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)

Immunocytochemical analyses revealed the presence and distribution of apolipoprotein E (apo E) in normal human brain tissue as well as in 77 human intracranial neoplasms. In normal brain tissues, the perikarya of astrocytes exhibited a strong positive reaction, whereas the Bergmann glia were stained to a moderate degree. However, no immunoreactivity was observed with neurons, oligodendrocytes, ependymal cells, and choroidal epithelium. Among the intracranial neoplasms, oligodendroglioma, choroid plexus papilloma, hemangioblastoma, primary malignant lymphoma, neurinoma, meningioma, pituitary adenoma, and craniopharyngioma were all negative. Immunoreactivity in the peripheral neuroblastoma was nil. However, the perikarya of astrocytomas and glioblastomas showed a positive reaction. Analyses on the degree of anaplasia and the amount of apo-E as an intensity of immunostaining showed a negative correlation. The astrocytic elements were stained in mixed oligoastrocytomas and medulloblastomas with glial differentiation. A few cases of ependymomas showed weak perikaryal immunostaining. Western blot analyses with anti-apo E antibody of a freshly prepared surgical specimen with astrocytomas revealed a single band with a molecular weight of approximately 37,000. The well differentiated cultured human astrocytoma cells secreted apo E into the medium. These lines of evidence suggest that apo E may serve as a potential marker specific for astrocytomas and glioblastomas, as well as an indicator of astrocytic tumor cell differentiation. The apo E localization in human brain tumors could be clinically relevant and diagnostically useful.
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PMID:Immunohistochemical localization of apolipoprotein E in human glial neoplasms. 339 6

For the determination of their possible utility as tumors markers, 2 neural-associated isozymes, neuron-specific enolase [(NSE) EC 4.2.1.11] and creatine kinase BB [(CK-BB) EC 2.7.3.2], were quantitated by radioimmunoassay in human neuroectodermal-derived cell lines, primary brain tumors, and sera and cerebrospinal fluid (CSF) from brain tumor patients. The NSE content of neuroblastoma cell lines was more than sixfold that of the glioma and medulloblastoma lines; the CK-BB content of neuroblastoma and medulloblastoma lines was fourfold to nineteen-fold that of the glioma and other lines. Expression of NSE in neuroblastoma cell lines was not related to time in culture and was cell line specific. NSE in ex vivo medulloblastomas was raised six to ten times that in astrocytomas and gliomas, although no significant differences were noted for the CK-BB content. Serum and CSF NSE levels were markedly raised above control values in 10 of 29 and 6 of 10 cases of astrocytoma, respectively. Raised CK-BB levels in serum (greater than 10 ng/ml) and CSF (greater than 12 ng/ml) were found in 9 of 18 and 2 of 10 patients, respectively. These data suggest that NSE is preferentially expressed by neuroblastoma lines and medulloblastomas and that NSE and CK-BB may have clinical utility as markers for prognosis, diagnosis, and monitoring of response to therapy.
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PMID:Differential expression of neural isozymes by human medulloblastomas and gliomas and neuroectodermal cell lines. 346 6

A multicentre registry of children who had been successfully removed from therapy for some common childhood cancers (Hodgkin's disease, non-Hodgkin's lymphoma, neuroblastoma, nephroblastoma, acute lymphatic leukaemia and other leukaemias) was established in Italy in 1981. The present study describes mortality and occurrence of second primary malignancies (SPMs) among 1467 children who were alive when the registry was established. Follow-up ended on December 31, 1983 for mortality and 1 year later for the occurrence of SPMs. Sixty-seven deaths were recorded, 11 of which were due to causes other than progression of the original disease. Eleven incident SPMs were identified (i.e. 3 acute myeloid leukaemias, 3 thyroid carcinomas, 1 bilateral breast carcinoma, 1 liver malignant mesenchymoma, 1 astrocytoma, 1 chondrosarcoma and 1 osteosarcoma) corresponding to an incidence rate of 2.1/1000 patient-years at risk. Anecdotal reports were collected regarding 2 further SPMs (a thyroid carcinoma and a myeloid leukaemia) as well as several benign tumours, including 2 mammary fibroadenomas.
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PMID:Late deaths and second primary malignancies among long-term survivors of childhood cancer: an Italian multicentre study. 365 74

