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 possible role of surface glycosaminoglycans (GAGs) in neuronal maturation occuring in neuroblastoma cultures has been investigated. GAGs of neuroblastoma cells, grown in suspension and monolayer, were labelled with 3H-glucosamine and 35S-sulfate. Neuron maturation, following cell adhesion to culture dishes, is accompanied by an increased ability of the cells to retain heparan sulfate (HS) on their surface, which is otherwise lost into the culture medium. The role of surface HS as a cofactor of cellular differentiation is discussed.
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PMID:Surface glycosaminoglycans as a differentiation cofactor in neuroblastoma cell cultures. 13

Ecto-ATPase and ecto-5'-nucleotidase activities of hamster astroblasts, clonal line NN, and mouse neuroblasts, clonal line Ml in coculture, have been studied. The originally low ecto-ATPase activity in both cell lines increased many fold when these cell lines were cocultured. An increase of ecto-ATPase activity was also found in coculture of neuroblastoma cells with chick fibroblasts. Neuroblastoma Ml cells were separated from coculture with hamster astroblasts after 7 days and 2 months. Reisolated M1 cell lines exhibited higher ecto-ATPase activity than the original M1 cell line. The M1 cell line separated after 2 months of coculture had higher ecto-ATPase activity than the M1 cell line separated after 7 days of coculture with hamster astroblasts. This higher ecto-ATPase activity continued for more than 20 replications after separation of the M1 cells from the glial cells.
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PMID:Neuroblasts-glia interaction in tissue culture as evidenced by the study of ectoenzymes. Ecto-ATPase activity of mouse neuroblastoma cells. 13 72

One to three-month-old A-strain mice, inoculated subcutaneously with 2 x 10(6) viable syngeneic C1300 neuroblastoma cells (clone NB9R) developed a palpable tumor within 9-12 days and died within 28-30 days. A transient glomerulopathy developed after 16-24 days. Despite a normal histologic appearance, the nephropathy was clearly demonstrated by electron microscopy and was classified as a focal mesangiopathic glomerulonephritis. Deposits of host 7S-G immunoglobulins and C3 complement fragments were detected in these same kidneys by immunofluorescence. Radioimmunoprecipitin determinations on sera obtained from mice at different intervals from tumor cell inoculation, revealed that untreated mice contained circulating antibodies capable of reacting with 125I-labeled gp69-71 glycoprotein from Gross murine leukemia virus (MuLV). Antibodies to p30 MuLV antigen and to crude membrane antigen (s) (CMA) solubilized from NB9R cells were found in sera only after tumor cell inoculation. Circulating immune complexes formed by host 7S-G immunoglobulins were clearly detected from day 16 to 22. Antibodies eluted from kidneys with nephropathy were shown to react with NB9R cells in vitro and to react specifically with CMA and the p30 MuLV antigen.
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PMID:Antibody formation and transient immune complex glomerulopathy in A-strain mice with C1300 neuroblastoma tumors. 14 55

The phenylalanine analogues p-chlorophenylalanine and alpha-methylphenylalanine were used to inhibit phenylalanine hydroxylase in animal models for phenylketonuria. The present report examines the affects of these analogues on the metabolism of neuroblastoma cells. p-Chlorophenylalanine inhibited growth and was toxic to neuroblastoma cells. Although in vivo this analogue increased cell monoribosomes by 42%, it did not significantly affect poly(U)-directed protein synthesis in vitro. P-Chlorophenylalanine did not compete with phenylalanine or tyrosine for aminoacylation of tRNA and was therefore not substituted for those amino acids in nascent polypeptides. The initial cellular uptake of various large neutral amino acids was inhibited by this analogue but did not affect the flux of amino acids already in the cell; this suggested that an alteration of the cell's amino acid pools was not responsible for the cytotoxicity of the analogues. In contrast with p-chlorophenylalanine, alpha-methylphenylalanine did not exert these direct toxic effects because the administration of alpha-methylphenylalanine in vivo did not affect brain polyribosomes and a comparable concentration of this analogue was neither growth inhibitory nor cytotoxic to neuroblastoma cells in culture. The suitability of each analogue as an inhibitor of phenylalanine hydroxylase in animal models for phenylketonuria is discussed.
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PMID:Effects of p-chlorophenylalanine and alpha-methylphenylalanine on amino acid uptake and protein synthesis in mouse neuroblastoma cells. 15 35

