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)

FcRs (Fc Receptors) have been detected on the cell surface of two human neuroblastoma cell lines; IMR 32 and SK-N-SH, by immunocytochemistry and flow cytometric analysis, using a previously characterized polyclonal antiserum raised against the Fc gamma R isolated from a human CLL line (Gorini, Medgyesi, Garavini, Dorrington and Down, 1987; Rozsnay, Sarmay, Szabo, Medgyesi, Gorini and Gergely, 1990). FcR is expressed on all the cells of both lines at least at the same level as on the HL60 promyelocyte cell line used as positive control. Two electrophoretic components displaying apparent molecular masses of 70 and 43 kDa respectively have been identified by SDS-PAGE followed by Western blotting analysis of crude cell membranes. In addition, "in situ" hybridization experiments seem to exclude a correlation between FcR expression and N-myc oncogene activity. The presence of FcR in neuroblastoma could be related to a possible functional role even on these cells which do not belong to the immune system; moreover, they could also be exploited for a diagnostic characterization of this tumor.
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PMID:Fc gamma receptors are expressed on human neuroblastoma cell lines: lack of correlation with N-myc oncogene activity. 130 13

High level expression of the nm23-H1 gene, which encodes for a nucleoside diphosphate kinase, has been found to correlate with diminished metastasis in some tumors but not in others. We have previously identified the protein product of the nm23-H1 gene in two-dimensional electrophoretic gels and have designated it p19/nm23. In neuroblastoma, higher levels of p19/nm23, which are associated with amplification of the N-myc oncogene, large tumor mass, and metastasis, were observed in advanced stage tumors compared with limited stage disease. Because of the variable expression of nm23-H1 in different tumors, we have investigated the relationship between amounts of the protein and cell proliferation. The levels of p19/nm23 were compared between resting and mitotically stimulated normal human PBLs and in leukemia cells. The amount of p19/nm23 increased in normal lymphocytes in response to mitotic stimulation and paralleled the increase in DNA synthesis. In leukemia cells obtained from patients with different subtypes of acute leukemia, p19/nm23 levels were also increased relative to resting normal lymphocytes. Treatment of mitotically stimulated lymphocytes with cyclosporin, which inhibits proliferation, blocked the increase in p19/nm23; treatment of the leukemia cell line HL-60 with dimethylsulfoxide, which induces terminal differentiation, resulted in diminished levels of p19/nm23. Our data therefore provide evidence that nm23-H1 expression is related to cell proliferative activity.
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PMID:Proliferation-related expression of p19/nm23 nucleoside diphosphate kinase. 131 21

Gene expression of nerve growth factor receptor (NGFR), epidermal growth factor receptor(EGFR), chromogranin A (CGA) and neuropeptide Y (NPY) in 4 neuroblastoma cell Lines without N-myc amplification was studied by using Northern blot technique. N type cells expressed more NGFR mRNA than S type cell's and have only little or no EGFR expression. S type cells had stronger expression of EGFR mRNA than that of N type cells accompanying with only less or even no NGFR expression. The results indicated that difference of gene expression of these growth factor receptors might be due to the various directions of tumor cell differentiation. Cells differentiating toward neurons gave more NGFR expression and cells prepared to be differentiating toward other direction might give more EGFR gene expression. Various gene expression of CGA and NPY in neuroblastoma cell lines might be due to the presence of different stages of tumor cell differentiation and NGF only induced differentiation of those neuroblastoma cells ready to be differentiating to neurons afterwards.
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PMID:[Gene expression of NGFR, EGFR, CGA, NPY in 4 neuroblastoma cell lines]. 132 22

