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PubMed1983

Calcitonin, carcinoembryonic antigen and neuron-specific enolase in medullary thyroid carcinoma.

Calcitonin, carcinoembryonic antigen (CEA) and neuron specific enolase (NSE) were studied in the thyroid glands of patients with multiple endocrine neoplasia (MEN) type 2a, 2b, and with sporadic thyroid carcinomas (MTC). Calcitonin, CEA and NSE were localized in normal C-cells, hyperplastic C-cells, and in MTC. While the distribution of calcitonin and CEA was quite similar in most cases, a smaller proportion of cases were positive for NSE. C-cell hyperplasia was identified in all nine patients with MEN 2a and in four of six patients with MEN 2b. None of the four patients with sporadic MTC had C-cell hyperplasia. These results indicate that C-cell hyperplasia is present in patients with MEN 2a and 2b and that NSE in addition to calcitonin and CEA is a useful marker for the thyroid C-cells.

Adolescent↗
PubMed1996

Cloning the 5' flanking region of neuron-specific Hel-N1: evidence for positive regulatory elements governing cell-specific transcription.

A 5.4 kilobase-pair segment of DNA flanking the 5' end of Hel-N1 was isolated and characterized. Primer extension studies with normal human brain and neuroblastoma cells revealed a major and minor transcription-initiation site. Sequence analysis of the initial 536 bp upstream to the major start site revealed a core promoter (-1 to -181) which contained two CCAAT boxes, a weakly-conserved TATA box, and an SP1 site. This region was also moderately GC-rich (62%). Using a transient luciferase-reporter-gene assay, the core promoter was found to be essential for basal transcription both in neural (PC12) and non-neural (HeLa and glial) cell types. Two positive regulatory elements, however, were identified in the initial 536 bp (-1 to -181 and -182 to -350) which produced a five- to six-fold increase in transcriptional activity in PC12 cells vs. HeLa or glial cells. These elements, therefore, were sufficient to confer cell-specific enhanced transcription and likely contribute to the neuronal specificity of Hel-N1 mRNA expression.

Animals↗
PubMed1987

Serum neuron-specific enolase. A marker for responses to therapy in seminoma.

Neuron-specific enolase (NSE) was evaluated as a serum marker in 105 patients with testicular cancer and compared with the established tumor markers alphafetoprotein (AFP) and human chorionic gonadotropin (HCG). Increased serum NSE activity was measured in eight of 11 (73%) patients with metastatic seminoma. Serum NSE concentrations fell to within the normal range following chemotherapy. Localization of NSE in seminoma cells was demonstrated immunohistochemically. Only six of 40 (15%) patients with metastatic nonseminomatous germ cell tumors showed elevated serum NSE levels. AFP and HCG were both positive in 70% of patients in this group, and NSE determination gave no additional information. Serum NSE concentrations were normal in 53 of 54 testicular cancer patients after orchiectomy and there was no evidence of metastatic disease; only one had borderline NSE levels, indicating the specificity of serum NSE determination. NSE is a new marker of seminoma and its measurement may be of clinical value in monitoring chemotherapy in patients with metastatic seminoma.

Adolescent↗
PubMed1990

Neuron-specific enolase during chemotherapy of small cell lung cancer.

Serum neuron-specific enolase (NSE) has been measured in 28 patients with small cell lung cancer (SCLC) and 90 patients with other forms of lung cancer (NSCLC), i.e., 28 with adenocarcinoma and 62 with squamous cell carcinoma. Increased NSE (greater than 12.0 micrograms/liter) was found in 71.4% of SCLC patients and in 22.2% of NSCLC patients. The predictive value of an increased NSE in identifying SCLC was only 50%, whereas the predictive value of a normal NSE in differentiating SCLC for NSCLC was 91%. Serial studies during chemotherapy of SCLC patients showed that the doubling time of NSE ranged from 7 to 127 days and the mean apparent half-life (AHL) of NSE to be 14 days. AHL values in excess of 20 days suggest that the tumour is not in full remission. We believe that measurement of serum NSE and calculation of the AHL and DT are valuable in identifying the effectiveness of chemotherapy in patients with SCLC.

