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Query: UMLS:C0027819 (neuroblastoma)
 27,800 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The accumulation of [3H]triphenylmethylphosphonium cation in neuroblastoma N1E 115 cells in the presence of tetraphenylboron is reduced by 3,3'-diethylthiadicarbocyanine iodide and by 3,3'-dipropylthiadicarbocyanine iodide. This reduction in uptake of the lipophilic cation is not due to the carbocyanine dyes depolarizing the plasma membrane of these cells but due to an interaction between the carbocyanine dyes and tetraphenylboron leaving less of the lipophilic anion free in solution to assist uptake of the lipophilic cation. This interaction is shown to have a 1:1 stoicheiometry.
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PMID:Reduction in accumulation of [3H]triphenylmethylphosphonium cation in neuroblastoma cells caused by optical probes of membrane potential. Evidence for interactions between carbocyanine dyes and lipophilic anions. 687 Dec 53

The fluorescence photobleaching recovery method has been used to determine the lateral mobilities of membrane lipids and proteins during the cell cycle of synchronized C1300 mouse neuroblastoma cells (clone Neuro-2A). As probes for lipid mobility, 3,3'-dioctadecylindocarbocyanine iodide and a fluorescein-labeled analog of ganglioside GM1 were used. Membrane proteins were labeled with rhodamine-labeled rabbit antibodies against mouse E14 cells. For both lipid probes the diffusion coefficients reach a minimum in mitosis, increase 2- to 3-fold during G1, remain constant at maximal values during S, and decrease again shortly before mitosis. Membrane proteins also exhibit minimum diffusion coefficients in mitosis, followed by a similar rise in G1. However, as cells proceed through S and G2, the lateral mobility of the membrane proteins gradually decreases. It is argued that lipid mobility is controlled by the fluidity of the membrane lipid matrix whereas protein mobility is governed also by other constraints.
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PMID:Lateral diffusion of membrane lipids and proteins during the cell cycle of neuroblastoma cells. 692 4

The case of a thirty two years old patient with a frontal syndrome developing over the last three years is reported. CT scan showed a large calcified lesion, situated on the median line enhanced by iodine. The patient was operated. Ultrastructural and histologie studies concluded that it the tumor was a neuroblastoma. After operation an unquestionable amelioration of the frontal disorders appeared. Facial paralysis with a inverse automatic-voluntary dissociation and an underuse of motricity, both left-sided, after cortectomy of the right-sided premotor area were observed. We therefore suggest that the lesion of the external premotor cortex was responsible of the facial paralysis with an inverse automatic voluntary dissociation and of the underuse the left side.
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PMID:[Cerebral neuroblastoma in the adult. Clinical and C.T. scan aspects (author's transl)]. 729 46

The actions of two structurally related tricyclic antidepressants on neuronal nicotinic acetylcholine receptors were investigated in human neuroblastoma (SY-SY5Y) cells, using whole-cell patch-clamp recordings. Both desipramine and imipramine reversibly inhibited inward currents evoked by application of the nicotinic receptor agonist dimethylphenylpiperazinium iodide (30-300 microM) with IC50 values of 0.17 microM and 1.0 microM respectively (holding potential -70 mV). The degree of current inhibition caused by either tricyclic compound was unaffected by agonist concentration (30-300 microM). The effects of desipramine were voltage-independent over the range -40 mV to -100 mV, and inhibition caused by imipramine only increased very slightly with membrane hyperpolarization over the same range. These results indicate that tricyclic antidepressants can inhibit neuronal nicotinic acetylcholine receptors by mechanisms which are distinct from their actions at non-neuronal nicotinic acetylcholine receptors.
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PMID:Inhibition of neuronal nicotinic acetylcholine receptors by imipramine and desipramine. 750 83

