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PubMedDate not supplied

14-3-3 protein, neuron-specific enolase, and S-100 protein in cerebrospinal fluid of patients with Creutzfeldt-Jakob disease.

We explored simultaneously 14-3-3 protein, neuron-specific enolase (NSE), and one astroglial protein, S-100, recently proposed as Creutzfeld-Jakob disease (CJD) markers, in the cerebrospinal fluid (CSF) of 129 patients with suspected CJD. Cutoff values for NSE and S-100 were established at 25 and 2.5 ng/ml, respectively. The highest sensitivity was observed for S-100 (94.2%) followed by 14-3-3 (89.8%) and NSE (79.7%), while the highest specificity in CJD diagnosis was obtained with 14-3-3 protein (100%) as compared with NSE (91.5%) and S-100 (85.4%). No influence of sex, genotype at codon 129 of the prion protein gene, time between sampling, and death or disease duration has been found. Based on 90 cases initially referred as 'probable' or 'possible' CJD, with 14-3-3, NSE, or S-100 we could correctly discriminate between 'CJD' or 'non-CJD' categories in 94.4, 86.5, and 90% of the cases, respectively. When limited to 'possible CJD' cases, diagnosis based on one of the three CSF proteins was accurate in 98, 90.7 and 87.3%, respectively. In view of the fact that the CSF 14-3-3 protein test alone has the highest specificity and good sensitivity, it appears that there is no additional advantage at the moment to include NSE and/or S-100 protein in the exploration of clinically suspected CJD cases.

14-3-3 Proteins↗
PubMed2005

The prognostic significance of circulating neuroendocrine markers chromogranin a, pro-gastrin-releasing peptide and neuron-specific enolase in patients with advanced non-small-cell lung cancer.

BACKGROUND: Chromogranin A (CGA), Pro-gastrin-releasing peptide (ProGRP) and neuron-specific enolase (NSE) are known as immunohistochemical tissue markers closely associated with neuroendocrine differentiation in non-small-cell lung carcinoma (NSCLC). The aim of the present study was to assess the value of serum levels of these markers in predicting response to chemotherapy and survival of patients with unresectable NSCLC. METHODS: The study included 67 patients with advanced NSCLC treated with chemotherapy. Before treatment, serum levels of CGA, ProGRP and NSE were measured with commercial kits. RESULTS: No association was found between serum NSE and age, gender, histology, performance status or extent of the disease. Distribution of serum CGA differed significantly according to gender and histology, with higher levels being found in men (p = 0.01) and in squamous cell carcinoma (p = 0.01). Serum ProGRP levels correlated with disease extent, being higher in patients with metastatic disease (M1) than in those with locoregional disease (M0; p = 0.02). The association of NSE, CGA and ProGRP levels with response to chemotherapy was not significant. While NSE had no impact on survival, the median survival was shorter for patients with elevated serum CGA and longer for patients with high ProGRP levels. Association with survival was significant when the Classification and Regression Tree (CART)-derived or median cutoff points were explored. On inclusion in multivariate Cox models, both CGA and ProGRP retained significance with high levels showing an opposite effect on survival [CART-derived cutoff points: CGA, relative risk (RR) -4.0; p < 0.001, and ProGRP, RR -0.4; p = 0.006, and median cutoff points: CGA, RR -1.8; p = 0.04, and ProGRP, RR -0.5; p = 0.03]. The combined use of CGA, ProGRP and NSE allowed for definition of two sets of patients with significantly different median survival times (25.2 vs. 8.8 months, p = 0.0001). CONCLUSIONS: In the circulation, CGA and Pro-GRP appear to bear important information related to the prognosis for NSCLC patients before chemotherapy. While a high CGA before treatment was found as an unfavorable prognostic determinant, a high ProGRP conferred a survival advantage. The combined use of serum CGA, ProGRP and NSE may supply additional information to prognosis.

Adult↗
PubMed1989

[Measurement of carcinoembryonic antigen, squamous cell carcinoma related antigen and neuron-specific enolase in the bronchoalveolar lavage fluid in patients with peripheral lung cancer].