Adenocarcinoma↗
PubMed1998

Human and mouse chromosomal mapping of Stac, a neuron-specific protein with an SH3 domain.

Stac is a novel neuron-specific protein consisting of a cysteine-rich domain and an SH3 domain. We determined the chromosomal location of both the mouse and the human Stac genes (Stac and STAC). By linkage analysis using a mouse recombinant inbred (RI) strain panel (BXD), it was determined that Stac is located between D9mit15 and D9mit20 at the distal region of chromosome 9, around which two neurological disease genes, du and tip, have been found. This result was also supported by analysis using an interspecific backcross panel BSS. The mouse chromosomal location around Stac was syntenic with the human chromosome around 3p21-p23, where the gene for cerebellar ataxia (ADCA type II) was recently mapped. By radiation hybrid mapping, STAC was assigned to human chromosome 3p22-p24, and it was found to be distinct from the ADCA type II locus.

Animals↗
PubMed1986

Neuron-specific enolase immunoreactivity in the developing mouse cochlea.

Onset of neuron-specific enolase reactivity was observed on gestation day 17 in spiral ganglion cells of the basal coil, and 2 days later in cochlear inner (IHC) and outer (OHC) hair cells. IHCs and OHCs were similarly reactive up to postnatal day 7, then the reactivity began to decrease in OHCs.

Animals↗
PubMed1988

[Neuron-specific enolase as a tumor marker in small cell bronchial carcinoma].

Neurone specific enolase (NSE) was measured in serum from 54 patients with untreated bronchial carcinoma. Serum NSE was elevated (greater than 12.5 micrograms/l) in 24 of 31 patients (77.4%) with small cell bronchial carcinoma, but in only 4 of 23 (17.4%) with non-small cell bronchial carcinoma. The median serum NSE level was significantly higher for small cell bronchial carcinoma than for the other forms (23.6 micrograms/l vs. 8.0 micrograms/l; P less than 0.001). NSE levels had a positive correlation to the tumour stage for the small cell tumour: median of 16.5 micrograms/l in "limited disease" (16 cases) and 43.2 micrograms/l in "extensive disease" (15 cases). Serum NSE levels seem to be suitable markers for documenting the course of small cell bronchial carcinoma: 15 patients with tumour regression or remission had normal NSE values while elevated levels were found in 7 of 8 patients with progression. NSE was demonstrated immunohistologically both in small cell and non-small cell bronchial carcinoma tissue, but high NSE levels were predominantly present in small cell carcinomas.

Adenocarcinoma↗
PubMed1989

Molecular characterization of GP50: a neuron-specific, synaptic-enriched glycoprotein.

The molecular properties of the neuron-specific, synaptic-enriched glycoprotein GP50 have been investigated with the aid of the monoclonal antibody MabSM-GP50. GP50 immunoreactivity was detected in the brains of the frog, trout, pigeon, snake, rabbit, mouse, cow, and human, although variation in quantity and electrophoretic mobility of the immunoreactive protein between species was apparent. Deglycosylation of synaptic membranes (SMs) with endoglycosidase H, peptide:N-glycosidase F, trifluoromethane-sulfonic acid, and alkaline sodium borohydride indicated that GP50 is associated primarily, if not exclusively, with high-mannose and/or hybrid-type oligosaccharides and lacks complex N-linked and O-linked sugar chains. GP50 remained associated with the membrane fraction following extraction of SMs with alkaline sodium carbonate, was partially (55%) present in the detergent phase following the phase partitioning of SMs in the presence of Triton X-114, and was resistant to proteolytic digestion with trypsin when present as a component of intact membranes. Taken together, these results indicate that GP50 is an integral component of the SM. Sucrose gradient centrifugation of Triton X-100 extracts of SMs or of forebrain and cerebellar homogenates resolved GP50 into two fractions with sedimentation coefficients of 3.6S and 7.3S, which accounted for 45 and 55% of the total, respectively. The 7.3S form occurred exclusively in the aqueous phase following partitioning with Triton X-114, whereas the 3.6S species was found in both the aqueous and detergent phases.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2005

Spatial learning of mice lacking a neuron-specific epidermal growth factor family protein, NELL2.