In vitro and in vivo neuroblastoma models were used to determine whether improvements in tumour targeting in vivo and therapeutic efficacy in vitro could result from the use of no-carrier-added (n.c.a.) [131I]MIBG. Results were compared with use of the conventional therapy MIBG preparation (ex. [131I]MIBG) of lower specific activity which is produced by iodide exchange reaction. The efficacy of n.c.a. [131I]MIBG was compared with that of [131I]MIBG over a range of specific activities by the assessment of neuroblastoma spheroid growth delay. Whereas n.c.a. [131I]MIBG at a radioactivity concentration of 2 MBq/ml prevented the regrowth of 84% of spheroids, toxicity was significantly reduced by the addition of non-radiolabelled MIBG to the incubation medium. The time-dependent biodistribution of n.c.a. [131I]MIBG in nude mice bearing human neuroblastoma xenografts was compared with that of the conventional therapy radiopharmaceutical. The n.c.a. agent gave improved tumour uptake but also significantly greater accumulation in normal tissues known to accumulate MIBG such as heart, adrenal and skin. However, uptake and retention in the blood was unaltered. For all tissues examined, the 3-day calculations were undertaken to predict organ to tumour dose ratios which would result in human neuroblastoma patients with each of the [131I]MIBG preparations. These results suggest that significant therapeutic gain may be achieved by the use of n.c.a. [131I]MIBG as a treatment agent in neuroblastoma. neuroblastoma.
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PMID:Enhanced tumour uptake and in vitro radiotoxicity of no-carrier-added [131I]meta-iodobenzylguanidine: implications for the targeted radiotherapy of neuroblastoma. 757 72

The purpose of this work was to compare technetium-99m-diphosphono-propanedicarboxylate (DPD) and iodine-123-metaiodobenzylguanidine (MIBG) scans in the diagnosis and follow-up of neuroblastoma, and to study the role of histological differentiation in the uptake of MIBG. The uptake of MIBG and of DPD were studied retrospectively in 27 patients with neuroblastoma (primary, residual and recurrent tumours as well as bone and bone marrow metastases). The findings were related to the histological classification of the tumours as neuroblastoma (N1), differentiating neuroblastoma (N2) or ganglioneuroblastoma (N3). Uptake of MIBG by the primary tumour occurred in 17 of 19 patients, either at diagnosis or during follow-up. There were only two false-negatives with MIBG, both of which were N3. Ten patients were studied preoperatively with both MIBG and DPD. The primary tumour showed MIBG uptake in nine of the ten and DPD uptake in eight of them. Thirty-five sites of cortical bone metastasis were shown in eight patients by both MIBG and DPD, 12 sites in seven patients by MIBG only and seven sites in five patients by DPD only. In 14 patients both MIBG and bone scan were negative. Overall, MIBG demonstrated more lesions than DPD. Retrospectively several hot spots seen only with the bone scan are to be considered as false-positive. The highest incidence of false-negative MIBG and bone scans was observed in ganglioneuroblastoma with a predominance of the more mature component (ganglioneuroma).
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PMID:Diagnosis and follow-up of neuroblastoma by means of iodine-123 metaiodobenzylguanidine scintigraphy and bone scan, and the influence of histology. 760 62

Dimethylphenylpiperazinium iodide (a nicotinic agonist) evokes noradrenaline release from human neuroblastoma SH-SY5Y cells that have been pretreated with 12-O-tetradecanoylphorbol 13-acetate for 8 min. This effect of dimethylphenylpiperazinium iodide was inhibited by 1 microM mecamylamine but not by 1 microM atropine, which suggests that SH-SY5Y cells express nicotinic receptors coupled to the release of noradrenaline. Dimethylphenylpiperazinium iodide-evoked release was enhanced by 5 microM Bay K 8644 (an L-type calcium agonist) and inhibited by 1 microM nifedipine. Dimethylphenylpiperazinium iodide depolarised SH-SY5Y cells and enhanced the level of intracellular calcium in cells loaded with fura 2. The effects of dimethylphenylpiperazinium iodide on noradrenaline release, depolarisation, and intracellular calcium levels were all inhibited by 1 microM desmethylimipramine. The results of this study show that nicotinic receptors in SH-SY5Y cells stimulate noradrenaline release by activation of L-type calcium channels.
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PMID:Nicotinic receptor-mediated release of noradrenaline in the human neuroblastoma SH-SY5Y. 768 69

Iodine labeled metaiodobenzylguanidine (MIBG) is a radiopharmaceutical employed for both diagnosis and metabolic radiotherapy of neuroblastoma (NB). Resistance to the radiotherapeutic effects of MIBG is common, due to lack of MIBG accumulation by NB cells. MIBG enters competent cells via the noradrenaline transporter; this function requires a relative cellular maturation and is missing in most NB cell lines. In vitro differentiation of NB cells can be achieved with gamma-interferon (gamma-IFN) and other agents. We have verified that gamma-IFN-induced differentiation of NB cells is specifically associated with an increase in their ability to incorporate MIBG. This phenomenon is due to enhancement of MIBG transporter activity, according to pharmacological sensitivity and semiquantitative PCR-based analysis of specific MIBG transporter mRNA. New therapeutic strategies based on both differentiation therapy and targeted radiotherapy of NB can so be devised.
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PMID:Interferon-gamma-induced differentiation of human neuroblastoma cells increases cellular uptake and halflife of metaiodobenzylguanidine. 776 44

