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)

1. The mouse neuroblastoma cell line N-115 was used as a model system to study neuronal differentiation induced by treatment of cells with different agents. 2. The extent of morphological differentiation obtained with dibutyryl cyclic AMP (dbc-AMP), dimethyl sulfoxide (DMSO), retinoic acid (RA), and serum-free medium was correlated to the expression of the mRNA for the gamma isoform of the glycolytic enzyme enolase, a recognized neuron-specific marker. 3. A 4-day treatment of the cells with any of the differentiation inducing agents used in this study resulted in the extension of long neurites, though differences in cell body shape were observed depending on the agent used. 4. Northern blot analysis revealed that changes in the level of gamma enolase-specific mRNA correlate with the extent of morphological differentiation, with a 5- to 20-fold increase depending on the differentiation inducing agent used. 5. Finally, we found that a high cell density causes a significative increase in the level of the gamma enolase-specific message in cells maintained in growing conditions.
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PMID:Differential expression of neuron-specific enolase mRNA in mouse neuroblastoma cells in response to differentiation inducing agents. 839 14

A case of olfactory neuroblastoma is reported. Light microscopic examination showed various arrangements of poorly differentiated tumour cells forming either uniform sheets or convoluted cords of multiple cell layers orientated toward a richly vascular stroma. Electron microscopic examination showed the presence of abundant cytoplasmic filaments and processes, and dense core endocrine vesicles ranging from 100-160 nm in diameter in both the perinuclear region and tumour cell processes. Immunohistochemical staining was positive in most of the tumour cells for neuron specific enolase, and in a few cells for S-100 protein, vimentin, and serotonin, but staining for desmin and keratin produced no reaction.
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PMID:Electron microscopic and immunohistochemical findings in a case of olfactory neuroblastoma. 843 97

The toxic effects of two metabolic inhibitors, dinitrophenol and iodoacetic acid, were compared. Mouse neuroblastoma cell cultures (Neuro-2a) were exposed to different concentrations of the toxic compounds for 24, 48 and 72 h to study basal toxicity effects (cell proliferation by quantification of total protein content (PR) and relative neutral red uptake (RNRU) by lysosomes). The following biochemical indicators assessed in the in vitro test system were: cytosolic phosphofructokinase (PFK) and enolase (ENL) activities in glycolysis; mitochondrial succinate dehydrogenase (SDH) activity in the citric acid cycle; lysosomal beta-galactosidase (GAL) activity; and neuronal acetylcholinesterase (AChE) activity. The effects of the two metabolic inhibitors on the various indicators differed. Iodoacetic acid was found to be far more toxic than dinitrophenol to neuroblastoma cell proliferation at 24 h exposure. Though 2,4-dinitrophenol and iodoacetic acid both inhibited cell proliferation of the neuroblastoma cells, their effects on the other endpoints were opposite. Dinitrophenol was a general activator of the metabolism, particularly affecting lysosomal function. Iodoacetic acid did not significantly alter general metabolism, but considerably modified lysosomal function and AChE activity. The modification of lysosomal function of Neuro-2a cells by the two compounds was quite different: dinitrophenol increased RNRU and GAL activity, and iodoacetic acid decreased both parameters.
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PMID:Comparative effects of the metabolic inhibitors 2,4-dinitrophenol and iodoacetate on mouse neuroblastoma cells in vitro. 865 53

Immortalized rat mesencephalic cells (1RB3AN27) produced dopamine (DA) at a level that was higher than produced by undifferentiated or differentiated murine neuroblastoma cells (NBP2) in culture. Treatment of 1RB3AN27 and NBP2 cells with a cAMP stimulating agent increased tyrosine hydroxylase (TH) activity and the intensity of immunostaining for the DA transporter protein (DAT). 1RB3AN27 cells were labelled with primary antibodies to neuron specific enolase (NSE) and nestin and exhibited very little or no labeling with anti-glial fibrillary acidic protein (GFAP). 1RB3AN27 cells exhibited beta- and alpha-adrenoreceptors, and prostaglandin E1 receptors, all of which were linked to adenylate cyclase (AC). Dopamine receptor (D1) and cholinergic muscarinic receptors linked to AC were not detectable. The levels of PKC alpha and PKC beta isoforms were higher than those of PKC gamma and PKC delta in 1RB3AN27 cells. The 1RB3AN27 cells were more effective in reducing the rate of methamphetamine-induced turning in rats with unilateral 6-OHDA lesion of the nigrostriatal system than differentiated NBP2 cells. The grafted 1RB3AN27 were viable as determined by DiI labelling, but they did not divide and did not produce T-antigen protein; however, when these grafted cells were cultured in vitro, they resumed production of T-antigen and proliferated after the primary glia cells and neurons of host brain died due to maturation and subsequent degeneration. Examination of H&E stained sections of the grafted sites revealed no evidence of infiltration of inflammatory cells in the grafted area suggesting that these cells were not immunogenic. They also did not form tumors.
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PMID:Characterization and transplantation of two neuronal cell lines with dopaminergic properties. 872 72

