human Thy-1 was determined by mixed hemadsorption assays with two monoclonal antibodies (mAb), K117 and L127, shown to detect authentic human Thy-1 through analysis of COS-7 monkey kidney cells transfected with a cloned human Thy-1 gene. Three different patterns of human Thy-1 expression were observed when hybrid cells, constructed with different human and rodent cell types, were tested with mAb K117 and L127. Hybrids formed between Thy-1+ human neuroblastoma cells and Thy-1- mouse neuroblastoma cells, or hybrids between Thy-1+ human fibroblasts and the Thy-1- mouse kidney carcinoma, RAG, retain human Thy-1 expression. In contrast, hybrids formed between either Thy-1+ human neuroblastoma cells or Thy-1+ human fibroblasts and Thy-1- mouse L cells lose expression of human Thy-1 even though chromosome 11 is retained. Finally, hybrids formed between Thy-1- human peripheral lymphocytes or a Thy-1- lymphoblastoid B cell line and Thy-1- Chinese hamster fibroblasts begin to express human Thy-1. These studies suggest that both positive and negative trans-acting signals may play a role in the tissue-specific regulation of the human Thy-1 gene.
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PMID:Differential expression of the human Thy-1 gene in rodent-human somatic cell hybrids [corrected]. 288 61


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