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)

Two patients, 14 and 46 years of age, presented with diffuse, rapidly growing intracerebral tumors leading to death 6 1/2 and 9 1/2 months, respectively, after diagnosis. Histological examination showed sheets of moderate-sized tumor cells with clear cytoplasm and central nuclei interrupted by delicate arciform vasculature, an appearance distinctly different from that of neuroblastoma. Malignant features were present in the form of significant nuclear pleomorphism, numerous mitotic figures, and small foci of necrosis with some suggestion of adjacent pseudo-palisading in one case. Ultrastructural examination showed neuronal differentiation, including prominent neuritic processes, microtubules, dense-core neurosecretory-type granules, and synaptic bouton-like structures containing small, empty-appearing synaptic-type vesicles and synapse-like membrane "thickenings." Immunohistochemistry showed focal immunopositivity for synaptophysin, neurofilaments, neuron-specific enolase, and S100 protein. Immunoreactivity for glial fibrillary acidic protein (GFAP) was found at the margins of the tumors adjacent to some intratumoral blood vessels and in some tumor cells. These tumors seem to occupy a nosological "middle ground" between neuroblastoma and central neurocytoma.
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PMID:Malignant neurocytic tumor. 805 20

We report a case of spinal cord neurocytoma in a 67-year-old man who had experienced a progressive numbness of the left foot during the previous 4 years. Magnetic resonance imaging showed a well-defined intramedullary tumor located at the T10-T11 level. The pathological examination revealed histological characteristics described in neurocytomas. The tumor cells showed a uniform small nucleus and clear or slightly eosinophilic cytoplasm with frequent perinuclear halos, resembling the picture of oligodendroglioma. Some tumor cells exhibited mature ganglion cell appearance. Electron microscopy showed cells with microtubules and dense-core vesicles in their cytoplasm and cytoplasmic process. Immunohistochemically, the majority of tumor cells expressed synaptophysin and neuron-specific enolase. We conclude that this tumor is an exceptional case of neurocytoma located in the spinal cord, and consider that the term neurocytoma can be applied to tumors with neuronal differentiation intermediate between neuroblastoma and ganglioneuroma, even if arising in CNS outside of the intracranial ventricular system.
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PMID:Neurocytoma of spinal cord. 805 8

A case of olfactory neuroblastoma in a 36-year-old woman who presented with florid Cushing's syndrome is reported. A nasal polyp, which proved to be an olfactory neuroblastoma, was resected. The procedure was followed by complete remission from the endocrinologic abnormalities. Postoperatively, the patient was well for 5 years until recurrence of both Cushing's syndrome and the nasal polyp was noted. Following combined transnasal-transcranial resection of the tumor, which extended into the anterior cranial fossa, the patient again experienced complete remission of Cushing's syndrome. Immunohistochemistry showed the tumor to be positive for neuron-specific enolase, synaptophysin, chromogranin, adrenocorticotropic hormone, beta-endorphin, and S-100 protein. Electron microscopy revealed neuritic processes containing microtubules and neurosecretory granules. This is the first reported case of Cushing's syndrome secondary to olfactory neuroblastoma.
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PMID:Cushing's syndrome secondary to olfactory neuroblastoma. 819 48

The sensitive and specific biochemical indicators for assessing chemical-induced neurotoxic insults in cell culture models have not been sufficiently explored. This study was designed to assess the usefulness of glia-specific beta-S100 protein and neuron-specific enolase (NSE) as indices of in vitro neurotoxicity of heavy metals. Glioma C6 and neuroblastoma N18TG-2 cells were grown in Dulbecco's modified Eagle's medium containing various concentrations of mercuric chloride (HgCl2) or cadmium chloride (CdCl2) for 5 days. Toxic response patterns of the neurospecific endpoints (beta-S100 and NSE), which were monitored with enzyme immunoassays, were compared with those of the non-neurospecific endpoints such as cell viability, total cellular protein, lactate dehydrogenase (LDH) activity, and cumulative glucose consumption in the two cell lines. Both HgCl2 and CdCl2 produced dose-dependent inhibition of neurospecific endpoints and non-specific endpoints. However, by ranking the EC50 values (effective concentration producing half-maximal inhibition) for various endpoints, the lowest values were found for beta-S100 in C6 cells, and for NSE in N18TG-2 cells. In lower and intermediate concentrations, the inhibitory effects of the heavy metals on the content of beta-S100 and NSE occurred in the absence of any detectable effect on intracellular LDH activity, and independently of total cellular protein inhibition. The sensitive and excess responses of the neurospecific endpoints relative to that of the non-specific endpoints may reflect the specific neurotoxic insults of the heavy metals on the cultured cells.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Neuron and glial cell marker proteins as indicators of heavy metal-induced neurotoxicity in neuroblastoma and glioma cell lines. 823 98

