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)

We have studied the regulation of lysosomal glycosidases during morphological differentiation of NB2a neuroblastoma cells. Cells treated with dibutyryl cAMP induced axon-like neuritis and showed a 2-4 fold increase in the activity of 6 lysosomal glycosidases, reaching their highest level after 5 days of treatment. Cells treated with retinoic acid, which induced dendrite-like neurites, did not show significant changes in the glycosidases activity although cell proliferation was also inhibited. There was no change in the pattern of the enzyme secretion during the dibutyryl cAMP treatment and morphological analysis using electron microscopy and cytochemical staining with acid phosphatase indicated the presence of lysosomes in the induced neurites.
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PMID:Induction of lysosomal glycosidases by dibutyryl cAMP in neuroblastoma cells. 242 67

Ultrastructural study of neuroblastoma group tumors including 7 neuroblastomas, 4 ganglioneuroblastomas, and 2 ganglioneuromas was performed by using both TEM and SEM. Tumor cells showed a wide variation comparable to the developmental stages of nerve cells and were classified into four types according to the neuritic process projections; namely apolar, monopolar, bipolar, and multipolar. Neuroblastoma was composed of small cells of apolar, monopolar, and bipolar types with few multipolar cells. Tumor cells ganglioneuroblastoma and ganglioneuroma were multipolar type. SEM observation demonstrated characteristic varicosities in the elongated neuritis processes, and by TEM examination the dilated portions of these varicosities revealed disruption or disappearance of parallel runnings of the microtubules and microfilaments. TEM examination demonstrated presence of Schwann cells in ganglioneuroblastoma and ganglioneuroma, and satellite cells and perineurial cells in ganglioneuroma. The hitherto undescribed cells with caveolar structure which are thought to be a precursor of these stromal elements were disclosed in ganglioneuroblastoma. In order to evaluate the maturation and prognosis of tumors of this group, stromal differentiation seems to be equally important as ganglionic differentiation because both stromal elements and tumor cells have a common origin of neural crest.
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PMID:Transmission and scanning electron microscopic studies on the tumors of neuroblastoma group. 628 64

In Alzheimer's disease (AD), in aging, and under conditions of oxidative stress, the levels of reactive carbonyl compounds continuously increase. Accumulating carbonyl levels might be caused by an impaired enzymatic detoxification system. The major dicarbonyl detoxifying system is the glyoxalase system, which removes methylglyoxal in order to minimize cellular impairment. Although a reduced activity of glyoxalase I was evident in aging brains, it is not known how raising the intracellular methylglyoxal level influences neuronal function and the phosphorylation pattern of tau protein, which is known to be abnormally hyperphosphorylated in AD. To simulate a reduced glyoxalase I activity, we applied an inhibitor of glyoxalase I, p-bromobenzylglutathione cyclopentyl diester (pBrBzGSCp(2)), to SH-SY5Y neuroblastoma cells to induce chronically elevated methylglyoxal concentrations. We have shown that 10 microM pBrBzGSCp(2) leads to a fourfold elevation of the methylglyoxal level after 24 hr. In addition, glyoxalase I inhibition leads to reduced cell viability, strongly retracted neuritis, increase in [Ca(2+)](i), and activation of caspase-3. However, pBrBzGSCp(2) did not lead to tau "hyper"-phosphorylation despite activation of p38 mitogen-activated protein kinase and c-Jun NH(2)-terminal kinase but rather activated protein phosphatases 2 and induced tau dephosphorylation at the Ser(202)/Thr(205) and Ser(396)/Ser(404) epitopes. Preincubation with the carbonyl scavenger aminoguanidine prevented tau dephosphorylation, indicating the specific effect of methylglyoxal. Also, pretreatment with the inhibitor okadaic acid prevented tau dephosphorylation, indicating that methylglyoxal activates PP-2A. In summary, our data suggest that a reduced glyoxalase I activity mimics some changes associated with neurodegeneration, such as neurite retraction and apoptotic cell death.
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PMID:Pathological effects of glyoxalase I inhibition in SH-SY5Y neuroblastoma cells. 1655 97