Carcinoembryonic antigen (CEA), squamous cell carcinoma related antigen (SCC) and neuron-specific enolase (NSE) in bronchoalveolar lavage fluid were measured in 30 patients with peripheral lung cancer, 11 patients with benign lung disease and 19 healthy controls. The mean levels and positive rates of lavaged fluid CEA were 128.0 +/- 16.9 ng/mg and 33.3% in patients with lung cancer, 68.1 +/- 25.9 ng/mg and 9.1% in patients with benign lung disease, and 68.3 +/- 11.6 ng/mg and 5.2% in healthy controls, respectively. The mean levels and positive rates of lavaged fluid CEA in patients with lung cancer were significantly higher than those in patients with benign lung disease (p less than 0.05) and those in healthy controls (p less than 0.05). The mean levels of lavaged fluid SCC and NSE showed no significant difference between cases of lung cancer and benign lung disease or healthy controls. No lavaged tumor marker level in patients with lung cancer showed any close correlation with histologic types and serum levels. In conclusion, measurement of lavaged fluid CEA was considered to be useful in the differential diagnosis of peripheral lung cancer.

Adenocarcinoma↗
PubMed1986

Bronchial carcinoids and phaeochromocytomas. A comparative study with special emphasis on S-100 protein, serotonin and neuron-specific enolase (NSE) immunoreactivity.

A comparative study of bronchial carcinoids (9 cases) and phaeochromocytomas (8 cases) were performed. Both types of tumour exhibited neuron-specific enolase (NSE) immunoreactivity and an argyrophil reaction, and displayed a few scattered argentaffin and serotonin immunoreactive tumour cells. In addition, four of the nine bronchial carcinoids and six of the eight phaeochromocytomas were S-100 protein immunoreactive. The stained cells were located mainly in the periphery of the tumour cell aggregates and possessed long cytoplasmic processes surrounding unreactive tumour cells. The similarity between the two tumour types, especially in their morphology and S-100 protein immunoreactivity, indicates that bronchial carcinoids, or at least some of them, are histogenetically closely related to phaeochromocytomas and might derive from the peripheral nervous system.

Bronchial Neoplasms↗
PubMed1995

Significance of serum neuron-specific enolase as a predictor of relapse of small cell lung cancer.

We conducted a prospective study to evaluate the significance of serum neuron-specific enolase (NSE) as a predictor of relapse of small cell lung cancer (SCLC). Patients entered into the study were drawn from those who had shown a complete or partial response to first-line chemotherapy with a concurrent decline in the NSE level to less than 10 ng/ml. When the serum NSE level increased to more than 15 ng/ml, the patient was restaged on the basis of clinical, radiological, and bronchoscopic examinations. During the period from August 1988 to December 1990, 57 patients with SCLC were enrolled and followed up until May 1992. Of these patients, 45 had clinical relapses, and 14 (31%) of them showed a clear elevation of the serum NSE level prior to the clinical recognition of relapse. Although one false-positive case was noted, this involved only a transient elevation of the NSE level. In patients who showed increased NSE levels, the relapses occurred in more difficult to detect silent sites such as the adrenal gland, liver, and deep lymph nodes. In addition, the percentage of patients demonstrating high NSE levels who were able to benefit from salvage chemotherapy was higher than for those who did not (RHO < 0.05). Our results indicate that serial NSE measurements are useful for the early prediction of SCLC relapse and should help to facilitate early administration of salvage chemotherapy for affected patients.

Adult↗
PubMed1993

[Level of carcinoembryonic antigen, neuron-specific enolase and ferritin in serum of small cell lung cancer patients: correlation with performance status, disease extent and prognosis].