NELL2 is a neuron-specific thrombospondin-1-like extracellular protein containing six epidermal growth factor-like domains. We previously disrupted the NELL2 gene in mice by gene targeting and showed that long-term potentiation is enhanced in vivo in the dentate gyrus of NELL2-deficient mice. To further elucidate the physiological roles of NELL2, we performed a behavioral characterization of NELL2(-/-) and their heterozygous control mice. NELL2-deficient mice exhibited learning impairment in the Morris water maze task. However, we observed no difference in passive avoidance learning between NELL2(-/-) and NELL2(+/-) mice. These observations suggest that NELL2 plays an important role in hippocampus-dependent spatial learning and that emotional learning does not depend critically on NELL2.

Animals↗
PubMed1992

[A clinical study on neuron-specific enolase activities in cerebrospinal fluid of neonates].

Activities of neuron-specific enolase (NSE) in the cerebrospinal fluid (CSF) were measured in 104 neonates (24 cases with CNS diseases and 80 cases without CNS diseases) aged from 0 to 27 days and 50 children without CNS diseases aged 3 months to 15 years. They were determined by using the radioimmunoassay of the Eiken Kit. The enzyme activity in neonates without CNS diseases was significantly higher than that in children. No significant correlation was found between the level of NSE activity and gestational age, birth weight or the days after birth. The mean level of NSE activity in the CSF of neonates with CNS diseases was significantly higher than that of neonates without CNS diseases. Those activities gradually decreased with the clinical course. It was considered that the appropriate cut-off level of NSE activities in CSF for anticipating CNS damage and neurological sequelae was 20.0 ng/ml.

Adolescent↗
PubMed1989

Combined measurements of neuron specific enolase and bombesin/gastrin releasing peptide in lung cancer.

Pretreatment serum neuron specific enolase (NSE) and plasma bombesin/gastrin releasing peptide (BN/GRP) were measured in 92 lung cancer patients and 17 controls. The mean level of NSE (p less than 0.001) and BN/GRP (p less than 0.05) was significantly raised in patients with small cell lung cancer (SCLC, n = 62) compared to non-SCLC (n = 30) and controls. The mean concentration of NSE in extensive SCLC was significantly greater (p less than 0.005) than in limited stage but with a substantial overlap of values. Forty-seven out of 62 SCLC patients had at least one of the two markers raised (sensitivity 76%, specificity 83%), 44 had raised NSE (sensitivity 71%, specificity 89%) but only 24 had BN/GRP raised (sensitivity 42%, specificity 91%). At restaging, 16 of 19 patients with SCLC responsive to chemotherapy showed a significant fall of NSE; on the other hand, BN/GRP fell significantly in only 3 patients, remaining unchanged in the majority of responding patients. In conclusion, the combined determination of NSE and BN/GRP in SCLC, at diagnosis and during the follow-up, was not found to be superior to NSE determination alone.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1987

[The changes in serum neuron-specific enolase in patients with small cell lung cancer].

Serum neuron-specific enolase (NSE) was measured in 48 newly diagnosed untreated patients with small cell lung cancer (SCLC) by radioimmunoassay. Serum NSE level elevated (greater than or equal to 15 ng/ml) in 50% of all patients. The positive ratio of NSE in patients with extensive disease (64%) was significantly higher than those in the patients with limited disease (30%) (p less than 0.05). The positive ratio of NSE in the patients with one metastatic site was 50%, that with two or more metastatic sites was 100% (p less than 0.05). No significant correlation was found between serum NSE levels and metastatic site as well as between serum NSE levels and response to the chemotherapy. In the patients with extensive disease, survival time was shorter in the patients with positive NSE levels than the patients with normal NSE levels. These findings indicate that serum NSE may be a useful marker for staging, monitoring and prognosis in patients with SCLC.

