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)

Plasmacytomagenesis provides a murine model to decipher progressive genetic events culminating in a B-cell neoplasia. Activation of the c-myc protooncogene by chromosomal translocation is considered an initiating event. Intracisternal A-type particles (IAPs) are defective retroviral-like structures present in the endoplasmic reticulum of plasmacytomas (PCTs). IAP proviral insertions have been documented to engender negative or positive effects on the expression of nearby cellular genes. We have isolated a gene, PANG (plasmacytoma-associated neuronal glycoprotein), that is ectopically transcribed in a number of PCTs due to IAP long terminal repeat (LTR) activation. A full-length PANG cDNA was isolated from an MPC-11 plasma cell tumor cDNA library and encodes a polypeptide of about 113 kDa with six immunoglobulin C2-like and four type III fibronectin-like domains. PANG bears a striking resemblance to axonal glycoproteins TAG-1 and F11 known to function in neuronal outgrowth. An extensive survey revealed a predominant 3.6-kb PANG transcript in 60% (30 of 50) of PCTs as well as unique smaller and larger species. All other normal and transformed lymphoid and nonlymphoid cell lines and normal tissues were negative for PANG expression except for the brain, wherein unique 4.0- and 6.1-kb transcripts were detected. Reverse transcriptase PCR analysis revealed IAP LTR fusion to PANG mRNAs in five PCTs and in a neuroblastoma line. The 5' end of a mouse brain PANG cDNA was identical to the MPC-11 PANG transcript except for the precise replacement of its 5' LTR sequence.
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PMID:PANG, a gene encoding a neuronal glycoprotein, is ectopically activated by intracisternal A-type particle long terminal repeats in murine plasmacytomas. 810 13

We reported previously (S. L. Rogers, P. J. Gegick, S. M. Alexander, and P. G. McGuire, Dev. Biol. 151, 191-203, 1992) that transforming growth factor-beta 1 (TGF beta 1) inhibited proliferation, up-regulated fibronectin synthesis, and suppressed melanogenesis in a population of quail neural crest cells in vitro. Here, we report that cell lines derived from the parent SK-N-SH neuroblastoma line (R. A. Ross, B. A. Spengler, and J. L. Biedler, J. Natl. Cancer Inst. 71, 741-747, 1983) respond differentially to TGF beta 1, and their responses provide further insights into the actions of this growth factor on neural crest subpopulations. The SH-EP cell line exhibits primarily nonneuronal traits and responded to TGF beta 1 with increased thymidine uptake after 6 days of culture, increased expression of fibronectin mRNA and protein, and decreased laminin synthesis. Many SH-EP cells also acquired a dramatically elongated morphology, reminiscent of Schwann cells in culture. Thymidine uptake by the neuronal SY5Y cell line was not substantially altered. Neither fibronectin mRNA nor protein was detectable in either TGF beta 1-treated or untreated cultures, although laminin synthesis was upregulated by the growth factor. In TGF beta 1-treated cultures of the intermediate SH-IN cell line, which has been reported to display both neuronal and nonneuronal characteristics, there was marked flattening of many cells, a steady decrease in thymidine uptake, and increased expression of both fibronectin and laminin. The observed responses of SH-IN cells mimic those observed in primary neural crest cultures and appear to represent similar differentiation toward a mesenchymal phenotype. These results substantiate the idea that closely related but diverging neural crest-derived cell types respond selectively to TGF beta 1 and demonstrate that these SK-N-SH-derived cell lines will be useful in experimental approaches that will allow us to infer mechanisms underlying regulation of neural crest differentiation.
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PMID:Transforming growth factor-beta 1 differentially regulates proliferation, morphology, and extracellular matrix expression by three neural crest-derived neuroblastoma cell lines. 814 71