Carcinoembryonic antigen (CEA), neuron-specific enolase (NSE) and ferritin serum levels were assessed before treatment in 109 small cell lung cancer patients. CEA and ferritin serum levels were estimated by immunoenzymatic method: Abbott kits were used. NSE serum level was assessed by radioimmunoassay Pharmacia kits. In 38 patients the disease was localized, in 27 metastases were found in one organ and in 48-in two or more organs. CEA levels above 5 ng/ml were found in 41%, NSE above 12.5 micrograms/l in 86% and ferritin above 250 ng/ml in 41% of patients. The levels of CEA and NSE, but not of ferritin were correlated with the disease extent. The levels of CEA and ferritin, but not of NSE were correlated with performance status of the patients. In the patients with NSE serum levels above 50 micrograms/l and ferritin serum levels above 600 ng/ml the prognosis was significantly worse than in remaining patients.

Carcinoembryonic Antigen↗
PubMed1992

Cerebrospinal fluid and serum levels of neuron-specific enolase in patients with schizophrenia.

Some patients with schizophrenia appear to have brain abnormalities, including enlarged third and lateral ventricles and reduced volumes of temporal lobe structures. These abnormalities could be attributed to a developmental abnormality or a neurodegenerative process. Neuron-specific enolase (NSE), a protein that is found primarily in neurons and neuroendocrine cells, has been used as an index of neuronal damage or degeneration. Levels of NSE in cerebrospinal fluid (CSF) and serum from 50 patients with acute and chronic schizophrenia were compared with those in normal and neurological control subjects. A double-antibody, solid phase iodinated radioimmunoassay was used to determine NSE levels. There was no evidence of elevated levels in patients with schizophrenia, whereas control subjects with neurological illnesses had increased levels of NSE in CSF. Because NSE is rapidly cleared from CSF, however, elevated levels could have been missed. Unmedicated patients tended to have lower levels than medicated patients.

Adult↗
PubMed1994

Neuron-specific enolase concentrations in blood as a prognostic parameter in cerebrovascular diseases.

BACKGROUND AND PURPOSE: To investigate the clinical relevance of plasma concentrations of neuron-specific enolase (NSE) in patients with severe cerebrovascular diseases, serial analyses were performed during the first 10 days after the acute event. METHODS: Plasma samples taken from 61 patients (30 with brain infarction, 13 with intracerebral hemorrhage, 11 with cardiogenic hypoxia-ischemia, and 7 with myocardial infarction [as control group]) were analyzed for NSE concentration using an enzyme immunoassay. The time course of plasma NSE was correlated with clinical findings, clinical outcome, cranial computed tomography, intracranial pressure, and other laboratory data. RESULTS: In cases of hypoxia-ischemia there was close correlation between plasma NSE values during the first 72 hours and the clinical outcome. In brain infarction and intracerebral hemorrhage, high plasma NSE mostly indicated an unfavorable outcome, but low values did not permit a reliable prognostic estimation. In cases of cerebral infarction and intracerebral hemorrhage with secondary neuronal destruction (for example, due to malignant edema), increasing NSE concentrations in plasma preceded the change of clinical or other diagnostic parameters. CONCLUSIONS: The course of plasma NSE levels is seen as a relevant parameter for assessing the prognosis of cerebral hypoxia-ischemia. Additionally, it may prove to be a useful tool for monitoring space-occupying brain infarctions and intracerebral hemorrhages and therefore may contribute to improved therapeutic management of severe cerebrovascular diseases.

Adult↗
PubMed1984

Neurone specific enolase and S100 protein as possible prognostic indicators in melanoma.

Fourteen cases of primary melanoma and 25 of their subsequent metastases were stained for Neurone Specific Enolase (NSE) and S100 protein. Intensity of staining for NSE and S100 protein broadly corresponded in 11 of the primary lesions and was disparate in three. Staining intensity for NSE or S100 was independent of tumour thickness. Primary lesions showing marked or moderate staining for NSE and S100 protein took a shorter time to metastasize than those showing slight or no staining. Assessment of staining intensity for NSE and S100 thus identified prognostic categories corresponding to disease free interval obtained by division according to tumour thickness. Staining intensity for S100 protein appears to give a clearer indication as to expectation of disease free interval. Staining intensity in individual cases showed an increase both for NSE and S100 protein between primary and metastatic lesions. The data presented are not sufficient to assign statistical significance but may lead to the incorporation of functional studies into the pathological assessment of malignant melanocytic lesions. The simultaneous occurrence of a functional neuronal and Schwann cell marker in melanoma is discussed.