Cells from an established human neuroblastoma cell line, SH-SY5Y, were demonstrated to grow and form solid tumours in nude rats. This cell line, which is an adrenergic subclone of the SK-N-SH cell line, has previously been used in differentiation model studies. The tumours retained the neuronal phenotype of the cultured cells, as evidenced by the expression of neuron-specific enolase (NSE) and chromogranin A + B. The transcription factor Isl-1, a protein expressed in subsets of neurons and endocrine cells as well as in neuroblastoma cells, was also expressed in the transplanted tumours, thus further verifying the retained phenotype of the cells under in vivo conditions. At scintigraphy utilizing 123I-MIBG the optimal tumour/background ratio was obtained 20 h after injection. The assessment of tissue/serum ratios showed the highest uptake in the spleen (0.067% per gram of inj. activity), neuroblastoma tumours (0.067% per gram of inj. activity) and in the adrenals (0.065% per gram of inj. activity).
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PMID:Characterization and uptake of radiolabelled meta-iodobenzylguanidine (MIBG) in a human neuroblastoma heterotransplant model in athymic rats. 830 41

A comparative study concerning the histogenesis of Ewing's sarcoma and its relationship with peripheral primitive neuroectodermal tumor (PNET) was undertaken using histological, immunohistochemical and ultrastructural techniques. The cases studied included 22 Ewing's sarcomas, 17 (ganglio) neuroblastomas, 3 peripheral PNETs, 1 peripheral neuroblastoma, 1 Askin's tumor and a case in which it was difficult to distinguish between Ewing's sarcoma and neuroblastoma. Almost all the cases of Ewing's sarcoma showed neural differentiations. Immunohistochemical study using antibodies for neuron-specific enolase, protein gene product 9.5, Leu 7 and neurofilament (200 kD) was most useful for examining the neural differentiation of these tumors. These results suggest that Ewing's sarcoma is in a broad sense one of such peripheral PNETs as (ganglio) neuroblastoma, peripheral neuroblastoma and Askin's tumor.
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PMID:[Clinicopathological study of Ewing's sarcoma and primitive neuroectodermal tumor]. 830 11

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

When established in culture, human neuroblastoma cell lines typically are comprised of heterogeneous cellular subpopulations, including neuroblastic (N-type), substrate-adherent (S-type), and intermediate (I-type) cells that can be distinguished by their characteristic morphologies and expression of differentiation-associated antigens. Here we examined the relative levels of the Bcl-2 oncoprotein in 15 clones derived from four different neuroblastoma cell lines. Among six clones isolated from the SK-N-SH line, levels of p26-Bcl-2 correlated with morphology and differentiation markers with the hierarchy of bcl-2 expression being: N-type cells > N/I-type > I-type > S-type. Furthermore, stimulation of one of the N-type clones, SH-SY5Y, with the phorbol ester, 12-O-tetradecanoylphorbol-13-acetate, induced differentiation toward a more neuronal-like phenotype and resulted in a 5- to 10-fold elevation in the relative levels of Bcl-2 protein. High relative amounts of p26-Bcl-2 protein were also found in an N-type clone derived from the SMS-KCN line. In two N-type clones derived from the LA-N-1 line, however, levels of Bcl-2 protein were only moderately elevated, and in one N-type clone from the SK-N-BE(2) line the levels of Bcl-2 protein were low. Thus, high relative levels of Bcl-2 oncoprotein are not a universal feature of N-type cells (three of six clones tested). In contrast, all 5 of the S-type clones evaluated contained relatively low levels of Bcl-2 protein, suggesting that these cells (which may represent embryonic precursors of Schwann, glial, and melanocytic cells) do not typically express the bcl-2 gene at high levels. Consistent with this inverse correlation between Bcl-2 protein levels and S-type characteristics, stimulation of an I-type clone derived from the SK-N-BE(2) line with 5-bromodeoxyuridine was accompanied by an accumulation of S-type cells in these cultures, decreased Bcl-2 protein, diminutions in the neuronal markers neurofilament-M and neuron-specific enolase, and an increase in the relative levels of the S-type marker proteins vimentin and beta-2-microglobulin. Conversely, stimulation of this I-type clone with retinoic acid resulted in an accumulation of N-type cells (which are thought to represent embryonic precursors of sympathetic neurons), decreased vimentin and beta-2-microglobulin, increased neurofilament-M, and a marked elevation in p26-Bcl-2.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Regulation of Bcl-2 oncoprotein levels with differentiation of human neuroblastoma cells. 840 88