Carcinoma, Small Cell↗
PubMed1983

Serum markers for pancreatic islet cell and intestinal carcinoid tumors: a comparison of neuron-specific enolase, beta-human chorionic gonadotropin and pancreatic polypeptide.

Neuron-specific enolase (NSE) (a glycolytic enzyme that occurs only in neuroendocrine cells), human pancreatic polypeptide (hPP) (a probable peptide hormone), and the beta-subunit of human chorionic gonadotropin (beta hCG) (a glycoprotein hormone), have been suggested as serum markers for the diagnosis and management of apudomas of the pancreas and intestinal tract. Serum levels of NSE, hPP, and beta hCG were measured in 21 patients with pancreatic islet cell cancer (including nine "nonfunctioning" tumors, six gastrinomas, three glucagonomas, two insulinomas, and one somatostatinoma) and in five patients with intestinal carcinoid tumors. Sixteen of the 26 patients (62%) had elevated circulating levels of at least one tumor marker. All three markers were elevated in only one patient, a woman with a "nonfunctioning" islet cell carcinoma. Five patients had increased levels of two serum markers. In three patients both NSE and hPP levels were above normal and in two patients both NSE and beta hCG levels were above normal. In nine patients only one marker was elevated. These included six with elevated NSE levels, two with elevated hPP levels, and one with elevated beta hCG levels. Thus NSE levels were elevated in 12, hPP levels in six, and beta hCG levels in four of the 26 patients. While no single marker was elevated in all patients, each of the three can be elevated in an individual case. When elevated, these markers may be valuable to estimate prognosis or monitor response to therapy.

Adenoma, Islet Cell↗
PubMed1993

Neuron-specific expression of GABAA-receptor subtypes: differential association of the alpha 1- and alpha 3-subunits with serotonergic and GABAergic neurons.

GABAA-receptors in the brain display a striking structural heterogeneity, which is based on a multiplicity of diverse subunits. The allocation of GABAA-receptor subtypes to identified neurons is essential for an analysis of the functional significance of receptor heterogeneity. Among GABA-receptive neurons, well-characterized examples include the serotonergic and GABAergic neurons in the raphe nuclei. The GABAA-receptor subtypes expressed in these two types of neurons were analysed using antisera which recognize selectively the alpha 1- and alpha 3-subunits, and their co-localization with serotonin and glutamate decarboxylase was assessed by confocal laser microscopy in double and triple immunofluorescence staining in the rat. The vast majority of serotonergic neurons express strong alpha 3-subunit-immunoreactivity, but are devoid of alpha 1-subunit staining. In contrast, both the alpha 1- and alpha 3-subunit-immunoreactivities are present in glutamate decarboxylase-positive neurons. Thus, serotonergic and GABAergic neurons selectively express distinct patterns of alpha subunits, suggesting that they possess distinct subtypes of GABAA-receptors. The occurrence of neuron-specific GABAA-receptor subtypes may open new possibilities for the targeting of drugs with selective therapeutic actions.

Animals↗
PubMed1999

Combinatorial control of a neuron-specific exon.

The mouse c-src gene contains a short neuron-specific exon, N1. N1 exon splicing is partly controlled by an intronic splicing enhancer sequence that activates splicing of a heterologous reporter exon in both neural and nonneural cells. Here we attempt to dissect all of the regulatory elements controlling the N1 exon and examine how these multiple elements work in combination. We show that the 3' splice site sequence upstream of exon N1 represses the activation of splicing by the downstream intronic enhancer. This repression is stronger in nonneural cells and these two regulatory sequences combine to make a reporter exon highly cell-type specific. Substitution of the 3' splice site of this test exon with sites from other exons indicates that activation by the enhancer is very dependent on the nature of the upstream 3' splice site. In addition, we identify a previously uncharacterized purine-rich sequence within exon N1 that cooperates with the downstream intronic enhancer to increase exon inclusion. Finally, different regulatory elements were tested in multiple cell lines of both neuronal and nonneuronal origin. The individual splicing regulatory sequences from the src gene vary widely in their activity between different cell lines. These results demonstrate how a simple cassette exon is controlled by a variety of regulatory elements that only in combination will produce the correct tissue specificity of splicing.

