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)

The binding of [3H]cyclosporine A (CsA) to BALB/c mouse spleen cells was examined with a novel centrifugation assay which rapidly removes free [3H]CsA from cell surfaces with a minimal loss of low affinity specifically bound [3H]CsA. A single class of specific and saturable CsA binding sites was found under equilibrium binding conditions. Scatchard analysis of the data resulted in a straight line with KD and Bmax values of 95 nM and 2.4 million binding sites/cell, respectively. Kinetic studies conducted with a wider range of [3H]CsA concentrations revealed two distinct binding sites, with KD's of 290 nM and 9.6 microM, respectively. [3H]CsA bound only nonspecifically to phosphatidylcholine:cholesterol liposomes. Specific [3H]CsA binding sites were found in murine WEHI-5 B-lymphoma cells, murine N1E-115 neuroblastoma cells and human A204 rhabdosarcoma cells. We conclude from these results that there are at least two nonlipid CsA binding sites in BALB/c mouse spleen cells and that CsA binding sites are present in both lymphoid and nonlymphoid tissue.
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PMID:A novel cyclosporine binding assay. 348 40

Statistical procedures were used to estimate lectin receptor distribution on the surface of ascite lymphoma cells, neuroblastoma C-1300 cells and of transformed human T- and B-derived lymphoid cell lines. Relationships between the arithmetic means and mean square variances for sample populations from each cell and ferritin- or colloidal gold-lectin combination were used to define four types of topographical distributions: uniform-ordered, uniform-random, random and clustered.
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PMID:[Evaluation of the distribution of lectin receptors on the surface of tumor and transformed cells using methods of variation statistics]. 360 7

Graft-versus-host disease is a complication of transfusion of nonirradiated blood products into an immunocompromised patient, and it has been reported in hematologic and lymphoid malignancies as well as in neuroblastoma in children. We report the first case of acute graft-versus-host disease in a child undergoing chemotherapy for a rhabdomyosarcoma, who received transfusions during an intercurrent illness. The graft-versus-host disease was accompanied by an allogeneic lymphoid graft and was diagnosed on the basis of HLA studies on the patient's and her family's circulating lymphocytes and confirmed by HLA typing of the patient's skin fibroblasts.
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PMID:Graft-versus-host disease in rhabdomyosarcoma following transfusion with nonirradiated blood products. 385 32

A cell-surface receptor for the mammalian reovirus type 3 hemagglutinin was isolated by using antiidiotypic anti-receptor antibodies. The receptor is a glycoprotein with a molecular mass of 67,000 daltons and a pI of 5.9. Evidence that the isolated structure represents the reovirus receptor was obtained by electrophoretic immunoblot studies, which demonstrated that the 67,000-dalton glycoprotein is the only cell-surface structure recognized by both reovirus type 3 and the anti-receptor immunoglobulin. Comparison of the reovirus receptor on murine thymoma (R1.1) and rat neuroblastoma (B104) cells indicated that similar structures on the cell surface are recognized by the reovirus type 3 and the anti-receptor antibodies as previously suggested from cellular and binding studies. This receptor was found on mouse, rat, monkey, and human cells. Furthermore, diverse tissue types, including lymphoid and neuronal cells, express the receptor structure. The receptor structure is discussed in terms of its role in mediating viral tropism and as an essential cell-surface protein.
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PMID:Isolation and biochemical characterization of the mammalian reovirus type 3 cell-surface receptor. 387 49

Single cells were prepared from mouse tail epidermis by a method which gives high viability counts and so permits their use in cytotoxicity tests. According to tests with standard alloantisera, the antigen phenotype of mouse epidermal cells is H-2(+)theta(+)Sk(+)H-Y(+)TL(-)Ly-A(-)Ly-B,C(-)PC(-). The skin differentiation alloantigen Sk, which is responsible for homograft reactions directed selectively against skin, is expressed also on brain, but not on other cell types; it is present on the transplanted neuroblastoma C1300. Cytotoxicity tests with epidermal cells of H-2 congenic mouse stocks confirm that the Sk locus is not closely linked to H-2. The lymphoid cell differentiation antigen theta also is present on both epidermal cells and brain. Mice frequently retain theta-incompatible or Sk-incompatible skin grafts although they have formed substantial titers of theta or Sk antibody in response to grafting. Male (H-Y) antigen is demonstrable on epidermal cells by cytotoxicity tests with H-Y antibody, as it is also on one other type of cell, spermatozoa.
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PMID:Serologically demonstrable alloantigens of mouse epidermal cells. 455 16

