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)

A 49-year-old man had a malignant soft tissue tumor of the right thigh with metastasis to the femoral region and lower quadrant of the anterior abdominal wall on the right side and the left supraclavicular lymph nodes. The neoplasm showed features of chondrosarcoma and primitive neuroectodermal tumor (combined neuroblastoma, ependymoma, astrocytoma, and oligodendroglioma). The gliomatous part of the mixed tumor was confirmed by identification of the glial fibrillary acidic protein (GFAP). The diverse cellular population suggests a tumor origin from the ectomesenchymal remnant of the neural crest. The mesenchymal component of the neural crest would differentiate into the chondrosarcoma and the neuroectodermal component into the primitive neuroectodermal neoplasm. These various neoplastic elements, then, would form a neoplasm of mixed mesenchymal and neuroepithelial origin or an ectomesenchymoma.
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PMID:Malignant neoplasm of mixed mesenchymal and neuroepithelial origin (ectomesenchymoma) of thigh. 649 17

In normal conditions, neuron-specific enolase (NSE) is histochemically demonstrable only in neurons and cells of the amine precursor uptake and decarboxylation (APUD) system. This has been found not to be true for neoplastic cells. Several types of CNS tumors, including glioblastoma, astrocytoma, oligodendroglioma, ependymoma, medulloblastoma, pineocytoma , meningioma, and choroid plexus papilloma, focally stained positively for NSE. Reactive astrocytes were also frequently positive. In the peripheral nervous system, neuroblastoma, ganglioneuroma, and paraganglioma stained positively for NSE. A number of non-APUD tumors were focally positive. These included schwannoma, carcinoma and fibroadenoma of the breast, renal cell carcinoma, giant cell tumor of the tendon sheath, and chordoma. Caution should be exercised in relying on the immunohistochemical demonstration of NSE as a diagnostic marker in those tumors that do not belong to the APUD cell system. It seems of little value as evidence of differentiation in CNS tumors.
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PMID:Immunohistochemical demonstration of neuron-specific enolase in neoplasms of the CNS and other tissues. 654 18

A blocking microcytotoxicity assay was used to detect soluble astrocytoma-associated antigen. The richest source of soluble antigen was found in spent culture media from an established glioblastoma (GF) tissue culture line. Also assayed were fractions of sonicated membrane antigen from another (GM) glioblastoma and pellets of GF and GM cultured glioblastoma tissue. Blocking by media conditioned by cultured normal human brain, breast cancer, neuroblastoma, meningioma, or 2-year-old astrocytoma cell lines was 41-82% lower. A monomer was isolated that blocked cytotoxicity and migrated in molecular exclusion chromatography with alpha-macroglobulins rather than the beta-2-microglobulins usually associated with histocompatibility antigens.
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PMID:Microcytotoxicity blocking assay for the detection and isolation of soluble astrocytoma association antigen. 654 96

A patient with Stage III paratesticular neuroblastoma diagnosed in infancy was treated with radiotherapy and chemotherapy. Typical depigmented "ash leaf" skin lesions of tuberous sclerosis appeared during early childhood. At 7 years of age he underwent craniotomy for a subependymal giant cell astrocytoma. The occurrence of neuroblastoma, tuberous sclerosis, and astrocytoma is unique, and supports the suggested relationship between neural crest tumors and hamartoma syndromes.
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PMID:Neuroblastoma, tuberous sclerosis, and subependymal giant cell astrocytoma. 661 97

The inhibitory actions of phenacetin and paracetamol and of their desacetylation products on prostaglandin synthesis were studied on enzyme preparations originating from a neuronal cell line (mouse neuroblastoma, clone N2A), a glial cell line (rat astrocytoma, clone C6) and rat renal medulla. All compounds tested inhibited cultured cell and kidney prostaglandin synthetases to similar extents. p-Phenetidine and p-aminophenol, the desacetylated metabolites of phenacetin and paracetamol, were either 7-10 times or 4 times more potent than paracetamol. Thus, p-Phenetidine inhibited prostaglandin synthesis as efficaciously as did acetylsalicylic acid. The possible roles of p-phenetidine as the active metabolite of phenacetin for cyclo-oxygenase inhibition in brain and of phenacetin as an organ pro-drug are discussed.
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PMID:Inhibitory actions of desacetylation products of phenacetin and paracetamol on prostaglandin synthetases in neuronal and glial cell lines and rat renal medulla. 680 77

