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)

The spectrum of enolase enzyme forms has been examined in several lines of neuroblastoma cells and compared to those present in whole brain. The neuron specific enolase (NSP) is greatly decreased in the cultured cells as judged by activity profiles and radioimmunoassay. The synthesis of neuronal enolase appears to be extensively depressed in these cells while the total enolase activity is not affected. The non-neuron form of enolase (NNE) apparently compensates for the lack of the neuronal forms in the cultured cells. The preponderance of NNE in cultured neurons suggests that this enzyme is present in immature neurons, and that neuroblastoma cells are not fully differentiated with respect to the enolase function. Dibutyryl cyclic adenosine monophosphate treatment does increase NSP levels in mouse neuroblastoma cells, but not to the levels expected for fully differentiated neurons. The results indicate that NSP is a molecular correlate of fully differentiated neurons.
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PMID:Neuron specific protein (NSP) in neuroblastoma cells: relation to differentiation. 63 82

To verify the practical utility of immunohistochemical analysis of bone marrow biopsy specimens in patients with neuroblastoma, we compared the results of routine histologic examination of 68 specimens with the results of immunohistochemical detection of tumor cells using an antibody to neuron-specific enolase (NSE). A commercially available polyclonal antibody to this enolase isoform consistently reacted with the neoplastic cells in biopsy specimens with histologic features diagnostic of (24 specimens) or suspicious for (one specimen) metastatic neuroblastoma. Immunohistochemical double-staining techniques documented that the NSE-positive neoplastic cells also reacted with antibodies to chromogranin and synaptophysin. Notably, anti-NSE detected small foci of metastatic neuroblastoma in two of 43 biopsy specimens that showed no evidence of metastatic tumor in the initial histologic sections. Rare NSE-reactive hematopoietic cells were present in approximately a third of the specimens with and those without neuroblastoma and were easily distinguished from metastatic tumor by morphologic examination. We conclude that this antibody to NSE consistently detects neuroblastoma cells in routinely processed bone marrow specimens, including small foci of tumor cells not evident in initial histologic sections.
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PMID:Detection of metastatic neuroblastoma in bone marrow biopsy specimens with an antibody to neuron-specific enolase. 149 35

The effect of estradiol-17 beta on the activities of glycolytic enzymes from female rat brain was studied. The following enzymes were examined: hexokinase (HK, EC 2.7.1.1), phosphofructokinase (PFK, EC 2.7.1.11), aldolase (EC 4.1.2.13), glyceraldehyde-3-phosphate dehydrogenase (EC 1.2.1.12), phosphoglycerate kinase (EC 2.7.2.3), phosphoglycerate mutase (EC 2.7.5.3), enolase (EC 4.2.1.11) and pyruvate kinase (PK, EC 2.7.1.40). The activities of HK (soluble and membrane-bound), PFK and PK were increased after 4 h of hormone treatment, while the others remained constant. The changes in activity were not seen in the presence of actinomycin D. The significant rise of the activities of the key glycolytic enzymes was also observed in the cell culture of mouse neuroblastoma C1300 treated with hormone. Only three of the studied isozymes, namely, HKII, B4 and K4 were found to be estradiol-sensitive for HK, PFK and PK, respectively. The results obtained suggest that rat brain glycolysis regulation by estradiol is carried out in neurons due to definite isozymes induction.
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PMID:Rat brain glycolysis regulation by estradiol-17 beta. 153 2

Neuroblastoma is the most common nonhematopoietic solid tumor of childhood and has been intensively studied for at least 4 decades. Despite this, few predictive histopathologic clues to its behavior exist. Age, anatomic sites of occurrence, and clinical stage have traditionally been the only reliable prognostic factors in this disease. A number of laboratory studies that focus on biologic features such as neurotransmitter synthesis (adrenergic and noradrenergic catecholamines), neurotransmitter enzyme expression (dopamine beta hydroxylase, choline acetyl transferase), cytogenetics (homogeneously staining regions, double minute chromosomes, chromosome 1p deletions), molecular genetics (N-myc oncogene amplification and expression), and immunophenotype (surface epitopes such as HLA antigens and GD2 ganglioside and intracytoplasmic determinants such as neurofilament protein, synaptophysin, chromogranin, and neuron specific enolase) now enable the pathologist to predict clinical course in many cases and to distinguish bona fide neuroblastomas, regardless of age, site, or histologic appearance, from a host of related but distinctly separate neuroectodermal tumor entities with apparent different histogenesis, treatment sensitivity, and prognosis.
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PMID:Neuroblastoma and other childhood neural tumors: a review. 169 Apr 16

There is evidence that the gene for gamma-gamma enolase (neuron specific enolase, NSE) is regulated during cell differentiation and development, conserved in a variety of organisms and contains mRNA destabilizing sequences. In order to investigate further the mechanisms of these processes and to obtain large quantity of this protein, the NSE gene was isolated from neuroblastoma cells and cloned in E. coli using standard molecular biology techniques. The NSE gene expression was studied and the expressed protein (recombinant NSE) was characterized extensively. The recombinant NSE behaves like parental NSE in antisera specificity, resistance for chaotropic agents like urea, thermal stability at higher temperatures etc. The physical parameters like secondary structure, hydrophilicity, antigenic index and flexibility of the expressed protein were studied. The results of the present investigation collectively form the basis for initial investigations of how the expression of NSE gene is regulated. This is the first report where the recombinant NSE gene has been characterized so extensively.
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PMID:Expression of DNA sequences containing neuron specific enolase gene in Escherichia coli. 170 32