NADH-dichlorophenol-indophenol oxidoreductases (PMOs) were purified from synaptic plasma membranes or synaptic vesicles (small recycling vesicles) from both bovine and rat brains and from a neuroblastoma cell line, NB41A3. Several isoforms could be identified in purified plasma membranes and vesicles. Purification of the enzyme activity involved protein extraction with detergents, (NH4)2SO4 precipitation, chromatography under stringent conditions and native PAGE. PMO activity could be attributed to a very tight complex of several proteins that could not be separated except by SDS/PAGE. SDS/PAGE resolved the purified complex into at least five proteins, which could be micro-sequenced and identified unambiguously as hsc70, TOAD64 and glyceraldehyde-3-phosphate dehydrogenase tightly associated with the brain-specific proteins aldolase C and enolase-gamma. Enzyme activity could be purified from both synaptic plasma membranes and recycling vesicles, yields being much greater from the latter source. Highly purified plasma membranes (prepared from a neuroblastoma cell line NB41A3 by iminobiotinylation of intact cells and affinity purification with avidin and anti-avidin antibodies under very stringent conditions) also displayed PMO activity tightly associated with TOAD64. The association of PMO in a tight complex was confirmed by its immunoprecipitation from cellular and membrane extracts of NB41A3 using antibodies directed against any component protein of the complex followed by immunodetection with antibodies directed against the other members. Antibodies also inhibited the enzyme activity synergistically. In addition, induction of the different components of the complex during dichlorophenol-indophenol stress was demonstrated by the S1 RNase-protection assay in synchronized NB41A3 cells. The role of the complex in membrane fusion and cellular response to extracellular oxidative stress during growth and development is discussed.
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PMID:Purification of a dichlorophenol-indophenol oxidoreductase from rat and bovine synaptic membranes: tight complex association of a glyceraldehyde-3-phosphate dehydrogenase isoform, TOAD64, enolase-gamma and aldolase C. 918 18

This study was to determine the extent of alteration of enolase specific activities in chicken embryo retina primary cells in culture when exposed to an ELF (extremely low frequency) electric field at 60 Hz. Results showed no alteration of enolase activity and enolase mRNA levels. In this study, sham vs. control experiments were also conducted to neutralize ambient AC magnetic fields, stray magnetic fields and variations in field uniformity. Under similar conditions, the specific activity of enolase is decreased in neuroblastoma cell line (NG108). It is apparent from this study that primary cells either are not affected by these exposure conditions or the effect is transient and warrants no damage.
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PMID:Enolase activity in chicken embryo primary retina cells is not affected by exposure to a 60-Hz electric field. 992 66

Chlorpromazine and other phenothiazine derivatives are neuroleptic drugs of widespread use for clinical situations beyond the realm of psychiatry, such as to control nausea, vomiting and intractable hiccups. The present study investigated in vitro different cytotoxic effects of chlorpromazine in cultures of mouse neuroblastoma cell line Neuro-2a exposed to different concentrations of this compound. Indicators assessed were cell proliferation by quantification of total protein content of the cell culture, lysosomal function evaluated by the relative uptake of neutral red cytosolic phosphofructokinase (PFK) and enolase (ENL) activities in glycolysis, mitochondrial succinate dehydrogenase (SDH) activity in the citric acid cycle, lysosomal beta-galactosidase (GAL) activity, and neuronal acetylcholinesterase activity. Marked inhibitory effects were found for cell proliferation and relative neutral red uptake; PFK, ENL and GAL activities had no significant differences from control. Stimulation was specifically detected on SDH and the Krebs cycle at concentrations up to 30 microM. Chlorpromazine did not have high toxicity for cytotoxic effects on lysosomes.
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PMID:Biochemical effects of chlorpromazine on mouse neuroblastoma cells. 1050 25