Cytoskeletal components play an important role in maintaining cellular architecture and internal organization, with clear involvement of defining cell shape, in cell division and other cellular processes, such as neurite extension and maintenance. Alterations of cytoskeleton in human neuroblastoma SK-N-SH cells after exposure to different concentrations of tri-ocresyl phosphate (TOCP) for 12 hr were investigated. TOCP decreased the cell viability in a dose-dependent manner; the viability of SK-N-SH was reduced to approximately 50% of baseline after a 12-hour exposure to TOCP at high concentration (5 mM). Biochemical characterization by western blotting revealed that 1 and 5 mM concentrations of TOCP significantly inhibited the expression of neurofilament high molecular weight protein (NF-H), and that 5 mM TOCP inhibited expression of microtubule-associated protein 2c and tau protein, but not beta-actin. Indirect immunofluorescence analysis revealed that higher concentrations of TOCP decreased the length of neuritis and changed the structure of microfilaments, which are associated with NF-H. In addition, activities of neuropathy target esterase and acetylcholinesterase were significantly reduced after exposure to 5 mM TOCP for 12 hr. Together, these results suggested that the loss of cytoskeletal components is the early event during the process of TOCP toxicity towards human neuroblastoma SK-N-SH cells.
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PMID:Effect of tri-o-cresyl phosphate on cytoskeleton in human neuroblastoma SK-N-SH cell. 1690 9

Notch proteins are definitely recognized as key regulators of the neuronal fate during embryo development, but their function in the adult brain is still largely unknown. We have previously demonstrated that Notch pathway stimulation increases microtubules stability followed by the remodeling of neuronal morphology with neurite varicosities loss, thicker neuritis, and enlarged growth cones. Here we show that the neurite remodeling is a dynamic event, dependent on transcription and translation, and with functional implications. Exposure of differentiated human SH-SY5Y neuroblastoma cells to the Notch ligand Jagged1 induces varicosities loss all along the neurites, accompanied by the redistribution of presynaptic vesicles and the decrease in neurotransmitters release. As evaluated by time lapse digital imaging, dynamic changes in neurite morphology were rapidly reversible and dependent on the activation of the Notch signaling pathway. In fact, it was prevented by the inhibition of the proteolytic gamma-secretase enzyme or the transcription machinery, and was mimicked by the transfection of the intracellular domain of Notch. One hour after treatment with Jagged1, several genes were downregulated. Many of these genes encode proteins that are known to be involved in protein synthesis. These data suggest that in adult neurons, Notch pathway activates a transcriptional program that regulates the equilibrium between varicosities formation and varicosities loss in the neuronal presynaptic compartment involving the expression and redistribution of both structural and functional proteins.
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PMID:Notch activation induces neurite remodeling and functional modifications in SH-SY5Y neuronal cells. 1926 17

Cyanoacrylate adhesive has been suggested as an alternative to suturing when repairing severed peripheral nerves. The authors examined the cytotoxic effect of ethyl-cyanoacrylate on the human neuroblastoma cell line SH-SY5Y and compared it with the effects of butyl-cyanoacrylate (Histoacryl), an adhesive approved for skin closure. Ethyl-cyanoacrylate or butyl-cyanoacrylate was applied in confluent SH-SY5Y cultures. Immediately, at 24h and at 7, 14, 21 and 28 days, cultures were photographed and analysed digitally. At corresponding intervals, cell death was quantified using a (51)Cr release assay. In cultures exposed to ethyl-cyanoacrylate or butyl-cyanoacrylate, cell death was observed predominantly in conjunction with the adhesive, causing a halo devoid of cells. Surviving cells showed neurodegenerative properties with loss of neuritis and reduction of body size up to 3 days post exposure. The inhibition halo diminished over time in both groups and at 28 days cells reached the margin of the adhesive in the ethyl-cyanoacrylate group. (51)Cr assay indicated significant cell death in exposed cultures, which rapidly decreased during the first 14 days. No significant differences were found between the adhesives. This study demonstrates that ethyl-cyanoacrylate and butyl-cyanoacrylate have a transient cytotoxic effect, which may explain the promising results when using cyanoacrylate for nerve repair.
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PMID:Cyanoacrylate in nerve repair: transient cytotoxic effect. 2043 10

We describe the case of a 16-month-old girl with neuroblastoma and chronic lymphocytopenia due to chemotherapy and treosulfan-containing megatherapy who developed cytomegalovirus retinitis and neuritis. Intravenous ganciclovir and anti-cytomegalovirus immunoglobulin were used with a transient benefit; however, retrobulbar gancyclovir resulted in a complete remission. This report emphasizes the need for close monitoring of viral infections in patients undergoing treosulfan-containing megatherapy, highlighting the immunosuppressive effects of this agent, and indicates the potential use of retrobulbar ganciclovir as the alternative method of drug delivery.
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PMID:Effective treatment of cytomegalovirus retinitis and neuritis with retrobulbar ganciclovir after treosulfan-based autologous bone marrow transplant. 2663 47