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)

Removal of sialic acid from intact mammalian nervous system cells in tissue culture is accompanied by an immediate increase in cellular cholinesterase activity. Treatment of hamster astroblast cells (clonal line NN) and mouse neuroblastoma cells (clonal lines S21, N18, and N115) for brief periods with a low level of Clostridium perfringens sialidase, 5 X 10(-3) units/ml, removed 1-15 mug of sialic acid per mg of cell protein and brought about a large increase in v0 and Vmax of cellular acetylcholinesterase (EC 3.1.1.7). Butyrylcholinesterase (EC 3.1.1.8) activities also increased upon careful enzymatic removal of cellular sialic acid, and cells with characteristically low butyrylcholinesterase activity, e.g., adrenergic clonal line N115 neuroblasts displayed relatively high activity after treatment with sialidase. These findings open the possibility that adaptive regulation of cholinesterases in mammalian cells may be mediated rapidly through changes in their sialic acid content.
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PMID:Activation of acetyl- and butyrylcholinesterase by enzymatic removal of sialic acid from intact neuroblastoma and astroblastoma cells in culture. 17 21

Single subcutaneous inoculation of human adenovirus type 12 (Ad.12), 0.05-0.1 ml of 10(8.0) TCID50 HEK cells/0.1 ml, was made on the back of 0-day-old hamsters. In 21 of 25 hamsters (84.0%), multiple solid tumors developed close to the inoculation site within 3 months. No control hamsters developed tumors. Tumor histopathology revealed the characteristic Homer Wright rosettes of neuroblastoma. Ad. 12-specific tumor antigens were demonstrable in both the primary and the cultured tumor cells by the immunofluorescein technique. Histochemical demonstration of cholinesterase and NADH oxidoreductase gave rise to a predominantly positive intracytoplasmic granule within the tumor cells. Electron microscopy showed remarkably uniform cell morphology: small, undifferentiated neuroblastic cells with poorly developed intracytoplasmic organelles; many possessed characteristic solitary cilia in a 9 + 0 tubules pattern. Intercellular junctions were poorly developed. Search for an incipient tumor cell aggregate by means of immunofluorescein T-antigen detection was carried out through a 240-h period following Ad. 12 inoculation. A sequential study in parallel with electron microscopic examination of the normal subcutaneous tissue proved that neuroblastic cells closely associated with the muscle spindle anlage could preferentially become the most sensitive target for Ad. 12 tumorigenesis.
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PMID:Cell origin of human adenovirus type 12-induced subcutaneous tumor in Syrian hamsters. 44 84

In vitro, we were able to induce a differentiation of human (SK-N-MC, IMR-32, Leo-2) and murine neuroblastoma cells (NA-2, C-1300, NIE-115) with dibutyryl cyclic 3'5'-adenosine monophosphate (dbcAMP), hypothalamic factor (HF), and somatostatin. As morphological criteria of cellular differentiation we used the decrease in cell proliferation and the formation of neurites. Functional parameters were the increase of A cholinesterase activity, cAMP level, and protein content, and the decrease of cGMP level. After application of dbcAMP and HF, the effects were stronger than after somatostatin. We believe that the action of HF and somatostatin is caused by an increase in cAMP levels. In the in vivo experiments, human and murine neuroblastoma cells (NA-2, C-1300, and Leo-2) were transplanted into nude/nude mice. After HF treatment of 14 mice with NA-2 tumors, 4 of the mice were tumor-free, and mean tumor weight was reduced to one-third of the controls. Of the animals with C-1300 and Leo-2 tumors, half became tumor-free, and mean tumor weight was reduced to one-fourth. The results indicate that the induction of cellular differentiation by factors and hormones may in future become a method of therapy for human neuroblastoma.
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PMID:Research on the differentiation of human and murine neuroblastoma cells. 167 82

