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 presence of antibodies to the virus capsid antigen of the Epstein-Barr virus was established in the sera of children from different forms of neoplasms with the aid of the indirect method of immunofluorescence according to Henle. 69 sera were studied from children with Wilm's tumor, teratoblastoma, reticulosarcoma, neuroblastoma, sarcoma and also from children with benignant tumors. As control served sera from healthy children of corresponding age. As test cells synthesizing the virus capsid antigen the authors utilized a suspension culture of P3HR-I cells, being one of the clones of Burkitt's lymphoma. The performed investigations have shown that in no one group of children with tumor could there be discovered an increase in the content of antibodies to the Epstein-Barr virus in comparison to controls. It has also been revealed that the spread of the Epstein-Barr virus in different groups of patients and healthy children fluctuated between 83 and 100%.
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PMID:A study on the relation between the Epstein-Barr virus and some forms of malignant tumors in children. 18 36

The presence of antibody to virus capsid antigen (VCA) of Epstein-Barr virus (EBV) was determined in sera from children with various forms of neoplasia by the indirect immunofluorescence procedure of Henle. Eighty-one sera from children with Wilms tumor, teratoblastoma, reticulosarcoma, neuroblastoma, soft tissue sarcoma, as well as from children with benign tumors were examined. The controls included sera from normal children of the same ages. The test cells synthesizing VCA were suspension cultures of P3HR-1 cells which are one of the clones of Burkitt lymphoma. The studies showed no increase in the content of antibody to EBV in any of the groups of children with tumors as compared with the controls. It was also found that the percentage of EBV infection in various groups of sick and normal children varied from 82 to 100.
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PMID:[Antibodies to Epstein-Barr virus in the sera of children with different neoplasms]. 19 3

Expression of the N-myc oncogene is an important determinant of tumor behavior in human neuroblastoma. To study the regulation of N-myc, we have subcloned fragments of the 5' flanking region of the human N-myc gene upstream of the chloramphenicol acetyl transferase (CAT) reporter gene, and assayed for promoter activity in transient transfections into neuroblastoma and other cell lines. Upstream sequences were found to possess promoter activity to within 121 bp of the major cap site (-121). Negative regulatory elements were identified in regions approximately 2 kb and 500 bp upstream from the major cap site, as well as 150-1000 bp downstream. Promoter constructs containing downstream elements from bp +150 to +1000 were active in N-myc-expressing neuroblastoma cell lines, but not in non-expressing Epstein-Barr virus (EBV)-transformed 729-6 B-cell or HeLa cell lines, while those lacking this element were active in all cell types tested. All tested constructs retaining promoter activity showed decreased activity in parallel with the down-regulation of endogenous N-myc in response to treatment of transfected cells with retinoic acid. These studies suggest that N-myc regulation may be controlled at different levels, and provide a basis for further characterization of N-myc regulation in neuroblastoma.
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PMID:Cell type-specific expression and negative regulation by retinoic acid of the human N-myc promoter in neuroblastoma cells. 156 67

Malignant glioma is the most common brain tumor. The molecular basis of glioma tumorigenicity has not been defined. Cultured glioma cells accumulate high levels of insulin-like growth factor I (IGF-I) transcripts. We asked whether IGF-I expression is coupled to tumorigenicity, using a combined in vivo/in vitro system employing antisense RNA for IGF-I. An antisense IGF-I expression construct in an expression vector that incorporates Epstein-Barr virus replicative signals and the ZnSO4-inducible metallothionein I transcriptional promoter was assembled. Stable glioma transfectants were derived from C6 glioma cells, which constitutively express IGF-I. B-104 neuroblastoma cells, derived originally from the same tumor but not expressing IGF-I, were also transfected as controls. In the absence of ZnSO4, the C6 transfectants expressed high levels of IGF-I mRNA and protein as detected by in situ hybridization and immunocytochemistry, respectively. Addition of ZnSO4 in the culture medium resulted in high levels of antisense transcript accumulation and dramatically decreased levels of endogenous IGF-I mRNA and IGF-I protein. Subcutaneous injection of either nontransfected C6 parental cells or C6 cells transfected with vector without IGF-I sequences into rats resulted in large tumors after 2 weeks, as did transfected and nontransfected B-104 cells. However, the rats injected with transfected C6 cells yielded no tumors after 40 weeks of observation. Two weeks after injection of the transfected C6 cells a small cyst was apparent in six rats. Histologic sections revealed a few glioma cells infiltrated by a large number of mononuclear cells. No infiltration of mononuclear cells was apparent in the glioma tumors resulting from injection of parental (nontransfected) cells, suggesting that the parental cells, but not the antisense IGF-I transfectants, escape the host immune response.
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PMID:Loss of tumorigenicity of rat glioblastoma directed by episome-based antisense cDNA transcription of insulin-like growth factor I. 159 87