Addition of 6-AN (0.01 mg/ml) to growing cultures of C-1300 neuroblastoma cells strongly reduced cell division. This growth inhibition was accompanied by a higher cell volume and a lower protein content per cell as compared to controls. Concurrently the specific activity of AChE increased markedly incontrols and 6-AN-treated cultures. During the experimental periods the specific activity of AChE was significantly higher after 6-AN. Morphologically, 6-AN-treated cultures showed characteristic signs of differentiation, i.e. enlarged, flattened cells with long branched processes. The described effect of 6-AN on growth and differentiation of neuroblastoma cells was less pronounced if cells received the antimetabolite after a subcultivation period of 5 days.
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PMID:Effects of 6-aminonicotinamide on growth and acetylcholinesterase activity during differentiation of neuroblastoma cells in vitro. 15 76

A biological system consisting of a cell membrane enzyme (Na+-K+)-ATPase responded to exposure to a weak A.C. magnetic field. Analysis of Na+ pump activity in normal mouse (A/J) tissue--(a) Kidney cortex and diaphragm after 11 days of exposure to a magnetic field of 55-60 gauss, 60Hz showed a significant reduction as did (b) liver tissue but at day 17 the levels had returned to the control values. Neuroblastoma cells (C1300) transplanted to A/J mice also showed a reduction in the (Na+-K+)-ATPase activity but this persisted at day 17.
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PMID:Weak A.C. magnetic field effects: changes in cell sodium pump activity following whole animal exposure. 15 71

A cerebral neuroblastoma removed surgically from a female child is presented. Electron microscopy showed numerous neuronal processes with growth cones which are a feature of the developing neurone. In addition there were some rosettes with distinct lumina. The luminal surfaces were covered with a smooth plasma membrane lacking any surface differentiation and the lateral surface of these cells had many cell junctions (terminal bars), reminiscent of a primitive neural tube. These features in a nerve cell tumor help to substantiate it as a neuroblastoma arising from immature rather than differentiated cells. The nature of this rare tumor is discussed.
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PMID:Cerebral neuroblastoma. 15 41

We studied two children with neuroblastoma in whom hypercalcemia developed as the initial manifestation in one and during the course of therapy in the other. Serum parathyroid hormone activity was elevated in the patient in whom the test for it was performed. Mithramycin controlled the hypercalcemia in one patient and tumor resection with radiation therapy and chemotherapy was sufficient for control of this complication in the other.
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PMID:Hypercalcemia associated with neuroblastoma. 15 70

Adult A/J mice inoculated with 1 x 10(6) syngeneic C1300 neuroblastoma cells had a palpable tumor after 1 week, and the tumor grew uniformly. The hypertonic KCl extract of the tumor induced blastogenic response of syngeneic spleen cells from tumor-bearing mice, and tumor antigens were considered to be solubilized by KCl from tumor cells. Although a higher blastogenic response to insoluble tumor antigens coupled to Sepharose 4B beads could have been expected as demonstrated in this mixed lymphocyte-tumor cell reaction (MLTR) assays, the blastogenic activity, which was approximately equal to that of soluble tumor antigens, was less than one-third of that in MLTR. The initial information of blastogenic response was found to be transmitted to the responder cells with out the entrance of tumor antigens into the cells by the use of insoluble tumor antigens. Blastogenic responses to soluble tumor antigens and to irradiated tumor cells (MLTR) in spleen cells from tumor-bearing mice were serially assayed after tumor inoculation. The response to soluble tumor antigens reached a peak 2 weeks after inoculation but a progressive depression of the responses was observed after a marked tumor growth. Although the blastogenic activity of soluble tumor antigens was small, changes in consecutive response to soluble tumor antigens in tumor-bearing mice were well correlated with those in MLTR. The blastogenic responses to soluble tumor antigens and MLTR were considered to be the manifestation of tumor-specific cell-mediated immunity. Furthermore, the serial blastogenic responses to concanavalin-A and lipopolysaccharide were also coincident with those of tumor-specific immunity.
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PMID:Blastogenic response of spleen cells from C1300 neuroblastoma-bearing mice to tumor cells or soluble and insoluble tumor antigens. 15 10

Mixed lymphocyte--tumor cell cultures were made with materials from patients with various histological types of cancer. In 25 out of 89 patients, positive lymphocyte response to tumor cells was observed. There appeared to be an inverse relationship between the frequency of positive responses and extent of the disease. Patients with neuroblastoma, however, showed more frequent positive responses in cases of widespread disease. The data obtained may have valuable clinical implications, supporting the possibility of immunotherapy of cancer patients.
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PMID:Lymphocyte response to autochthonous human solid tumor cells: relationship to histological types and tumor load. 16 Dec 40


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