A variety of solid and hematological human tumors and normal human bone marrow specimens were assayed for colony formation in a short-term soft-agar culture system. The effect of human fibroblast, lymphoid, and myeloid interferons on inhibition of colony formation was assessed. The effect of interferon on colony formation formed a continuum from complete inhibition to stimulation of growth. Of 40 evaluable tumor specimens, 18 showed at least a 70% inhibition of colony formation in the presence of interferon, at concentrations of 1000 units/ml or less. Four specimens (acute myelogenous leukemia, osteogenic sarcoma, neuroblastoma, ovarian carcinoma) showed at least 3-fold stimulation of colony formation with interferon. Two of 12 normal bone marrow specimens grown with colony-stimulating, factor-conditioned media showed greater than 70% colony inhibition with interferon. A dose-response relationship was seen in all tumor specimens tested. While fibroblast interferon was the most active in this system, all interferons showed the same magnitude and direction of activity. Continuous exposure and 1-hr incubation of tumor cells with interferon were identical in terms of colony inhibition. These data support the ability of this assay system to select tumors responsive in vitro to interferon, suggest the optimal species and concentration for inhibition or stimulation of growth, and support a direct role of interferon in the regulation of cell growth independent of other immunoregulatory actions of interferon. Such information may prove useful for predicting response in vivo to interferon in Phase II trials.
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PMID:Effect of fibroblast, lymphoid, and myeloid interferons on human tumor colony formation in vitro. 616 Sep 5

Monoclonal antibodies to beta 2-microglobulin (beta 2m), and to the native two-chain molecule, were used to assess the expression of the HLA-A, B, C molecules on human neuroblastoma-derived cell lines. In radioimmuno-, cytotoxic, and microscopic assays, employing fresh and fixed cells, neuroblastoma cells show at best weak activity as compared to glial or lymphoid cells. In binding inhibition assays, neuroblastoma extracts were 200- to 1800-fold less efficient in inhibiting the antibodies than were glial or lymphoid extracts. Immunoprecipitation and SDS-PAGE analysis confirmed that a beta m-like chain is synthesized by the neuroblastoma cells, but the HLA chain could not be visualized by this technique. HLA-A, B, C and beta 2m levels are known to vary among tissues and cell lines. Yet the magnitude of the differences between the neuroblastoma and lymphoid lines is much greater than the reported differences in expression between some of these same lymphoid lines and many other nonlymphoid malignant or nonmalignant cell types. Metastatic neuroblastoma tumor in bone marrow also showed weak HLA-A, B, C activity, with the cells appearing negative in microscopic assays. Possible clinical implications are discussed.
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PMID:Striking paucity of HLA-A, B, C and beta 2-microglobulin on human neuroblastoma cell lines. 618 60

We attempted to determine the reliability of surface markers in distinguishing 21 small round cell tumors from lymphoid malignancies. Using immunofluorescence on tumor cell suspensions and immunoperoxidase on fresh frozen sections, we found that specimens of neuroblastoma (n = 7), rhabdomyosarcoma (n = 7), Ewing's tumor (n = 5), and two unclassified small round cell tumors all lacked human HLA-DR antigens. Each of eight tumors tested also lacked common leukocyte antigen (T200). In each of 13 cases studied, neither polyvalent surface immunoglobulin (sIg) nor receptors for sheep erythrocytes (E), complement (EAC), or the Fc portion of IgG immunoglobulin (EA) were found. Conversely, we found HLA-DR and/or T200 antigens, usually one or more receptors for E, EAC, or EA, and not infrequently, monoclonal sIg on malignant cells in each of 42 cases of lymphocytic lymphoma and leukemia. We conclude that study of surface DR and T200 antigens, sIg, and receptors for E, EAC, and EA aids the differential diagnosis of small round cell tumors from lymphocytic lymphoma and leukemia.
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PMID:Immunologic markers in the differential diagnosis of small round cell tumors from lymphocytic lymphoma and leukemia. 618 65

alpha 2-Macroglobulin (alpha 2M) was identified in chemically defined spent medium of cultured human melanoma cells. This wide-spectrum protease inhibitor was subsequently shown to be synthesized and was secreted by 10 of 13 cultured melanoma cells but not by neoplastic cells of other histologic origins (0/5 breast, 0/2 colon, 0/2 lung, 0/2 glioblastomas, 0/1 neuroblastoma, 0/4 lymphoid). alpha 2M was also produced by one strain of fetal lung fibroblasts, as was previously shown, but not by two strains of normal fetal uveal melanocytes or two strains of fetal skin fibroblasts. Biochemical characterization of melanoma alpha 2M indicated that it has a similar tetrameric structure but is smaller in size than authentic serum alpha 2M. Preliminary studies indicated that melanoma alpha 2M can bind to protease and has possible functional capability.
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PMID:alpha 2-macroglobulin production by cultured human melanoma cells. 619 43

The Manchester Children's Tumour Registry data for the period 1954-1977 have been analysed. The overall incidence of malignant disease in children aged 0-14 years in the north-west of England is estimated to be 100 per million person-years. The most common disease group is leukaemia, which forms about one third of the total number of cases. Among solid tumours, by far the most common presenting site is the central nervous system, representing nearly a quarter of all neoplasms. Wilms' tumour, neuroblastoma and soft-tissue sarcomas comprise approximately 5%, 6.5% and 6% respectively of the total. The tumours most frequently seen in adults (e.g. carcinoma of colon, lung and breast) are extremely rare in childhood. A significant excess of males was seen in acute lymphoid leukaemia, non-Hodgkin's lymphoma, Hodgkin's disease, medulloblastoma and hepatoblastoma. A female excess was found among germ-cell tumours. During the study period significant increases in incidence were seen among acute lymphoid leukaemia and epithelial tumours, and an increase in germ cell tumours approached significance.
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PMID:Incidence of malignant disease in childhood: a 24-year review of the Manchester Children's Tumour Registry data. 625 25


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