In vitro culture of metastatic melanoma fragments with 150 units of recombinant interleukin 2 resulted in the successive expansion of CD4+ and then CD8+ tumor-infiltrating lymphocytes (TIL) throughout a 2-month period. TIL cultured for 43 days and consisting of 95% CD8+ and 10% CD4+ T lymphocytes were cloned by limiting dilution (LD). Thirteen CD8+ and thirty-one CD4+ clones were obtained, indicating that the frequency of clonogenic CD8+ proliferative T lymphocytes was much lower than that of their CD4+ homologues. When LD was performed in the presence of autologous melanoma cells the frequency of CD8+ clones was increased by factor 4. The DNA from TIL of day 43 bulk culture and of six CD8+ clones was hybridized with T cell receptor (TcR) beta and gamma probes. Identical configuration of the nonfunctional gamma and functional beta TcR genes was found in "bulk culture" and cloned TIL. The CD8+ clones therefore derived from a clonal population of CD8+ cells which had expanded in vitro before the LD. All the CD8+ clones tested were strongly cytotoxic for autologous melanoma cells but did not kill autologous fibroblasts or concanavalin A blasts, or any of the 10 allogeneic tumor targets tested, including 5 melanomas, 2 breast cell lines, 1 neuroblastoma, K-562 and the Epstein-Barr virus-transformed cell line used as a feeder. Furthermore, specific killing was inhibited by monoclonal antibodies against CD3, CD8, TcR alpha/beta and against class I major histocompatibility complex antigens indicating that these cytotoxic T lymphocyte clones recognized autologous tumor cells through the TcR, in an HLA class I-restricted manner. These data show that it is feasible to obtain tumor-specific cytotoxic T lymphocytes from melanoma TIL with a simple culture technique and that a single clone could be expanded to more than 10(10) cells which should allow testing of immunotherapeutic potential of these cells by adoptive transfer into melanoma patients.
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PMID:Selective expansion of a specific anti-tumor CD8+ cytotoxic T lymphocyte clone in the bulk culture of tumor-infiltrating lymphocytes from a melanoma patient: cytotoxic activity and T cell receptor gene rearrangements. 197 94

Activation of peripheral blood lymphocytes from a neuroblastoma patient by co-cultivation with autologous neuroblastoma cells in a mixed lymphocyte-tumor cell culture (A-MLTC) resulted in the generation of cytotoxic activity against the autologous neuroblastoma cell line HNB-MS. A-MLTC was set up in the presence of recombinant human interleukin-2 (IL-2). HNB-MS stimulator was treated with recombinant human interferon-gamma (IFN-gamma) prior to A-MLTC. CTL generated in short-term culture effectively lysed HNB-MS, while they had no effect on an Epstein-Barr virus transformed autologous B-cell line EB-MS. Moreover, CTL lysed 3 different allogeneic neuroblastoma cell lines, but not a rhabdomyosarcoma cell line RBB. Recombinant human tumor necrosis factor-alpha (TNF-alpha) and interleukin-4 (IL-4) enhanced and suppressed CTL generation, respectively, when added to the A-MLTC from the beginning of culture. CD3+ CD4- CD8+ T cells were the major anti-tumor effectors. Furthermore, 111indium-labeled CTL clearly accumulated in metastatic sites. These results indicate that CTL can be used for adoptive immunotherapy in neuroblastoma.
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PMID:Autologous tumor-specific cytotoxic T-lymphocytes in a child with neuroblastoma. 208 62

GM2 ganglioside is a common cell surface constituent of human melanoma and other tumors of neuroectodermal origin, and vaccination with GM2 ganglioside results in high levels of anti-GM2 antibodies in patients with melanoma. Lymphocytes from a GM2-vaccinated patient (VS) were transformed by Epstein-Barr virus and tested for production of antibodies with reactivity for GM2-positive tumor cells. A high percentage of antibody-producing B cells was detected, but antibody reactivity was generally lost during culture expansion. Two cultures, however, remained stable for antibody productivity and one was used to develop a stable hybrid line with mouse myeloma. The monoclonal antibody (designated 3-207) derived from patient VS has dual specificity for GM2 and GD2, despite the fact that only GM2 antibody could be detected in the patient's serum. Monoclonal antibody 3-207 shows high-titered reactivity with a range of melanoma, astrocytoma, neuroblastoma, and leukemia cell lines, cells with prominent cell surface expression of GM2 and GD2. The cell surface reactivity of monoclonal antibody 3-207 was not abolished by treatment of target cells with neuraminidase, as the enzyme converted GD2 to GM2, which was still detected by monoclonal antibody 3-207.
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PMID:Human monoclonal antibody with dual GM2/GD2 specificity derived from an immunized melanoma patient. 215 45