To study the molecular origin of the altered regulation of butyrylcholinesterase (BuChE) in nervous system tumors, BuChE complementary DNA (cDNA) sequences from human glioblastoma and neuroblastoma cDNA libraries were compared with BuChE cDNAs from normal fetal and adult tissues. A single 2.6-kilobase BuChE cDNA sequence was found in all normal tissues, whereas an additional alternatively terminated BuChE cDNA clone was found in both tumor libraries. The tumor-specific cDNA contained a 3',0.7-kilobase nontranslatable extension, as well as several nucleotide alterations in the normal polyadenylation site. Single-base mutations in the coding region of this unusual BuChE cDNA infer two amino acid substitutions: Asp70----Gly and Ser425----Pro. The Asp70----Gly change has recently been implicated with "atypical" BuChE, which is deficient in its capacity to hydrolyze succinylcholine. The 3.6-kilobase mRNA was less abundant in RNA blot hybridization than the 2.6-kilobase mRNA, which is in agreement with the low ratios between the 3.6- and 2.6-kilobase BuChE cDNA clones in glioblastoma and neuroblastoma libraries. Furthermore, size fractionation and microinjection of glioblastoma polyadenylated RNA, followed by enzyme activity and selective inhibition measurements, demonstrated two peaks of functional BuChE mRNA, the heavier one probably reflecting the longer transcripts. Chromosomal mapping of the 0.7-kilobase 3' fragment by in situ hybridization localized it to a unique 3q26-ter position, where we recently found an inheritably amplified "silent" defective CHE gene in a family exposed to the cholinesterase inhibitor methyl parathion. Our findings confirm previous genetic linkage mapping of the functional CHE gene to the 3q26-ter position and demonstrate that extended functional mRNA transcripts encoding a BuChE form with two modified amino acids are produced from this gene in glioblastoma and neuroblastoma cells.
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PMID:Expression of alternatively terminated unusual human butyrylcholinesterase messenger RNA transcripts, mapping to chromosome 3q26-ter, in nervous system tumors. 231 87

The method is suggested to isolate simultaneously microsomes and plasma membranes of neuroblastoma S 1300 N 18 cells by means of differential centrifugation in the step density gradient of Percoll/Ficoll with a high degree of purification determined from the activity of marker enzymes (acetyl cholinesterase Na+,K+-ATPase, alkali phosphatase, glucose-6-phosphatase, succinate-dehydrogenase, acid phosphatase) as well as from the content of DNA and RNA and with a sufficiently high protein yield. The purified fractions of microsomes and plasma membranes are established to contain no phosphatidyl glycerol and cardiolipin--safety markers of mitochondrial membrane purification. A degree of separation of microsomes, plasma membranes and proteins dissolved in cytosol may be estimated by the activity of the cholesterol-synthesizing system of enzymes with the use of sterol-transferring protein.
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PMID:[Rapid simultaneous isolation of microsomes and plasma membranes from neuroblastoma C 1300 N 18 cells]. 258 50

The commercially available kits (Test-Combination, Cholinesterase, Boehringer, Mannheim and Test-reagent, Cholinesterase EC 3.1.1.8, Pliva, Zagreb) and reagents prepared in own laboratory for measuring cholinesterase activity (Ellman method) were tested with respect to their stability and the reproducibility of the activity measurements. The reagents of the three sources were shown to be interchangeable and equally stable over a few weeks. The coefficient of variation for within-run measurements by the Ellman method was 2-3% and that for between-run measurements 6%. The stability of the few enzyme standards (Precinorm E, Precinorm U, NBS-serum and native human serum) for the quality control of the measurements was also tested: the most stable was native human serum.
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PMID:[Measurement of serum cholinesterase activity: comparison of commercial and laboratory test reagents, enzyme standards and statistical processing of the results]. 263 23

Long-term preincubation at 37 degrees of mouse neuroblastoma cells (clones NS-20 and N1E-115) with soman, a potent and irreversible cholinesterase inhibitor, resulted in a significant decrease in the number of [3H]N-methylscopolamine binding sites and in the inhibition of carbamylcholine-induced cyclic GMP formation. The disappearance of surface muscarinic receptors and the desensitization of the receptor-mediated response seem to occur via accumulation of acetylcholine in the culture medium. The significance of these findings is discussed.
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PMID:Modulation of the number of muscarinic receptors in mouse neuroblastoma cells by soman. 302 49