BACKGROUND AND METHODS. Genetic analysis of tumor tissue has provided considerable insight into mechanisms of malignant transformation and progression. Neuroblastomas have been studied by cytogenetics, flow cytometry, and molecular genetic techniques, and these studies have identified several specific abnormalities that allow subclassification of these tumors into genetic/clinical subtypes. RESULTS AND DISCUSSION. Four genetic abnormalities have been identified that are characteristic of certain neuroblastomas. These include: (1) loss of heterozygosity (LOH) for the short arm of chromosome 1, including band 1p36; (2) amplification of the N-myc protooncogene; (3) hyperdiploidy, or near triploidy; and (4) defects in expression or function of the nerve growth factor receptor (NGFR). Abnormalities of the NGFR are found in virtually all neuroblastoma cell lines, and some primary tumors. The latter have not been studied extensively. Hyperdiploidy is associated with lower stages of disease and with a favorable outcome in infants. LOH for chromomors. The latter have not been studied extensively. Hyperdiploidy is associated with lower stages of disease and with a favorable outcome in infants. LOH for chromosome 1, band p36, and N-myc amplification are more common in patients older than 1 year of age with advanced stages of disease. The latter two genetic abnormalities may be related, and LOH for 1p36 may precede the development of amplification. When these abnormalities are combined with assessment of DNA content, three distinct genetic subsets of neuroblastomas can be identified. The first is characterized by a hyperdiploid or near-triploid modal karyotype, with few if any cytogenetic rearrangements. These patients generally are younger than 1 year of age with localized disease and a good prognosis. The second has a near-diploid karyotype, with no consistent abnormality identified currently. These patients generally are older with more advanced stages of disease that progress slowly and are often fatal. The third group has a near-diploid or tetraploid karyotype, with deletions or LOH for 1p36, amplification of N-myc, or both. These patients generally are older with advanced stages of disease that rapidly are progressive. Thus, genetic analysis of neuroblastoma cells provides information that has prognostic significance and can direct a more appropriate choice of treatment.
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PMID:Neuroblastoma. Effect of genetic factors on prognosis and treatment. 132 79

The various members of the myc gene family, including c-myc and N-myc, are supposed to play a role in the regulation of cell cycle and proliferation. Whereas c-myc is expressed nearly ubiquitously, the N-myc gene product is found mainly in actively proliferating neural tissues such as early development tissues or in retinoblastomas and neuroblastomas. In this report, the upstream region of mouse N-myc gene was ligated to pSVPCAT, which carries the simian virus 40 (SV40) promoter and bacterial chloramphenicol acetyltransferase (CAT) gene, and transcriptional activities were examined by CAT and S1 protection assays after transfection of the DNAs into human cervical carcinoma HeLa or neuroblastoma IMR32 cells. Several regulatory regions were identified: two promoting regions (-980 to -860 and -279 to +108) and an inhibiting one (-860 to -797). The region spanning positions -980 to -860 increased CAT expression independently of orientation and distance to the SV40 promoter, indicating that the element is a typical enhancer. Moreover, the expression levels from this enhancer were higher in IMR32 cells than in HeLa cells, indicating that action has, if not cell-type specificity, cell-type preference. These findings may provide useful bases for the understanding of the cell-type specific regulation of N-myc expression.
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PMID:The upstream region of the mouse N-myc gene: identification of an enhancer element that functions preferentially in neuroblastoma IMR32 cells. 132 47

Neuroblastoma (NB), primitive neuroectodermal tumor (PNET), Ewing's sarcoma and rhabdomyosarcoma (RMS) are solid malignant tumors in childhood. Microscopically these tumors are grouped as small-round-cell tumors, and a different diagnosis is sometimes difficult. Cell surface membrane antigen, cytoskeletal protein and N-myc amplification and over-expression were analyzed in these cell lines and tumor tissues for the accurate diagnosis. NB and PNET could be distinguished from Ewing's sarcoma and RMS by the panel of monoclonal antibodies against cell surface membrane antigens. The cytoskeletal protein analysis is useful for the diagnosis of RMS and leiomyosarcoma. Alpha-smooth muscle actin and/or desmin were demonstrated in the S-type (epithelial-like) cells in 3 NB cell lines, suggesting the differentiation pathway of NB into smooth muscle cells. N-myc amplification and over-expression were observed in NB cell lines as well as one RMS cell line. The occurrence of N-myc amplification and over-expression in the RMS cell line cautions us against using N-myc as a distinguishable marker for NB.
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PMID:[Analysis of surface membrane antigens, cytoskeletal proteins and N-myc oncogene in pediatric solid malignant tumors, their diagnostic usefulness and relevant problems]. 132 30