A fast, inexpensive, and versatile technique for patterning the surface of glass coverslips with molecules of biological interest is described. The technique combines photolithographic, silane-coupling, and protein adsorption procedures to pattern coverslips with amines, alkanes, and proteins with micrometer spatial resolution. The attachment of amines and alkanes was verified using contact angle and X-ray photoelectron spectroscopic (XPS) measurements. XPS results showed that amines and alkanes were attached in 1-4 nm thickness covering approximately 20% and 45%, respectively, of the surface. Patterns of amines were visualized using fluorescent staining, and patterns of proteins were detected immunochemically. Patterned coverslips were used to investigate adhesion and neurite outgrowth of mouse neuroblastoma (N1E-115) cells. Cells were examined on the following patterns: alkane-glass, protein-glass, amine-alkane, and amine-protein. Cell attachment and neurite outgrowth on patterned coverslips displayed the following preferences: laminin, fibronectin, or collagen IV > amine or glass > alkane or bovine serum albumin. This patterning method should be useful for studies of cell-surface interactions, cell migration, nerve regeneration, and the formation of neural networks in vitro.
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PMID:A versatile technique for patterning biomolecules onto glass coverslips. 815 46

Sixty-seven childhood tumors were studied immunohistochemically for the extracellular matrix element type IV collagen, laminin, and fibronectin. Tumors included Ewing's sarcoma, primitive neuroectodermal tumor, small cell osteosarcoma, neuroblastoma or ganglioneuroblastoma, rhabdomyosarcoma, and lymphoma. It was found that small cell osteosarcoma was often positive for fibronectin but not type IV collagen or laminin, a new observation. In the lymphomas, matrix proteins were rarely found. Ewing's sarcoma was variably positive for type IV collagen and laminin, but fibronectin was absent. Extracellular laminin and fibronectin were found in one of two cases of primitive neuroectodermal tumor. In neuroblastoma and ganglioneuroblastoma, the matrix components were rarely found. These results, discrepant with findings in cultured cells, may reflect the altered capacity of tumors to produce these proteins in vitro, which suggests that caution should be exercised in drawing conclusions regarding the nature or histogenesis of tumors from data obtained with cultured tumor cells. Embryonal rhabdomyosarcoma frequently contained all matrix elements in the extracellular space and in a dotlike pattern in the cytoplasm; alveolar rhabdomyosarcoma rarely contained these proteins and never exhibited the dotlike pattern. The frequent finding of matrix proteins in embryonal rhabdomyosarcoma but only rarely in alveolar rhabdomyosarcoma and the unique immunostaining pattern in embryonal rhabdomyosarcoma may prove to be a useful adjunct in the diagnosis of childhood tumors.
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PMID:Extracellular matrix of small round cell tumors of childhood: an immunohistochemical study of 67 cases. 815 9

We have prepared a monoclonal antibody, Neuro-1, that recognizes the human homolog of the chicken contactin/F11 and mouse F3 cell adhesion molecules. The Neuro-1 antigen, structurally characterized as a 135 kDa glycosylphosphatidylinositol-linked glycoprotein, was immunoaffinity purified and partially sequenced. Comparison of an internal peptide sequence to that predicted from the chicken contactin/F11, mouse F3 and human contactin (reported herein) cDNA sequence identifies the Neuro-1 antigen as human contactin. Moreover, a polyclonal antisera generated against the purified Neuro-1 antigen was immunoreactive with a fragment of human contactin expressed in bacteria. The complete coding and deduced amino acid sequences of human contactin were determined and are 86% and 95% identical to the respective mouse F3 sequences. Structural features shared with contactin/F11/F3 include six immunoglobulin type C2 and four fibronectin type III-like domains, multiple sites for asn-linked glycosylation and a COOH-terminal signal peptide presumably removed during the generation of a phosphatidylinositol cell surface linkage. The potential for glycosylation and GPI-linkage is also consistent with protein chemical studies of human contactin. Contactin mRNA expression was characterized using Northern blot analyses of human tissues and cell lines. High level expression of a single contactin transcript in adult brain, and low level expression of multiple transcripts in lung, pancreas, kidney and skeletal muscle are observed. Highly expressed multiple transcripts, similar in pattern to that of pancreas, lung, kidney and skeletal muscle, are also observed in human neuroblastoma and retinoblastoma cell lines.
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PMID:Identification and characterization of the human cell adhesion molecule contactin. 816 10