Critical Evaluation of 200 tumours of meninges, brain and spinal cord showed that to be familiar with the ultrastructural features of meningioma and its variants was instrumental in differential diagnosis of other primary or secondary meningeal tumours (neurinoma, paraganglioma, xanthomatous and histiocytic tumours). A limited value of electron microscopy was found in astrocytoma and glioblastoma in contrast to its importance in low-differentiated ependymoma and oligodendroglioma. The examination had histogenetical and taxonomic values in medulloblastoma (CNS neuroblastoma and mixed tumours with a component featuring primitive neuroectodermal or neuroblastic differentiation). Ultrastructure was very important in the so-called primitive neuroectodermal CNS tumours where only the lack of conspicuous glial or neuroblastic differentiation confirmed the diagnosis. Electron microscopy was instrumental in rare primary CNS lymphomas as well as in some metastatic tumours.
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PMID:[Contribution of electron microscopy in the differential diagnosis of tumors of the meninges, brain and spinal cord]. 373 Dec 97

The immunohistochemical localization of the calcium-binding protein, S100 beta, in human nervous system tumors has been examined by using a monoclonal antibody with specificity for the S100 beta polypeptide. S100 beta-specific immunoreactivity is detected in astrocytoma, glioblastoma, Schwannoma, ependymoma, and craniopharyngioma, whereas no reactivity is seen in oligodendroglioma, meningioma, neuroblastoma, or medulloblastoma. These data suggest that analysis of S100 beta localization with these monoclonal antibodies may be useful for research or diagnostic purposes.
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PMID:Immunohistochemical localization of S100 beta in human nervous system tumors by using monoclonal antibodies with specificity for the S100 beta polypeptide. 373 19

Two established neural cell lines were used to examine the cytotoxicity of bilirubin in vitro. N2AB-1 is a subclone of Neuro 2a from the original C1300 mouse neuroblastoma and C6 glioma is a rat astrocytoma cell line. These cells were grown in monolayer cultures in medium with 10% fetal calf serum containing doses of 5 to 42 microM bilirubin. Morphologic and biochemical characteristics of cell viability were monitored for 72 h. Additional cultures of N2AB-1 were differentiated by treatment with prostaglandin E1/cyclic adenosine monophosphate before exposure to various bilirubin concentrations. The cells were examined every 24 h by phase contrast microscopy and protein synthesis was measured by incorporation of tritiated leucine for appropriate times. N2AB-1 cells were extremely sensitive to bilirubin within 24 h at doses greater than 11 microM. Cells showed swelling, vacuole formation, pigment accumulation, and lift off from the growing surface. Growth of N2AB-1 over 3 days was inhibited in a dose-dependent manner. Moreover, protein synthesis 6 h after bilirubin exposure and 24 h after bilirubin exposure was inhibited in the same dose dependency as cell growth. In contrast, N2AB-1 cells morphologically differentiated by drug treatment showed no effect of bilirubin exposure. Also, mitotically active rat glial cells were resistant to bilirubin toxicity under similar conditions. This study demonstrates that marked differences exist among neural cells in susceptibility in vitro to bilirubin toxicity and that mitotically active neuronal cells are more sensitive to bilirubin treatment than "mature" neurons.
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PMID:Differential sensitivity of neural cells to bilirubin toxicity. 378 Sep 13