Animals↗
PubMed1998

Neuron-specific enolase and chromogranin A as markers of neuroendocrine tumours.

Circulating neuron-specific enolase (NSE) and chromogranin A (CgA) were measured in 128 patients with neuroendocrine tumours (NET) to compare their sensitivity and specificity, to investigate factors associated with elevated serum levels and to determine the usefulness of these markers in the follow-up of NET patients. NSE (Cispack NSE, Cis Bio International, Gif-sur-Yvette, France; normal <12.5 microg l(-1)), and chromogranin A (CgA-Riact, Cis Bio International, normal <100 microg l(-1)) were measured in 128 patients without renal insufficiency. There were 99 patients with gastroenteropancreatic (GEP) NET, 19 with medullary thyroid carcinoma and ten with phaeochromocytoma. Fifty-three patients with non-NET were studied as controls. Serum NSE and CgA levels were elevated in 48 (38%) and 76 (59%) of the 128 NET patients respectively. In all groups of NET patients, CgA proved to be more sensitive than NSE. NSE and CgA had a specificity of 73% and 68% respectively. Immunostaining for NSE was positive in three out of eight controls with elevated CgA levels, whereas immunostaining for CgA and synaptophysin was negative in all cases. Elevated CgA levels were significantly associated with two independent parameters, namely the presence of other secretions (P = 0.0001) and a heavy tumour burden (P = 0.001). Elevated NSE levels were exclusively associated with poor tumour differentiation (P = 0.01). Among six patients with NET followed for 11-37 months, CgA appeared to be a better marker of tumour evolution than NSE. We suggest that CgA ought to be the only general marker screened in NET patients.

Adolescent↗
PubMed1992

Temporal and compartmental restriction of neuron-specific enolase expression in the rat mesostriatal system.

The striatum and the mesencephalic dopamine neurons which innervate it, are each organized into developmentally and biochemically distinct compartments. Striatal patches, characterized in the neonate by high concentrations of opiate receptors and substance P, are innervated prenatally by fibers originating in one group of midbrain dopamine neurons, the ventral tier. By the third postnatal day, a dense dopamine projection from neurons in the dorsal tier of the mesostriatal group innervates non-patch areas of the striatum, i.e. the matrix, and is followed by the appearance there of neurotensin, somatostatin and calcium binding protein. We have recently observed that the period of establishment of connections between dorsal tier dopamine neurons and their target cells in the striatal matrix is accompanied by a surge in expression of the gene coding for tyrosine hydroxylase (TH). In order to determine the overall metabolic state of mesencephalic and striatal neurons during the period of up-regulation of TH gene expression, we have applied immunocytochemistry for neuron specific enolase (NSE), and cytochrome oxidase histochemistry, known markers for neuronal activity, as well as TH immunohistochemistry to the mesencephalon and striatum of postnatally developing rats. At birth, both NSE and cytochrome oxidase were expressed almost exclusively in the patches, appearing in the matrix only after the 2nd postnatal day. Patches of NSE remained visible thru the 14th day. In the mesencephalon, cytochrome oxidase and immunoreactive NSE cells in adjacent sections, were present only in the pars reticulata (i.e. ventral tier). By day 8, both techniques identified nigral cells in the dorsal as well as ventral tiers.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Neuron-specific enolase-containing cells in the rhesus monkey trabecular meshwork.

Neuron-specific enolase (NSE) localizes immunohistochemically to a discontinuous band of cell clusters in the trabecular meshwork of the anterior segment of the rhesus monkey eye. To date, this enolase isomer has been found exclusively in neurons or in cells of the diffuse neuroendocrine system. On this basis, its presence provides presumptive evidence for neuroregulatory cells in the primate trabecular meshwork.

Animals↗