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)

To determine if immunohistochemistry might aid in the identification of neuroblastomatous foci in composite adrenal tumors, the authors analyzed two examples of composite adrenal pheochromocytoma-neuroblastoma, 18 pure pheochromocytomas, and six pure neuroblastomas using peanut agglutinin and a panel of antibodies directed against neuroendocrine and neural-associated antigens. Pure pheochromocytoma had the following immunopositivity: vimentin 14/18, chromogranin 18/18, synaptophysin 18/18, S100 protein 0/18 (tumor cells), neurofilament 14/18, J1 beta-tubulin (J1) 18/18, microtubule-associated protein-2 13/18, glial fibrillary acidic protein 13/18, and peanut agglutinin 17/18. Pure neuroblastoma reacted positively as follows: vimentin 0/6, chromogranin 5/6, synaptophysin 4/6, S100 protein 0/6 (tumor cells), neurofilament 5/6, J1 6/6, microtubule-associated protein-2 6/6, glial fibrillary acidic protein 1/6, and peanut agglutinin 6/6. Each component of both composite tumors reacted similarly to the pure neoplasms. Although the frequency of positive staining was similar for pheochromocytoma and neuroblastoma, the intensity and pattern differed for several antigens. Pheochromocytoma was diffusely positive for synaptophysin and chromogranin, whereas staining was focal and punctate in neuroblastoma. Microtubule-associated protein-2, J1, and neurofilament antibodies highlighted the fibrillar background of neuroblastoma, which pheochromocytoma lacked. Pheochromocytoma contained focal, ball-like immunoreactivity for glial fibrillary acidic protein and vimentin, which was absent in neuroblastoma. These immunohistochemical distinctions can assist the clinically important recognition of neuroblastomatous foci in composite adrenal pheochromocytoma-neuroblastoma.
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PMID:Immunohistochemical detection of neuroblastomatous foci in composite adrenal pheochromocytoma-neuroblastoma. 804 83

Malignant schwannomas are rare neoplasms that are seldom found in the head and neck. Few cases have been reported involving paranasal sinuses and none of them was of the "epithelioid" type. In this report, an unusual case of epithelioid malignant schwannoma involving the maxillary sinus, nasal cavity and orbit is presented. The patient was a 27-year-old male with a history of headache, nasal obstruction and epistaxis. Histologically, the tumour had a biphasic pattern with spindle and epithelioid elements which led to a differential diagnosis with malignant melanoma. It had also to be distinguished from other neoplasms, such as squamous cell carcinoma and olfactory neuroblastoma because of it location. Immunohistochemical positivity for S-100 protein, glial fibrillary acidic protein and vimentin together with negativity for HMB-45 and cytokeratins, as well as mesaxon formation detected with electron microscopy were conclusive in the diagnosis. The patient was treated with surgical excision and radiotherapy but local recurrence and metastases occurred, and he died within 1 year after initial diagnosis.
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PMID:Malignant sinonasal epithelioid schwannoma. 811 30

Vimentin is initially expressed by nearly all neuronal precursors in vivo, and is gradually replaced by neurofilaments shortly after the immature neurons become postmitotic (Cochard and Paulin, 1984, J Neurosci 4:2080; Tapscott et al., 1981, Dev Biol 86:40). A transient increase in neuritic vimentin filaments occurs within the first day of dbcAMP-mediated neurite induction in NB2a/d1 neuroblastoma, after which vimentin levels rapidly decline and neurofilaments increase (Shea, 1990, Brain Res 521:343). In the present study, we tested the possibility that vimentin filaments may function in neurite elaboration by inducing neuritogenesis under conditions where vimentin expression and assembly was inhibited. Intracellular delivery of anti-vimentin antiserum into transiently permeabilized NB2a/d1 cells prevented the initial elaboration of neurites, but did not retract existing neurites. By contrast, intracellular delivery of antiserum directed against the low molecular weight neurofilament subunit or normal rabbit antiserum did not affect neurite outgrowth. Treatment with vimentin antisense oligonucleotides reversibly depleted vimentin synthesis and steady-state levels, and prevented neurite initiation, but did not induce retraction of existing neurites. These findings point toward an hitherto undetected role for vimentin in the initiation of neurite outgrowth.
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PMID:Transient requirement for vimentin in neuritogenesis: intracellular delivery of anti-vimentin antibodies and antisense oligonucleotides inhibit neurite initiation but not elongation of existing neurites in neuroblastoma. 823 Mar 22

The cell line AG-F was isolated from the marrow of a neuroblastoma patient undergoing myeloablative treatment and autologous bone marrow rescue. A year later, the patient developed a Hodgkin's type lymphoma. AG-F cell line demonstrated an unusual phenotype, lacking surface CD2 and CD3, but expressing high levels of CD4, CD5, CD7, CD29, and CD45RO. Markers associated with Hodgkin's lymphoma cells, CD15 and CD30, were also positive. AG-F cells grow in suspension in clusters of 50-200 cells, with a doubling time of 9 h. They can also grow in serum-free medium and form tumors in nude mice. AG-F cells have amplified N-myc and c-myc and high levels of the corresponding mRNA transcripts. Cytogenetic analysis revealed a DNA index by flow cytometry of near tetraploid cells and a karyotype of 85-87 chromosomes, with consistent abnormalities in chromosomes 1, 5, and 9. Gene rearrangement studies revealed rearrangement of the beta gene of the T-cell receptor. AG-F cells secrete high levels of IL-6, IL-8, IL-10, and GM-CSF. Cell adherence and formation of long processes could be induced by fibronectin and were enhanced by exposure to PMA. Cells exposed to phorbol myristate acetate (PMA) had increased expression of CD11a, CD11b, CD18, CD45RO, and HLA-DR, whereas expression of CD15 and CD30 was markedly decreased. Similarly, the level of c-myc and N-myc oncoproteins and the levels of the cytoskeletal proteins, actin, tubulin, and vimentin markedly decreased early after PMA-induced differentiation.
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PMID:Isolation and characterization of an early T-helper/inducer cell line with a unique pattern of surface phenotype, constitutive cytokine secretion and myc oncogene expression. 825 4