Three cases of postirradiation osteosarcoma which presented in childhood are reported and the pertinent literature reviewed. The children had been treated in each instance before the age of 3 years for an astrocytoma, retinoblastoma, and neuroblastoma, respectively. An average latent interval of 9.5 years lapsed before the osteosarcomas were diagnosed. Two of the tumors occurred in unusual sites, the cervical vertebrae and maxilla but were within the fields of prior irradiation. The tumors were predominantly sclerotic and were high-grade osteosarcomas. Only one patient has remained free of disease after treatment. One tumor-related death has occurred and the third patient has had two wedge resections of pulmonary metatases.
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PMID:Postirradiation osteosarcoma in childhood. A clinicopathologic study of three cases and review of the literature. 693 66

This report presents five patients with cervical-area infection and four with spinal cord tumors who presented with torticollis early in the course of their illnesses. three children were found to have osteomyelitis of the cervical spine; two, retropharyngeal abscess; two, intramedullary astrocytoma; one, extradural neuroblastoma; and one, extradural sarcoma. Though torticollis is most frequently a benign condition, its persistence or its association with other objective findings should lead to search for an etiologic basis.
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PMID:Torticollis as the presenting sign in cervical spine infection and tumor. 705 9

The rates of utilization of [3-14C]-acetoacetate, [3-14C]-3-hydroxybutyrate, and [6-14C]-glucose were measured in four established cell lines from neuroblastoma of rat (B103) and mouse (N4TG1) and from rat astrocytoma (RGC6) and mouse oligodendroglia (G2620). The rates of incorporation of acetoacetate into lipid were 3-5 times higher than glucose in all cell lines. The incorporation of 3-hydroxybutyrate was similar to that of glucose. Thin-layer chromatography of the total lipid extracts showed the same relative rates of use of these substrates for synthesis of various phospholipids and neutral lipids. The rates of incorporation into neutral lipids and phosphatidylcholine were essentially linear for 12 hr; however, that into phosphatidylethanolamine was markedly higher in the second 6 hr interval than in the first. In all cases, the greatest percentage of label (35-50%) appeared in the phosphatidylcholine fraction. The distribution of label from each of the three substrates among the various lipids was similar in the glial cells, but there were marked differences in distribution of the two ketone bodies in the neuroblastoma lines. These cells also synthesized lipids that migrated to the same area on the chromatogram as cholesterol esters and free fatty acids. In three of the four cell lines the rates of oxidation were highest for glucose, intermediate for acetoacetate, and lowest for 3-hydroxybutyrate. The ratios of the rate of incorporation to the rate of oxidation were higher for ketone bodies (3.32 for 3-hydroxybutyrate and 5.29 for acetoacetate) than for glucose (0.41). This indicates that in these cells ketone bodies are directed toward lipid synthesis rather than oxidation, and glucose is preferentially used as an energy source.
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PMID:Utilization of ketone bodies and glucose by established neural cell lines. 716 45

Interaction of embryonic chick cerebral cells with the astrocytoma (C6) and neuroblastoma (N2a) cells were examined by SEM. When astrocytoma cells were added to the glial monolayer cell substratum the glial substratum was loosened and astrocytoma cells grew into the gaps of the loosened glial substratum. It is believed that the penetrating property of the astrocytoma cells may be related to the invasiveness of the tumour cells. When neuroblastoma (N2a) cells were added to normal glial substratum, no invasion of the glial substratum was observed. Instead, for the first 2 days the tumour cells rested on the glial substratum and sent out numerous fine filopodia (0.1-0.2 micrometers) closely adhered to the surface of the glial cells. On the third day, the groups of glial cells underneath the neuroblastoma cells, which have been covered by filopodia of the tumour cells were rounded and became retracted from the glial substratum. These morphologically altered cells showed features of the tumour cells. It is therefore speculated that neuroblastoma cells have the ability of changing (transforming?) the glial cells probably through their filopodia. When neuroblastoma cells were added to the astrocytoma substratum, there was an initial reaction on both cell types in which lamellipodia were extremely developed. This initial reaction subsided about 24 hours later and the neuroblastoma cells became more flattened, and grew on the astrocytoma substratum. In this case no rounding up of astrocytoma cells was observed. Normal neuronal cells when added to astrocytoma substratum, showed well differentiated neuronal characteristics. This indicates that neuronal differentiation can be maintained by a tumour substratum.
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PMID:Scanning electron microscopic observations on the interaction between normal neuronal and tumour cells in monolayer culture. 730 94

The presence of glia maturation factor (GMF)-like activity was demonstrated in rat astrocytoma cells (C6 cells). The extracts of C6 cells enhanced the DNA synthesis of cultured glioblasts 3-fold at the maximum, inducing such morphological changes as extrusion of processes. C6 cells also showed a proliferative response to the extracts, though the responsiveness in terms of effective concentration of C6 extracts was about a half of the glioblast responsiveness. The extracts lowered growth rate of neuroblastoma cells and especially decreased their DNA synthesis without a morphological differentiation.
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PMID:Glial cell growth-promoting factor in astrocytoma (C6) cell extracts. 730 29


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