We studied two cases of pigmented neuroectodermal tumor of infancy (PNTI) by routine light microscopy and immunohistochemistry on formalin fixed, paraffin embedded tissues using antibodies to HMB-45 "melanoma associated" antigen, S-100 protein, neuron specific enolase (NSE), Leu-7 antigen, chromogranin, epithelial membrane antigen, collagen Type IV, alpha-fetoprotein and muscle-specific actin and to the intermediate filaments cytokeratin (CK), vimentin, desmin and neural filaments. We found that the large epithelioid cells, many of which contained melanin pigment, were strongly positive for CK and HMB-45, and less intensively positive for vimentin and NSE. The small neuroblast-like cells revealed only focal, weak NSE positivity. Both cell types were negative for S-100 protein and for the other antigens examined. Our results suggest that: (1) the large and small cell populations in PNTI have different immunophenotypes; (2) the expression of CK and HMB-45, together with the S-100 negativity, appears unique for the pigmented cells; and (3) this profile may be helpful in the exclusion of melanoma and peripheral neuroblastoma from the differential diagnosis.
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PMID:Pigmented neuroectodermal tumor of infancy. A light microscopic and immunohistochemical study. 170 90

Fourteen patients with stage III-IV neuroblastoma were treated with alternating combination chemotherapy consisting of (a) VP16/cisplatin and (b) doxorubicin/vincristine/cyclophosphamide. The initial response to induction chemotherapy, especially to VP16/cisplatin was evaluated by determining t 1/2 for urinary vanillylmandelic acid (VMA), homovanillic acid and serum neuron specific enolase (NSE). The period prior to normalization of these parameters was also determined. The patients could be classified as 7 rapid responders, with less than 3 weeks of t 1/2 VMA, or t 1/2 NSE, and 7 slow responders longer than 4 weeks of t 1/2 VMA. An analysis of the data indicates that an initial rapid response correlated with subsequent high complete response rate, but did not necessarily predict better prognosis in these patients.
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PMID:Treatment for stage III-IV neuroblastoma patients: initial response to chemotherapy evaluated by biochemical parameters. 175 98

A 3 1/2-year-old girl with a diagnosis of common acute lymphoblastic leukemia antigen (CALLA)-positive acute lymphoblastic leukemia was noted to be hypertensive and developed a tonic-clonic seizure. Computed tomography scan of the head revealed a right orbital mass. Orbital fine needle aspiration biopsy demonstrated rosette-like arrangements of cells with fibrillar cytoplasmic processes suggesting neuroblastoma. The tumor cells were antineuron-specific enolase positive. The cytologic findings suggested neuroblastoma, a diagnosis confirmed on subsequent work-up. The difficulty in distinguishing neuroblastoma from acute lymphoblastic leukemia in the pediatric patient is discussed in terms of clinical and cytologic features.
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PMID:Neuroblastoma presenting as acute lymphoblastic leukemia but correctly diagnosed after orbital fine-needle aspiration biopsy. 183 97

Serum neuron specific enolase (NSE) was determined in 159 patients with neuroblastoma at diagnosis and in 183 children of various age groups. We found an age dependence of reference intervals for NSE and defined the 95th percentiles as upper normal limits. The specificity was 91.3% and the sensitivity 73.0%. The incidence of abnormal NSE levels increased with stage. The NSE serum levels were not influenced by histologic differentiation. Neuron specific enolase proved to be a reliable tumor-marker for monitoring the disease. Moreover, abnormal NSE values at diagnosis were of prognostic significance for patients with localized neuroblastoma (stages I-III) and for children with metastatic disease (stage IV), but not for infants with stage IV S. In comparison to catecholamine metabolite determination neuron specific enolase appeared to be a slightly less specific, equally sensitive tumor marker but with prognostic information for children with neuroblastoma.
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PMID:Age dependence and prognostic impact of neuron specific enolase (NSE) in children with neuroblastoma. 189 81

A new human neuroblastoma cell line (LS) that originated from an abdominal tumor of a 16-month-old girl is presented; it was classified, according to Evans, as being stage III. Morphological (dense-core particles) and biochemical characteristics (dopamine-beta-hydroxylase, acetylcholinesterase, neuron-specific-enolase) confirmed the diagnosis. In addition to a slightly variable modal chromosome number of 48 or 49 (because of marker-chromosomes and autosomal trisomies), cytogenetic analysis revealed two constantly appearing chromosomes with homogeneously stained regions (HSR's). The karyotype remained constant over 50 passages in vitro [49,XX, -12, +der5, + 17, + mar1, + mar2]. Double minutes were a rare phenomenon and appeared only in a few metaphases. In situ hybridization showed that some of the HSR's consisted of amplified N-myc copies. The distribution of the N-myc copies according to in situ hybridization signals along the HSR's was compared with the data of Southern and Northern blotting analyses.
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PMID:Cytogenetic and molecular characterization of a newly established neuroblastoma cell line LS. 202 21


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