Five primary and two metastatic rhabdomyosarcomas (RMS) with primary presentation in the skin were studied by conventional light microscopy and immunohistochemistry. These cases account for only 0.7% of the 682 cases of RMS collected at two large institutions with a main interest in soft tissue tumors. All but one tumor, which was an embryonal RMS, corresponded to the alveolar subtype. The myogenic nature of the tumor cells was supported by the immunophenotype including positive reactions for vimentin, desmin, and muscle actin. Clinical findings included a male predominance, young age of the patients and the location of all primary cutaneous RMS in the face. One of the two metastatic RMS presented at birth with a clinical picture highly suggestive of congenital metastatic neuroblastoma, notably because of a 100-fold amplification of the N-myc copy number. Thus, this case illustrates again that an amplification of the N-myc oncogene is not restricted to neuroblastoma, but may also occur in other tumor types.
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PMID:Rhabdomyosarcomas with primary presentation in the skin. 835 Dec 44

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

A case of olfactory neuroblastoma is reported. Light microscopic examination showed various arrangements of poorly differentiated tumour cells forming either uniform sheets or convoluted cords of multiple cell layers orientated toward a richly vascular stroma. Electron microscopic examination showed the presence of abundant cytoplasmic filaments and processes, and dense core endocrine vesicles ranging from 100-160 nm in diameter in both the perinuclear region and tumour cell processes. Immunohistochemical staining was positive in most of the tumour cells for neuron specific enolase, and in a few cells for S-100 protein, vimentin, and serotonin, but staining for desmin and keratin produced no reaction.
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PMID:Electron microscopic and immunohistochemical findings in a case of olfactory neuroblastoma. 843 97

The addition of the peroxovanadium (pV) derivatives potassium bisperoxo(1,10-phenanthroline)oxovanadate(v) (bpV[phen]) or potassium bisperoxo(pyridine-2-carboxylato) oxovanadate(v) (bpV[pic]), both of which are potent inhibitors of protein tyrosine phosphatases (PTPs) [Posner et al. (1994): J Biol Chem 269:4596-4604], to the culture medium of neuroblastoma NB 41 and glioma C6 cells resulted in a marked decrease in their proliferation rates and a progressive accumulation at the G2/M transition of the cell cycle. The effect was dependent on dose, cell type, and a pV compound employed. Mean values of the RNA-to-DNA and RNA-to-protein ratios in NB cells treated for 48 h with increased doses of bpV[phen] showed that general synthetic functions were not altered, nor did we observe oxidative damage to DNA using a sensitive DNA-nick detection assay. No changes in the expression and localization of vimentin, a component of the intermediate filament cytoskeleton, were observed by indirect immunofluorescence, showing that treatment did not disturb the cytoskeleton network. Measurements of BrdU incorporation into newly synthesized DNA showed that cells treated were not totally arrested. Furthermore, cells arrested G2/M were able to reenter the cycle rapidly after the release of inhibition. This progressive accumulation of G2/M coincided with the detection of tyrosine-phosphorylated p34cdc2 and a dramatic reduction in its kinase activity toward histone H1 by 48 h of culture. Both compounds were equally potent in inhibiting the catalytic activity of a yeast and the structurally distant mouse cdc25B in vitro, suggesting that augmented tyrosine phosphorylation of p34cdc2 derived from the in vivo inhibition of cdc25. Their equal in vitro potency contrasted with the considerably greater potency of bpV[phen] in vivo, in vivo suggesting that factors regulating the intracellular access of these compounds to cdc25 might be critical in determining in vivo specificity. In conclusion the final consequence of long-term exposure to potent and structurally defined PTP inhibitors on two highly proliferative nerve cell lines is to restrict cell growth. The corresponding hyperphosphorylation and reduced activity of p34cdc2 likely reflects the unusual sensitivity of cdc25 as an in vivo target for peroxovanadium compounds.
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PMID:Arrest at the G2/M transition of the cell cycle by protein-tyrosine phosphatase inhibition: studies on a neuronal and a glial cell line. 856 56

Vimentin is expressed initially by nearly all neuronal precursors in vivo, and is replaced by neurofilaments shortly after the immature neurons become post-mitotic. Moreover, both vimentin and neurofilaments can be detected transiently within the same neurite, leaving open the possibility that vimentin may play a role in the early stages of neuritogenesis. In the present study, cultured hippocampal neurons, which transiently express vimentin in culture, were treated with sense- and antisense-oriented deoxyoligonucleotides encoding regions of the vimentin sequence that overlap the translation initiation codon. Antisense oligonucleotide treatment reduced vimentin-immunoreactivity to background levels. Moreover, while 90-100% of cultured hippocampal neurons elaborated neurites within the first 24 hr following plating, only 24-30% did so in the presence of vimentin antisense oligonucleotides. Inhibition of neurite outgrowth was reversible following removal of antisense oligonucleotide. These findings substantiate earlier studies in neuroblastoma cells, indicating a possible role for vimentin in the initiation of neurite outgrowth.
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PMID:Role of vimentin in early stages of neuritogenesis in cultured hippocampal neurons. 896 Sep 81


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