The gamma-subunit of 2-phospho-D-glycerate hydrolyase, E.C. 4.2.1.11 (enolase), neuron-specific enolase (NSE), is present at high concentrations in neurons and neuroendocrine cells and has therefore recently been introduced as a marker for neuroendocrine tumors. By the indirect methods, immunocytochemistry and radioimmunoassay, NSE has been detected also in some nonneuroendocrine tumors, a finding that could reflect technical artifacts or the capacity for NSE expression in nonneuroendocrine tumor cells. This paper reports on the expression of NSE in human neuroendocrine and nonneuroendocrine tumor specimens and in a panel of permanent human cell lines, by using a direct (enzymatic) and an indirect (radioimmunoassay) method for determination of NSE. We detected NSE in all tested tumor specimens and neuroendocrine tumor cell lines and in a majority (21 of 24) of the nonneuroendocrine tumor cell lines. In general, neuroendocrine tumor specimens and derived tumor cell lines contained more NSE than the nonneuroendocrine tumor specimens and cell lines. However, some of the cultured hematopoietic cell lines (T leukemia and Epstein-Barr virus immortalized B lymphoblastoid cell lines) had NSE levels comparable to those found in some neuroblastoma and small-cell lung carcinoma cell lines. We conclude that NSE is not exclusively expressed in neuroendocrine tumor cells.
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PMID:Expression of gamma-subunit of enolase, neuron-specific enolase, in human non-neuroendocrine tumors and derived cell lines. 300 68

Multiple B cell lines established by Epstein-Barr viral transformation from six patients with Alzheimer's disease (AD) and six age-matched controls were screened immunocytochemically for their reactivities with AD and normal brains as well as to cell lines such as HeLa, fibroblasts and neuroblastoma. A higher incidence of reactivity with neurofibrillary tangles in situ was found among the cell lines from AD patients (23/866) in comparison with those from normals (6/803). Three cell lines from a patient with a definitive neuropathological diagnosis of AD were shown to secrete antibodies preferentially reactive with astrocytes in the grey matter of AD brain and one cell line from a normal elderly individual was shown to specifically react with neurofibrillary tangles and plaque neurites. These four antibodies were not reactive with normal brains or cell lines. These unique human antibodies may be useful in the diagnosis of AD and offer clues to its pathogenesis.
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PMID:Human antibodies to neurofibrillary tangles and astrocytes in Alzheimer's disease. 326 Sep 6

Human IgM kappa antibody to a membrane antigen of human tumors of neuroectodermal origin (melanoma, glioma and neuroblastoma) has been detected in the spent culture fluid of an Epstein-Barr virus (EBV)-transformed human B-lymphoblastoid cell line, L72. The chemical nature of the antigen was identified as ganglioside GD2. The antibody was purified by precipitation of L72 culture fluid with ammonia sulfate and hypotonic buffer followed by ultracentrifugation and Sephacryl S-300 super gel filtration. Approximately 27 mg of pure human IgM was obtained from 101 of spent medium. Total IgM and antibody activity recovery efficiency was 60% and 75%, respectively. The monoclonal character of the immunoglobulin produced by the L72 cell line was determined by agarose isoelectric focusing and immunofixation techniques. 1 mg of the purified IgM possessed an antibody titer endpoint to a GD2-positive melanoma cell line of 1:10,000 as assayed by immune adherence and 1:100 titer by complement-dependent cytotoxicity in vitro. The effect of pure anti-GD2 on suppression of melanoma growth in vivo was tested using a nude mouse model. Three-week-old CD-1 nude mice bearing 2-3 mm M14-A subcutaneous melanoma nodules were treated intraperitoneally with anti-GD2 and rabbit complement. Tumor growth was retarded for 25 days when compared to that of control mice receiving non-specific human IgM and complement. On Day 15, treated tumors were 80% smaller than control tumors. These result indicated that the pure human monoclonal antibody to GD2 may have potential for cancer therapy.
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PMID:Human monoclonal antibody to tumor-associated ganglioside GD2. 609 19


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