Adult↗
PubMed1985

Serum neuron-specific enolase in metastatic Merkel cell tumors.

Three patients with widely disseminated Merkel cell tumors of the skin are presented. In all three cases, neuron-specific enolase (NSE) was demonstrated in neoplastic tissue by immunohistochemical staining, and serum NSE levels were also elevated in all three patients. Serum NSE may prove to be a useful tumor marker in this and other malignancies of neuroendocrine origin.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed2000

[Diagnostic value of s-100 protein and neuron-specific enolase as serum markers for cerebral deficiency after general anesthesia. Study in patient with hip or knee replacement].

UNLABELLED: S-100 protein and neuron-specific enolase (NSE) serum concentrations serve as markers of cerebral damage in cardiac surgery, neurology, or after head injury. In these circumstances, S-100 and NSE levels correspond with the results of neuropsychological tests. The present study investigated the diagnostic value in orthopaedic patients after joint replacement. METHODS: Forty patients scheduled for elective hip or knee arthroplasty were investigated. Serum values of NSE and S-100 were determined preoperatively and 30 min and 4, 18, and 36 h postoperatively. Neuropsychological tests (syndrome short test, SKT, delirium assessment according to DSM IV) were performed preoperatively and two, three, and four days following surgery. General anaesthesia was induced with fentanyl and etomidate and maintained with isoflurane in oxygen/air. FINDINGS: The S-100 increased from a median of 0.04 ng/ml (range 0.004-0.19 ng/ml) preoperatively to 1.03 ng/ml (range 0.18-3.65 ng/ml) at 30 minutes postoperatively (P < 0.0001). These levels returned to normal in the course of the following 2 days. NSE values were 8.55 ng/ml (range 4.6-14.9 ng/ml) preoperatively and 7.07 ng/ml (range 4-16.4 ng/ml) postoperatively (P = 0.167). There were no differences in serum concentrations of S-100 and NSE between normal patients and those with postoperative cognitive deficit. Furthermore, no correlation was found between the serum marker and neuropsychological tests. INTERPRETATION: Obviously, increased NSE levels seem to indicate cerebral damage only in more severe cases. S-100 does not seem to be brain-specific in patients undergoing orthopaedic surgery. Therefore, the value of S-100 in the assessment of brain disorders is limited.

Aged↗
PubMed1989

Neuron specific enolase, carcinoembryonic antigen and lactate dehydrogenase as indicators of disease activity in small cell lung cancer.

The clinical value of the three serum biomarkers neuron specific enolase (NSE), carcinoembryonic antigen (CEA) and lactate dehydrogenase (LDH) were evaluated prospectively in 86 patients with small cell lung cancer (SCLC) entered into randomized clinical trials. The patients were monitored clinically very closely and biomarkers were measured before each course of chemotherapy. The correlation between disease extent and biomarker was significant for both NSE (2P: 0.001) and LDH (2P:0.05). Of those two biomarkers NSE was the most sensitive and was raised in 75% of all patients at diagnosis, in 67% of patients with limited disease, and in 86% of patients with extensive disease. All patients with three or more sites involved presented raised serum NSE levels but there was no significant correlation between definite number or specific sites known to have metastatic disease. There was a tendency towards a higher serum CEA level in extensive disease than in local disease. Only half the patients with metastatic disease had elevated (greater than 5.0 ng/ml) levels of CEA, and values above 50.0 ng/ml were unusual. In patients initially seropositive for NSE a close correlation was found during follow up between serum NSE and response (98%) or progressive systemic disease (100%). During a major response, either complete or partial, serum NSE showed minor fluctuations (mean 8 ng/ml, S.D. 1.79, range 4.6-12.1). At present serum NSE seem to be the most sensitive and valuable biomarker in the management of SCLC, while the gain by adding CEA is small. Furthermore, NSE may be a useful tool in the estimation of disease extent and response to treatment in patients in whom clinical or radiological evaluation is difficult.

Adult↗
PubMed1998

Neuron-specific enolase concentrations in serum and cerebrospinal fluid in patients with no previous history of neurological disorder.