Inhibitory coupling of receptors to adenylate cyclase previously has been shown to be relatively sensitive to inactivation by alkylation with N-ethylmaleimide (NEM). Modification of the inhibitory guanine nucleotide regulatory protein, Ni, has been proposed to be responsible for this effect. The effects of NEM on GTP-sensitive binding of carbachol to muscarinic cholinergic receptors has been compared in a cell line (1321N1 human astrocytoma cells) in which these receptors stimulate phosphoinositide breakdown and in a cell line (NG108-15 neuroblastoma X glioma cells) in which activation of these receptors results in inhibition of adenylate cyclase. Pretreatment of membrane preparations from 1321N1 cells with NEM resulted in a concentration-dependent decrease in the extent of pertussis toxin-catalysed [32P]ADP-ribosylation of a 41 000 Da protein previously proposed to be the alpha subunit of Ni. Under conditions where 32P-labelling of Ni in 1321N1 membranes was reduced by NEM by 90%, no effect was observed on the extent of guanine nucleotide-sensitive high-affinity binding of carbachol to muscarinic cholinergic receptors. In contrast, treatment of NG108-15 membranes with NEM under the same conditions resulted in complete loss of high-affinity guanine nucleotide sensitive binding of carbachol. These results illustrate another difference between the muscarinic receptor population of these two cell lines, and support the previous proposal that muscarinic receptors of 1321N1 cells couple to a guanine nucleotide regulatory protein that is not Ni.
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PMID:Further evidence that muscarinic cholinergic receptors of 1321N1 astrocytoma cells couple to a guanine nucleotide regulatory protein that is not Ni. 392 72

Uptake of amino acids by cultured neuroblastoma and astrocytoma cells was studied in the presence and absence of L-histidine. Intracellularly accumulated histidine was assumed to induce accumulation of radioactively labeled amino acids from medium by means of exchange transport. Neuroblastoma cells accumulated more histidine than astrocytoma cells and were more sensitive to the enhancement of uptake of other large neutral amino acids by histidine. Histidine also increased glutamic acid uptake in astrocytoma cells, but reduced it in neuroblastoma cells. The greatest differences between the cell lines in amino acid uptake without histidine were found with acidic amino acids (astrocytoma cells accumulated them more than neuroblastoma cells) and with taurine (the reverse was found). The uptake and exchange mechanisms for some neutral and acidic amino acids may thus be dissimilar in the plasma membranes of cultured cells of neuronal and glial origin.
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PMID:Stimulation of amino acid accumulation in neuroblastoma and astrocytoma cells by L-histidine. 400 Mar 98

Melanocytes derived from fetal or adult skin do not propagate in vitro unless cultured in the presence of factors such as 12-O-tetradecanoylphorbol 13-acetate (TPA). In a search for physiological factors regulating the growth of melanocytes, extracts of various cultured cell types were tested. Factors produced by melanoma and astrocytoma cell lines support continued proliferation of melanocytes in the absence of TPA. WI-38, a fibroblast cell line derived from human embryonic lung, was the most active source of melanocyte growth factors. No melanocyte growth-promoting activity was found in extracts of cultured neuroblastoma, renal cancer, normal keratinocytes, or renal epithelium. Nerve growth factor, epidermal growth factor, melanocyte-stimulating hormone, transforming growth factor-beta, and platelet-derived growth factor did not have growth-promoting activity for melanocytes. The presence of melanocyte growth factors and TPA together resulted in the strongest mitogenic activity for melanocytes, permitting the recovery (at 20 days) of 4 to 20 times as many cells as in growth factor or TPA alone.
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PMID:Growth regulation of human melanocytes: mitogenic factors in extracts of melanoma, astrocytoma, and fibroblast cell lines. 402 18

This report describes an exceptional example of cerebral neuroblastoma in association with neoplastic glial cells, which were frequently arranged in clusters around the supporting blood vessels. The neuroblastic nature of the tumor was confirmed by the presence of numerous dense-core vesicles in the cell processes. The glial nature of the associated cells was confirmed by their positivity for glial fibrillary acid protein by immunoperoxidase staining and by the presence of abundant cytoplasmic filaments of intermediate size on electron microscopy. Of particular interest was the presence of dense-core vesicles in some of the glial cells, and that of a basal lamina underlying the perivascular glial cells. The tumor was interpreted as a composite cerebral neuroblastoma and astrocytoma. No undifferentiated neuroepithelial stem cells could be identified. The cytogenesis of this mixed neuroepithelial neoplasm is uncertain.
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PMID:Composite cerebral neuroblastoma and astrocytoma. A mixed central neuroepithelial tumor. 402 75


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