Of all human tumors, neuroblastomas bear the most prominent genetic changes. Amplifications and deletions of chromosomal DNA can be identified by light microscopy on chromosomal spreads of neuroblastoma cells with remarkable frequency and consistency. Consequently, extensive studies have been undertaken to elucidate the molecular basis of these cytogenetic changes. A rich body of information has accumulated on the role played by dominant oncogenes and recessive tumor suppressor genes in the pathogenesis of this disease. Most notably, it was found that amplification of N-myc is responsible for the presence of double minutes and homogeneously staining regions in neuroblastoma chromosomes. It has also been discovered that N-myc amplification is a prognostic sign of malignancy. More recently, recessive genetic alterations in neuroblastoma, such as deletion of putative tumor-suppressing genes have received increasing attention, and considerable efforts are being made to identify such genetic elements. Finally, the susceptibility of neuroblastoma cells to differentiating stimuli has made them a popular in vitro system for neurobiological and pharmacological research. The need for suitable in vivo systems has spurred the development of several animal models employing tumor viruses and transgenic technologies.
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PMID:Dominant and recessive molecular changes in neuroblastomas. 134 34

Neuroblastomas are heterogeneous in terms of both their genotype and their clinical behavior. Recent studies suggest that these two features are related, and that the genotype frequently is predictive of response to treatment or the outcome of the patient. The genetic abnormalities that are characteristic of certain neuroblastomas include: (a) loss of heterozygosity (LOH) for the short arm of chromosome 1, including band 1p36; (b) amplification of the N-myc protooncogene; and (c) hyperdiploidy, or near-triploidy, determined either by flow cytometry or by karyotype. Hyperdiploidy is associated with lower stages of the tumor and with a favorable outcome in infants. However, LOH for chromosome 1 (band p36) and N-myc amplification are more common in patients over 1 year of age who have advanced stages of the tumor. Based on analysis of neuroblastomas for these genetic abnormalities, three distinct genetic subsets can be identified. The first is characterized by a hyperdiploid or near-triploid modal karyotype, with few, if any, cytogenetic rearrangements. These patients are generally less than 1 year of age, they have localized tumors, and have a good prognosis. The second genetic subset has a near-diploid karyotype, but with no consistent abnormality identified to date. They are generally older patients with tumors in the more advanced stages that progress slowly and are often fatal. Patients in the third group of genetic abnormalities have a near-diploid or tetraploid karyotype, with deletions or loss of heterozygosity for 1p36, amplification of N-myc, or both. These patients are generally older; they have advanced stage tumors that are rapidly progressive.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Molecular basis of clinical heterogeneity in neuroblastoma. 135 15

A methodology for rapid isolation of neuroblastoma cells from marrow with metastatic neuroblastoma cells was developed using a cocktail of five antibodies and magnetic microspheres coated with secondary antibodies. Cells bound to microspheres were released by brief exposure to chymopapain, followed by repeated culture of released cells in serum-supplemented Dulbecco's modified Eagle's medium and selection for adherent cells. Using this methodology, over 35 primary cell lines were obtained free of contaminating normal cells. Detailed analyses of over 14 cell lines revealed gross differences in cell phenotype, size, morphology development of neurite processes, and doubling time (40 to 80 h). All cell lines expressed the M(r) 145,000 neurofilament, and a few expressed the M(r) 200,000 neurofilament, with very little or no expression of the M(r) 68,000 neurofilament. Eight % of all cells lines had near-diploid DNA content. High expression of the MDR-1 protein was detected in six of the 22 cell lines tested. Great heterogeneity was observed in the expression of N-myc oncoprotein, with ten of 13 patients overexpressing the protein. c-myc oncoprotein was also expressed in all cell lines; however, the level of expression was 4- to 10-fold lower than the N-myc oncoprotein. Localization studies of c-myc and N-myc oncoproteins on the level of light microscopy and electron microscopy revealed exclusive nuclear localization of c-myc, whereas N-myc was localized to the nucleus and to the cytoplasm.
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PMID:Expression of N-myc, c-myc, and MDR-1 proteins in newly established neuroblastoma cell lines: a study by immunofluorescence staining and flow cytometry. 137 83

In different neuroblastoma cell lines and transfected clones, an increasing plasma membrane redox activity correlates with amplification and enhanced expression of the N-myc oncogene. Furthermore, plasma membrane redox activity is partially inhibited by retinoic acid in neuroblastoma cells with multiple copies of the N-myc oncogene but not in neuroblastoma cells with only one copy of this gene.
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PMID:Plasma membrane redox activity correlates with N-myc expression in neuroblastoma cells. 139 12


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