Much evidence suggests that apoptosis plays a crucial role in cell population homeostasis that depends on the expression of various genes implicated in the control of cell life and death. The sensitivity of human neuroblastoma cells SK-N-SH to undergo apoptosis induced by thapsigargin was examined. SK-N-SH were previously differentiated into neuronal cells by treatments with retinoic acid (RA), 4 beta-phorbol 12-myristate 13-acetate (PMA) which increases protein kinase C (PKC) activity, and staurosporine which decreases PKC activity. Neuronal differentiation was evaluated by gamma-enolase, microtubule associated protein 2 (MAP2) and synaptophysin immunocytochemistry. The sensitivity of the cells to thapsigargin-induced apoptosis was evaluated by cell viability and nuclear fragmentation (Hoechst 33258) and compared with pro-(Bcl-2, Bcl-x(L)) and anti-apoptotic (Bax, Bak) protein expression of the Bcl-2 family. Cells treated with RA and PMA were more resistant to apoptosis than controls. Conversely, the cells treated with staurosporine were more susceptible to apoptosis. In parallel with morphological modifications, the expression of inhibitors and activators of apoptosis was directly dependent upon the differentiating agent used. Bcl-2 expression was strongly increased by PMA and drastically decreased by staurosporine as was Bcl-x(L) expression. Bax and Bak expression were not significantly modified. These results demonstrate that drugs that modulate PKC activity may induce a modification of Bcl-2 expression as well as resistance to the apoptotic process. Furthermore, the expression of Bcl-2 was reduced by toxin B from Clostridium difficile and, to a lesser extent, by wortmannin suggesting a role of small G-protein RhoA and PtdIns3 kinase in the control of Bcl-2 expression. Our data demonstrate a relationship between the continuous activation of PKC, the expression of Bcl-2 protein family and the resistance of differentiated SK-N-SH to apoptosis.
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PMID:Resistance to induced apoptosis in the human neuroblastoma cell line SK-N-SH in relation to neuronal differentiation. Role of Bcl-2 protein family. 1123 Dec 87

We present an adrenal Ewing's sarcoma family of tumor (ESFT) arising in an 11-year-old Japanese boy. Although intensive chemoradiotherapy and radical surgery were performed, the patient died of obstinate disease 1 year and 3 months after the initial presentation. The primary site (adrenal gland) with radiologic findings (with foci of calcification), high titer of serum neuron specific enolase, and sheets of monotonous primitive rounded cells on histology mostly favored neuroblastoma. However, a diagnosis of ESFT was confirmed by immunohistochemical profile, including MIC2-positivity and molecular study disclosing EWS-FLI1 chimera gene verified by direct sequencing. Recognition of adrenal ESFT and use of newly developed diagnostic techniques are required for differential diagnosis of undifferentiated small round cell tumor of the adrenal gland.
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PMID:Ewing's sarcoma family of tumor arising in the adrenal gland--possible diagnostic pitfall in pediatric pathology: histologic, immunohistochemical, ultrastructural, and molecular study. 1156 33

Neuroblastoma, common in children, rarely develops in adults. We recently treated a patient with adult neuroblastoma. A 34-year-old man complained of a swelling in right inguinal region. CT scan showed swelling of retroperitoneal and inguinal lymph nodes, and bone scintigram by 99mTc-HMDP showed an abnormal uptake in the swollen lymph nodes. Chemotherapy with CDDP (cisplatinum), VP-16 (etoposide), BLM (bleomycin), ADM (adriamycin) was not effective. Histopathological examination of a biopsy specimen revealed neuroblastoma. Another chemotherapy with CPM (cyclophosphamide), VCR (vincristine), ADM, DTIC (dacarbazine), CDDP, VP-16 was effective in decreasing the tumor size. Further high dose chemotherapy with CPM, ADM, CDDP, VP-16 combined with peripheral blood stem cell transplantation led to almost complete disappearance of the tumor and normalization of blood tumor markers (neuron specific enolase and immunosuppressive acidic protein). Retroperitoneal lymph node dissection demonstrated well-differentiated neuroblastoma in the excised tissue. Six months postoperatively, the tumor recurred in the pelvic cavity. Although chemotherapy and radiotherapy were given, he died of the disease 12 months postoperatively.
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PMID:[A case of adult neuroblastoma arising in the retroperitoneal space]. 1159 7


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