Studies of cerebrospinal fluid (CSF) concentrations of neuron-specific enolase (NSE) in patients with neurological lesions indicate a quantitative relation between the degree of cell damage in the central nervous system (CNS) and the concentration of this CNS-specific protein. We collected serum and CSF from 63 males and 24 females undergoing various surgical procedures in spinal anaesthesia. The patients had no actual or previous history of neurological disease. The mean value of NSE in serum was 7.1 +/- 3.6 micrograms/L. NSE concentrations in CSF demonstrated age- and sex-dependency, with an increase with age from 21 to 84 years and significantly higher levels in males than in females. Therefore, age- and sex-matched reference values have to be used when NSE is evaluated in CSF in patients with different neurological disorders.

Adult↗
PubMed1991

Prognostic impact of histologic demonstration of chromogranin A and neuron specific enolase in pulmonary adenocarcinoma.

One hundred-fourteen patients with inoperable adenocarcinoma of the lung (ACL) were evaluated by immunohistochemistry with monoclonal antibodies against Neuron Specific Enolase (NSE) and Chromogranin A (Chr A) in order to determine the frequency and prognostic impact of such antigen expression. All patients were previously untreated and received chemotherapy according to a prospective randomized trial. The tumors of 18 patients (16%) had more than 10% positive cells stained with anti-NSE, 59 (52%) had 1-10% positive cells and those of 37 patients (32%) contained no NSE-positive cells. The corresponding figures for Chr A were: 22 patients (19%), 51 patients (45%) and 41 patients (36%), respectively. Forty-four per cent of the patients with more than 10% positive NSE cells responded to chemotherapy (either complete or partial remissions) compared to 17% of the patients with fewer than 10% positive cells (p less than 0.025). The corresponding values for Chr A were 30% responders versus 19% responders (not statistically significant). The median survival for patients with more than 10%, 1-10% or no NSE-positive cells was 262 days, 231 days and 159 days, while, for Chr A it was 245 days, 200 days and 238 days, respectively. The survival curves for both NSE and Chr A according to the various levels of positivity were not significantly different. The presence of neuroendocrine marker in pulmonary adenocarcinoma seems to be associated with increased sensitivity to chemotherapy.

Adenocarcinoma↗
PubMed1987

Isolation and characterization of non-neuronal enolase (NNE) from Neurospora crassa and comparison with neuron specific enolase isolated from neuroblastoma cell line NG108.

Enolase is a vital enzyme of the glycolytic pathway. It exists mainly in two forms, non-neuronal enolase (NNE) and neuron specific enolase (NSE). Neurospora crassa, a filamentous fungus, was used as the source of pure NNE, and by using DEAE-cellulose and a Sephadex G-150 column chromatography highly purified enzyme (20.4 fold purification with 54.7 percent recovery) was obtained. The development profile of the enzyme shows a peak value after 90 hours of mycelial growth from conidia of N. crassa. In this respect, it differs from neuroblastoma NSE where the peak value of the enzyme activity appears 7 1/2 hours after the splitting of the cells. N. crassa enolase (NNE) is more thermolabile than NG108 NSE and N. crassa enolase is more sensitive to urea, chloride, and fluorophosphate. The Km values for 2-phosphoglycerate and Mg++ were 0.34 mM and 0.47 mM, respectively, for N. crassa enolase, whereas these values were 1.1 mM and 3.1 mM, respectively, in the case of neuroblastoma NSE. N. crassa enolase is a dimer molecule of molecular weight 85,000 daltons. N. crassa enolase is not neutralized by NSE antisera and neutralized by NNE antisera as opposed to neuroblastoma NSE.

Cell Line↗
PubMed2005

Increased sensitivity to acute and persistent pain in neuron-specific endothelin-1 knockout mice.