The histogenesis of Ewing's sarcoma remains unknown. Recent studies have suggested a relationship to an unusual form of childhood neural tumor, often termed peripheral neuroepithelioma or primitive neuroectodermal tumor. Five Ewing's sarcoma tumor cell lines were studied for evidence of a neural phenotype. Under normal culture conditions, no morphologic evidence of neural differentiation was detected. Treatment with retinoic acid, an agent known to induce marked neural differentiation in neuroblastoma, had no demonstrable effect. Treatment with either cyclic AMP or TPA, in contrast, induced pronounced morphologic evidence of neural differentiation. Cells developed elongate processes with varicosities by phase-contrast microscopy; filaments, microtubules, and uraniffin-positive dense core granules were present by electron microscopy. Three neural markers (NSE, NFTP, and cholinesterase) were absent or barely detectable in untreated cells, but became abundant after treatment. These results provide convincing evidence for a neural histogenesis of Ewing's sarcoma. They also suggest a close relationship between Ewing's sarcoma and peripheral neural tumors, including the chest wall tumor described by Askin, but only a distant relationship to neuroblastoma.
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PMID:Experimental evidence for a neural origin of Ewing's sarcoma of bone. 303 30

Children undergoing ABMT, a procedure which entails massive doses of chemotherapy along with total-body irradiation, are candidate to develop severe gastrointestinal toxicity and prolonged anorexia requiring administration of Parenteral Nutrition (PN) for variable periods. We report a series of 35 consecutive children affected by malignancies who underwent 37 courses of PN after ablative therapy followed by ABMT. Age ranged from 8 months to 17 years; 16 were females, 19 males. There were 23 cases of neuroblastoma, 5 of Wilms' tumor, 3 of acute myelogenous leukemia, 2 of Ewing's sarcoma, 1 case each of rhabdomyosarcoma and acute lymphoblastic leukemia. All patients developed severe neutropenia for 9-42 days (median 18 d). Fever occurred in all patients; sepsis was documented in 10. Duration of PN ranged from 10 to 64 days (23 +/- 9; mean +/- SD). PN solution, containing crystalline L-Aminoacids (8.5%) mixed with 33% glucose, minerals, trace elements and vitamins provided for children a caloric intake of 49.8 +/- 17.3 Kcal/Kg/day with a nitrogen intake of 0.26 +/- 0.27 g/Kg/day. Nutritional assessment, utilizing percent ideal body weight, serum protein electrophoresis, C3, pseudocholinesterase and fibrinogen, was performed at the beginning and at the completion of each course of PN. Mean percent ideal body weight was 95.8 before PN, 98.5 on last day of PN (p less than 0.0005). Other parameters did not change significantly. No metabolic complication nor severe electrolyte imbalance were observed except for 5 patients who developed hypokalemia in coincidence with administration of Amphotericin B.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Autologous bone marrow transplantation in children. Use of parenteral nutrition]. 311 38

Mouse N1E-115 neuroblastoma cells were used to study carbachol induced changes in muscarinic cholinergic parameters. Cells were treated with carbachol (1 mM) for up to 96 hours. The number of muscarinic receptors, measured in 3H-3-quinuclidinyl benzilate binding experiments, decreased approximately 50% after 4 hours exposure to carbachol. This was followed by an increase in binding sites, and after 24 hours the number of binding sites was the same as in control cells. The changes observed in the choline esterase activity followed the same pattern. The increase in number of binding sites was not dependent on protein synthesis, while the increase in choline esterase activity was. The muscarinic receptor-stimulated uptake of 45Ca2+ showed an initial decrease, which was followed by a significantly increased basal uptake of 45Ca2+. It is suggested that all these changes are adaptations of long time exposure to carbachol.
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PMID:Exposure to carbachol induces several changes in muscarinic cholinergic parameters in N1E-115 mouse neuroblastoma cells. 335 74


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