bcl-x is a new member of the bcl-2 gene family and is highly expressed in neural tissues. The present study was designed to determine the expression of the bcl-x gene products in neuroblastoma (NB) and their role in the modulation of chemotherapy-induced apoptosis. Twenty-seven NB cell lines were screened by quantitative immunoprecipitation for Bcl-xL, Bcl-xS, and Bcl-2 expression. None of the cell lines expressed Bcl-xS. Twenty-four of 27 (88%) of the NB cell lines expressed Bcl-xL and 21 of 27 (78%) were positive for Bcl-2. The level of Bcl-xL and Bcl-2 expression was variable among the lines analyzed. Bcl-2 expression was restricted to cells of chromaffin lineage, whereas Bcl-xL was seen in both chromaffin and nonchromaffin lines. To determine whether Bcl-xL could mediate chemotherapy resistance, a NB cell line expressing negligible levels of Bcl-xL was transfected with a bcl-xL expression vector, and unique clones were generated expressing variable levels of Bcl-xL. Cells were treated either with cisplatinum (CP), 4-hydroperoxy-cyclophosphamide (4-HC), or etoposide (VP-16) to induce apoptosis, and cell viability and DNA degradation were determined. Following treatment with CP or 4-HC, Bcl-xL-expressing cells showed significantly increased viability as compared to vector-transfected controls (P < 0.005). Flow cytometric analysis of propidium iodide-stained nuclei following CP or 4-HC treatment revealed significantly increased DNA degradation in controls as compared to Bcl-xL-expressing lines (P < 0.004). DNA analysis by pulsed-field gel electrophoresis revealed high molecular weight (approximately 40 kb) DNA degradation in controls, whereas the DNA in cells expressing Bcl-xL was largely intact. In contrast to CP and 4-HC, results with VP-16 revealed a short-term delay in the onset of apoptosis in Bcl-xL-expressing cells with no long-term survival advantage. The results of these studies indicate Bcl-xL is expressed in NB cells and functions in a manner analogous to Bcl-2 by inhibiting chemotherapy-induced apoptosis.
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PMID:Bcl-xL is expressed in neuroblastoma cells and modulates chemotherapy-induced apoptosis. 778 Sep 71

Apoptosis influences early development and later refinement in adult tissues. Experiments in which embryonic neurons or multipotent neural precursor cells are transplanted into regions of neuronal degeneration following targeted photolytic cell death show similar regulation of neuronal migration and differentiation. In those experiments, transplanted cells sought to restore normal cytoarchitecture by preferential migration into neuron deficient regions, assumption of pyramidal morphology, and early process elongation. Control transplants into intact and kainic acid lesioned cortex failed to elicit similar responses. We investigated the possibility that mechanisms of neuronal death common to apoptosis and targeted photolysis could explain the similar developmental influences. We assessed the pathways of cellular injury and eventual cell death in neuroblastoma and PC12 cell cultures labeled with nanospheres carrying the chromophore NH4-chlorin e6 and subjected to photoactivation (1) pharmacologically by scavengers of singlet oxygen and inhibitors of lysosomal proteases, (2) histologically by electron, fluorescence, and light microscopy, and (3) biochemically with binding of cellular DNA by propridium iodide, 3'-OH DNA end terminal labeling, and gel electrophoresis. We found that nanospheres were incorporated into lysosomes, and exposure to light energy led to singlet oxygen (1O2) production and cell death within both neuroblastoma and PC-12 cell lines. Scavengers of 1O2 prevented cell toxicity, while inactivation of lysosomal proteases reduced cell death. Morphologically, degenerating cells revealed release of proteases from lysosomes and disruption of cytoskeletal proteins. Apoptotic characteristics including early loss of cell adhesion, plasma membrane blebbing, and nuclear condensation and convolution were observed. Biochemically, DNA fragmentation was present in cells stained with propridium iodide and observed by 3'-OH end terminal labeling and gel electrophoresis. Thus, cells targeted by photolytically generated 1O2 undergo a form of cell autolysis whose final common pathway is apoptotic. The slow, nonnecrotic process of targeted neuronal cell death in vivo may activate many of the same physiological cues activated by programmed cell death during normal development and during organizational refinement in the adult vertebrate nervous system. This may potentially explain the migration and differentiation of neocortical neurons and neural precursors transplanted into these regions of neuronal degeneration.
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PMID:Apoptotic mechanisms in targeted neuronal cell death by chromophore-activated photolysis. 782 98


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