The cell line AG-F was isolated from the marrow of a neuroblastoma patient undergoing myeloablative treatment and autologous bone marrow rescue. A year later, the patient developed a Hodgkin's type lymphoma. AG-F cell line demonstrated an unusual phenotype, lacking surface CD2 and CD3, but expressing high levels of CD4, CD5, CD7, CD29, and CD45RO. Markers associated with Hodgkin's lymphoma cells, CD15 and CD30, were also positive. AG-F cells grow in suspension in clusters of 50-200 cells, with a doubling time of 9 h. They can also grow in serum-free medium and form tumors in nude mice. AG-F cells have amplified N-myc and c-myc and high levels of the corresponding mRNA transcripts. Cytogenetic analysis revealed a DNA index by flow cytometry of near tetraploid cells and a karyotype of 85-87 chromosomes, with consistent abnormalities in chromosomes 1, 5, and 9. Gene rearrangement studies revealed rearrangement of the beta gene of the T-cell receptor. AG-F cells secrete high levels of IL-6, IL-8, IL-10, and GM-CSF. Cell adherence and formation of long processes could be induced by fibronectin and were enhanced by exposure to PMA. Cells exposed to phorbol myristate acetate (PMA) had increased expression of CD11a, CD11b, CD18, CD45RO, and HLA-DR, whereas expression of CD15 and CD30 was markedly decreased. Similarly, the level of c-myc and N-myc oncoproteins and the levels of the cytoskeletal proteins, actin, tubulin, and vimentin markedly decreased early after PMA-induced differentiation.
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PMID:Isolation and characterization of an early T-helper/inducer cell line with a unique pattern of surface phenotype, constitutive cytokine secretion and myc oncogene expression. 825 4

Electrical signals elicited by integrin interaction with ECM components and their role in neurite outgrowth were studied in two clones (N1 and N7) isolated from 41A3 murine neuroblastoma cell line. Although the two clones similarly adhered to fibronectin (FN) and vitronectin (VN), this adhesion induced neurite outgrowth in N1 but not in N7 cells. Patch clamp recordings in whole cell configuration showed that, upon adhesion to FN or VN but not to platelet factor 4 (PF4), N1 cells undergo a marked (approximately equal to 20 mV) hyperpolarization of the resting potential (Vrest) that occurred within the first 20 min after cell contact with ECM, and persisted for approximately 1 h before reverting to the time zero values. This hyperpolarization was totally absent in N7 cells. A detailed analysis of the molecular mechanisms involved in N1 and N7 cell adhesion to ECM substrata was performed by using antibodies raised against the FN receptor and synthetic peptides variously competing with the FN or VN binding to integrin receptor (GRGDSP and GRGESP). Antibodies, as well as GRGDSP, abolished adhesion of N1 and N7 clones to FN and VN, revealing a similar implication of integrins in the adhesion of these clones to the ECM proteins. However, these anti-adhesive treatments, while ineffective on Vrest of N7 cells, abolished in N1 cells the FN- or VN-induced hyperpolarization and neurite outgrowth, that appeared therefore strictly associated and integrin-mediated phenomena. The nature of this association was deepened through a comparative analysis of the integrin profiles and the ion channels of N1 and N7 cells. The integrin immunoprecipitation profile resulted very similarly in the two clones, with only minor differences concerning the alpha V containing complexes. Both clones possessed Ca2+ and K+ delayed rectifier (KDR) channels, while only N1 cells were endowed with inward rectifier K+ (KIR) channels. The latter governed the Vrest, and, unlike KDR channels, were blocked by Ba2+ and Cs+. By moving patched cells in contact with FN-coated beads, it was shown that KIR channel activation was responsible for the FN-mediated hyperpolarization of Vrest. Treatment with Pertuxis toxin (PTX) abolished this hyperpolarization and neurite outgrowth, indicating that a G protein is interposed between integrins and KIR channels and that the activation of these channels is required for neuritogenesis. In fact, the block of KIR channels by Cs+ abolished both hyperpolarization and neurite outgrowth, provided that the cation was supplied during the first two hours after N1 cell contact with FN.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Integrin-mediated neurite outgrowth in neuroblastoma cells depends on the activation of potassium channels. 835 96