Endothelin-1 (ET-1) exists in endothelial cells as well as a variety of other cell types. The presence of ET-1 and its receptors in neurons suggests its possible role as a neurotransmitter and/or neuromodulator. Studies utilizing exogenous ET-1 have suggested that ET-1 affects pain transmission. This study was designed to examine the possible role(s) of neuronal ET-1 in pain processing. We produced neuron-specific ET-1 knockout mice using the Cre/loxP system with a synapsin I promoter and examined the effects produced by the lack of neuronal ET-1 on pain behavior using common pain models and a model of stress-induced analgesia. In acute nociceptive pain models, paw withdrawal thresholds to radiant heat and mechanical stimuli applied with von Frey hairs were significantly lower in the knockout mice compared with control. This indicated that the absence of neuronal ET-1 leads to greater sensitivity to acute nociceptive stimuli. After inflammation was produced by intraplantar injection of carrageenan, there was a significantly greater degree of thermal hyperalgesia and mechanical allodynia in the knockout mice even after the difference in baseline values was compensated. Furthermore, in a neuropathic pain model produced by spinal nerve ligation, there was also a greater degree of mechanical allodynia in the knockout mice. Finally, in a swim-stress model, the magnitude of stress-induced analgesia was less in the knockout mice, indicating the involvement of neuronal ET-1 in stress-induced analgesia. The results suggest that there is a basal release of ET-1 from neurons that affect baseline pain thresholds as well as an additional release during persistent pain states that acts to suppress the pain. The involvement of neuronal ET-1 in stress-induced analgesia further suggests its role in endogenous pain inhibitory systems. To confirm that ET-1 is released in persistent pain states and to determine which part of the CNS is involved, we measured the concentrations of ET-1 before and after inducing peripheral inflammation in different parts of the CNS involved in endogenous pain inhibitory systems in normal mice. We found that ET-1 was increased in the hypothalamus while no significant increase was observed in the midbrain, medulla and spinal cord. The results of the present study suggest that neuronal ET-1 is involved in endogenous pain inhibitory control likely via pathways through the hypothalamus.

Acute Disease↗
PubMed1998

A neuron-specific gene transfer by a recombinant defective Sindbis virus.

We examined the possibility that Sindbis virus, an alpha virus with a single-stranded RNA genome, would be applied for neuronal gene transfer. The recombinant defective Sindbis viruses were constructed by replacing the structural genes of Sindbis virus with genes encoding beta-galactosidase (rdSind-lacZ) or enhanced green fluorescent protein (rdSind-EGFP). In neuron-glia cocultures prepared from the neocortex, hippocampus, and striatum, EGFP or beta-galactosidase was expressed selectively in neurons 24 h after infection with rdSind-EGFP or rdSind-lacZ. Most cortical neurons were infected with rdSind-lacZ at a multiplicity of infection (M.O.I.) of 5 while glial cells were little infected. In addition, transient neuron-specific expression of beta-galactosidase was observed near injection sites over the next 3 d following administration of rdSind-lacZ in adult rat. In the cortical neurons infected with rdSind-EGFP, treatment with NMDA induced neuritic blebs and cell body swelling in a Na+-dependent manner. Therefore, recombinant defective Sindbis viruses can be used as an efficient and selective vector for gene transfer into neurons and applied to investigate biological role of target genes delivered into neurons in vitro and in vivo.

Alphavirus Infections↗
PubMed1994

Culture from human leptomeninges of cells containing neurofilament protein and neuron-specific enolase.

Actively dividing cells cultured from human leptomeninges obtained at autopsy and from human pia obtained at neurosurgery expressed two antigens characteristic of a mature neuronal phenotype: the 160 kDa neurofilament protein (NF-M) and neuron-specific enolase (NSE). The cells lacked typical glial, epithelial and endothelial markers but did contain vimentin, a protein normally associated with but not limited to mesenchymally derived cell types. Immunocytochemical results using redundant antibodies were consistent over serial passage and were confirmed by Western blot analysis. Morphologically the cells were pleiomorphic with frequent long, NF-M + processes. The antigenic characteristics of the cultured leptomeningeal and pial cells were similar to those exhibited by human autopsy and biopsy brain-derived cultures described previously, suggesting that the latter may have originated from pial cells adherent to the autopsy and biopsy brain tissue specimens.

Adult↗