Two putative human oligodendroglioma cell lines were examined for the expression of the oligodendrocyte-associated genes, 2',3'-cyclic nucleotide-3'-phosphodiesterase, myelin basic protein, myelin proteolipid proteins, and myelin-associated glycoprotein. The expression of these genes also was examined in control astrocytoma and neuroblastoma cell lines. In addition, the expression of the non-oligodendrocyte-specific genes, glial fibrillary acidic protein (GFAP), neuron-specific enolase and neurofilaments (NF) NF-L and NF-M also were examined. All the cell lines expressed 2',3'-cyclic nucleotide 3'-phosphodiesterase, neuron-specific enolase, and vimentin, and none expressed myelin-associated glycoprotein. The "oligodendrocyte-specific" myelin proteolipid protein mRNAs and the "neuron-specific" NF-L mRNA were expressed in the two astrocytoma cell lines, which also expressed GFAP. Expression of intermediate filament protein genes was more restricted. The astrocytoma, neuroblastoma, and oligodendroglioma cell lines expressed only GFAP, NF-M, and cytokeratin K7, respectively. These results: (a) provide molecular data confirming the classification of the two cell lines as oligodendrogliomal and suggest that their molecular profiles are indicative of immature oligodendrocytes; (b) demonstrate the expression of cytokeratins in oligodendrogliomal cell lines and suggest that apparent GFAP expression in oligodendrogliomas detected by immunocytochemical methods may be due to cross-reactivity with cytokeratins, with which they share common polypeptide sequence; and (c) indicate that astrocytoma cell lines can exhibit a "mixed" phenotype, expressing genes associated with fully differentiated oligodendrocytes and neurons.
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PMID:Expression of oligodendrocyte-associated genes in cell lines derived from human gliomas and neuroblastomas. 841 42

Serum neuron-specific enolase (NSE) levels were studied by an enzymo-immunoassay method in 2 groups of patients: a group of epileptic patients, and a group of patients with refractory major depression after electroconvulsive therapy (ECT). In patients without organic neurological disease (n = 274) the mean serum NSE level (+/- S.D.) was 8.4 +/- 3.4 micrograms/l. No correlation with sex or age was observed. No significant difference was observed between epileptic patients without seizure or major electroencephalogram (EEG) abnormality, and a reference group. Significant increases were observed in 32 samples collected from patients with interictal EEG without spikes and waves before the 7th day after a seizure, in whom mean NSE was 21.5 +/- 9.4 micrograms/l, and in 26 samples from 4 patients without seizures but with spikes and waves in the interictal EEG, whose mean NSE was 20.6 +/- 11.5 micrograms/l. The increases of serum NSE levels in epileptic patients seem therefore to be linked to seizures and/or to EEG abnormalities. The consequences of these observations for the survey of epileptic patients, and for the diagnosis of cerebral tumors (mainly neuroblastoma) or for monitoring treatment after surgical resection, are discussed. In only 1 patient out of 6, an increase in serum NSE levels was observed with a peak about 12 h after ECT. No significant correlation with the ECT features (length of seizures, one- or two-sided electrodes) was observed.
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PMID:Increased serum levels of neuron-specific enolase in epileptic patients and after electroconvulsive therapy--a preliminary report. 871 37


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