Murine Neuro-2A neuroblastoma cells were exposed to ethanol in culture under two experimental paradigms: (1) short-term (24 hr or less) and low concentrations (0.05 to 0.5%; 8.5 to 86 mM) and (2) long-term (48 hr at 0.5%; 86 mM). Long-term ethanol exposure did not affect Neuro-2A viability, determined by DNA synthesis or the ability to exclude Trypan Blue. Similarly, long-term ethanol treatment did not inhibit differentiation, exhibited by the extension of neurites, promoted by either dibutyryl-cyclic-AMP or by incubation with exogenous ganglioside GM1. The incorporation of exogenous ganglioside GM1 into plasma membranes was not influenced by varying concentrations of ethanol (up to 1.2%; 204 mM). In contrast, ethanol did influence Neuro-2A cell attachment to collagen in a dualistic manner. During short-term ethanol exposure, cell attachment was enhanced. However, when cells were initially exposed to ethanol for 48 hr a marked inhibition of subsequent attachment was observed. Long-term ethanol exposure also inhibited attachment to other substrata, including laminin, fibronectin and vitronectin. Incubation of Neuro-2A cells with either exogenous ganglioside GM1 or a mixture of brain gangliosides partially reversed the inhibition of attachment to collagen. This reversal did not appear to be due to any one particular ganglioside structure, however. Mixed brain gangliosides were fractionated into three fractions, according to the number of sialic acid residues. Each of the three fractions were equally effective in partially restoring Neuro-2A cell attachment to collagen after long-term ethanol treatment. The results suggest that the mechanism by which these effects occur is at the level of plasma membrane fluidity, because both ethanol and glycosphingolipid content are known to influence membrane lateral mobility, although other mechanisms, such as changes in headgroup hydration, are possible.
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PMID:Effects of ethanol on neuroblastoma cells in culture: role of gangliosides in neuritogenesis and substrate adhesion. 858 6

This study was performed to develop and improve a completely defined in vitro ocular wound-healing model of fibroblast proliferation for glaucoma filtration surgery. This model is essential for the investigation of protein-sensitive drugs and cytokines. Tenon's capsule fibroblasts in their third passage were incubated overnight, washed free of serum, and fed defined media, Aim V or Clonetics FBM serum-free medium containing platelet-derived growth factor, basic fibroblast growth factor, epidermal growth factor, or fibronectin at various dilutions and in combinations at optimum concentrations. Proliferation was measured by 3H-thymidine incorporation at 1, 3, and 7 days. Morphology was compared to controls fed Minimum Essential Medium + 10% serum. Single factors stimulated the greatest amount of thymidine uptake on day 3. Optimum concentrations were epidermal growth factor at 5 ng/ml, basic fibroblast growth factor at 10 ng/ml and platelet-derived growth factor at 20 ng/ml. Identical combinations of factors stimulated nearly twice the thymidine uptake in Clonetics medium as in Aim V. Epidermal growth factor activity was inhibited by either basic fibroblast growth factor or platelet-derived growth factor. Basic fibroblast growth factor and platelet-derived growth factor together produced a less than additive effect. The performance of either serum-free medium may be improved by the addition of basic fibroblast growth factor or platelet-derived growth factor. The optimum serum-free medium (Clonetics FBM) with growth factors was unable to stimulate proliferation as much as Minimum Essential Medium + 10% NBS, but was successful in maintaining viability during the 7 day test period.
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PMID:The effects of growth factors on Tenon's capsule fibroblasts in serum-free culture. 863 Dec 1

Integrins belong to a large family of heterodimeric membrane glycoproteins which mediate cell-cell or cell-extracellular matrix interactions. These interactions could play a major role during the migration of tumor cells across the extracellular matrix and vascular endothelium and would thus appear to be a requisite for the metastatic process. Treatment of the Foss human melanoma cell line with LIF or OSM, two cytokines involved in acute-phase response, increased the expression of membrane alpha v beta 1 by 1.5-2 fold. The same phenomenon was observed on the SK-N-SH human neuroblastoma cell line. This modulation, which was inhibited by specific monoclonal antibodies against alpha v or beta 1 integrin subunits, was concomitant with improved tumor cell attachment to the fibronectin matrix. Similar results were obtained after TNF-alpha treatment. Our findings demonstrate the ability of LIF and OSM to modulate tumor cell capacity to adhere to the matrix component, suggesting a potential role for these cytokines in modulation of tumoral progression.
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PMID:[Modulation of integrin alpha-v-beta-1 expression on human tumor cells by leukemia inhibitory factor (LIF) and oncostatin M (OSM)]. 867 51


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