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PubMed1992

Activation of c-src neuron-specific splicing by an unusual RNA element in vivo and in vitro.

A conserved positive-acting RNA sequence was found to be required for the neuron-specific splicing of the mouse c-src N1 exon. The sequence lies in the intron between exons N1 and 4, close to the N1 donor site. Normally, only the neural-specific splicing of exon N1 required this sequence. When the intron downstream of N1 was shortened, splicing at the constitutive exon 4 acceptor also became dependent on the activating sequence. The neuronal and nonneuronal patterns of src splicing were reconstituted in vitro. HeLa cell extracts spliced exon 4 to exon 3, skipping exon N1. Weri-1 retinoblastoma cell extracts spliced exon 4 to exon N1 as well as to exon 3. Both patterns of splicing were dependent on the activating sequence. A 123 nt RNA containing just the activating sequence specifically inhibited both patterns of src splicing, indicating that factors bound to the activator were required for its effects.

Animals↗
PubMed1987

An immunocytochemical demonstration of calcineurin in human nerve cell tumors. A comparison with neuron-specific enolase and glial fibrillary acidic protein.

Human central and peripheral nerve cell tumors were examined in detail using antibodies to calcineurin, glial fibrillary acidic protein (GFAP) and neuron-specific enolase (NSE). Forty-eight formalin-fixed and paraffin-embedded specimens of human neuronal tumors, including 27 medulloblastomas, were examined. Calcineurin-positive cells were found in all peripheral nerve cell tumors and the two gangliogliomas, whereas 20 of the 27 medulloblastomas and one of the two cerebral neuroblastomas did not contain calcineurin-positive cells. Differentiation of cells along the neuronal lines was positively correlated with calcineurin immunoreactivity. NSE-positive cells were found in all of the tumors with the exception of the one cerebral neuroblastoma. NSE immunoreactivity was not invariably consistent with calcineurin immunoreactivity and non-neuronal cells were often positive. Calcineurin-positive cells were all devoid of GFAP, but NSE-positive cells expressed GFAP in some tumors. GFAP-immunoreactive cells were found only in central nerve cell tumors, and not in peripheral tumors. In addition, GFAP-positive cells in some tumors such as retinoblastoma and medulloblastoma morphologically revealed not only neoplastic but also reactive astrocytic features.

Biomarkers, Tumor↗
PubMed1982

Immunocytochemical study on the localization of neuron-specific enolase and S-100 protein in the carotid body of rats.

Light- and electron-immunocytochemical investigation with the peroxidase-antiperoxidase (PAP) procedure revealed neuron-specific enolase and S-100 protein-like immunoreactivities specifically localized in the chief cells and the sustentacular cells of the rat carotid body, respectively. This finding suggests a neuron-like nature of the chief cells and a glia-like nature of the sustentacular cells on both embryological and functional bases.

Animals↗
PubMed1997

Serum neuron-specific enolase levels do not increase after electroconvulsive therapy.

BACKGROUND: Cognitive disorders occurring after electroconvulsive therapy (ECT) are regarded as an expression of brain damage, despite computed tomography (CT) and magnetic resonance imaging (MRI) showing no signs of structural brain damage. Serum neuron-specific enolase (NSE) is a sensitive marker of neuronal damage (i.e., after stroke or cardiac arrest). The objective of this study was to investigate whether ECT leads to a rise in the serum NSE level as an expression of neuronal damage. METHODS: We investigated seven patients (four women, three men; mean age 6212 years) with major depressive disorder, who were treated with ECT for the first time. ECT was administered every 2 days, three times a week under standard conditions (anaesthesia: thiopental, succinylcholine, 100% oxygen, unilateral ECT, seizure duration more than 20 s). Blood samples were drawn at the following times. For the first ECT: 15 and 1 min before ECT, and 1, 5, 10, 15, 20, 25, 30, 45, 60, 75, 90, 105, 120 min, and 8, 12, 24 h after ECT. For all subsequent ECT: 1 min before and 4 h after every ECT. Serum NSE was measured by means of enzyme immunoassay (Cobas Core NSE, EIA, Hoffmann-La Roche). RESULTS: On average, each patient underwent ECT 10 times (range 5-20). In the first ECT there was no difference in serum NSE levels before and at all times following ECT. A comparison of serum NSE levels before and after each subsequent bout of ECT revealed no differences. Moreover, comparing the baseline serum NSE levels (before the first ECT) with the values after final ECT showed no differences either. CONCLUSION: ECT did not increase serum NSE values, indicating that electroconvulsive therapy does not cause neuronal damage.

Aged↗
PubMed1997

Mice lacking p35, a neuronal specific activator of Cdk5, display cortical lamination defects, seizures, and adult lethality.

The adult mammalian cortex is characterized by a distinct laminar structure generated through a well-defined pattern of neuronal migration. Successively generated neurons are layered in an "inside-out" manner to produce six cortical laminae. We demonstrate here that p35, the neuronal-specific activator of cyclin-dependent kinase 5, plays a key role in proper neuronal migration. Mice lacking p35, and thus p35/cdk5 kinase activity, display severe cortical lamination defects and suffer from sporadic adult lethality and seizures. Histological examination reveals that the mutant mice lack the characteristic laminated structure of the cortex. Neuronal birth-dating experiments indicate a reversed packing order of cortical neurons such that earlier born neurons reside in superficial layers and later generated neurons occupy deep layers. The phenotype of p35 mutant mice thus demonstrates that the formation of cortical laminar structure depends on the action of the p35/cdk5 kinase.

Animals↗
PubMed1999

Quinupristin/dalfopristin attenuates the inflammatory response and reduces the concentration of neuron-specific enolase in the cerebrospinal fluid of rabbits with experimental Streptococcus pneumoniae meningitis.

The inflammatory response following initiation of antibiotic therapy and parameters of neuronal damage were compared during intravenous treatment with quinupristin/dalfopristin (100 mg/kg as either a short or a continuous infusion) and ceftriaxone (10 mg/kg/h) in a rabbit model of Streptococcus pneumoniae meningitis. With both modes of administration, quinupristin/dalfopristin was less bactericidal than ceftriaxone. However, the concentration of proinflammatory cell wall components (lipoteichoic acid (LTA) and teichoic acid (TA)) and the activity of tumour necrosis factor (TNF) in cerebrospinal fluid (CSF) were significantly lower in the two quinupristin/dalfopristin groups than in ceftriaxone-treated rabbits. The median LTA/TA concentrations (25th/75th percentiles) were as follows: (i) 14 h after infection: 133 (72/155) ng/mL for continuous infusion of quinupristin/dalfopristin and 193 (91/308) ng/mL for short duration infusion, compared with 455 (274/2042) ng/mL for ceftriaxone (P = 0.002 and 0.02 respectively); (ii) 17 h after infection: 116 (60/368) ng/mL for continuous infusion of quinupristin/dalfopristin and 117 (41/247) ng/mL for short duration infusion, compared with 694 (156/2173) ng/mL for ceftriaxone (P = 0.04 and 0.03 respectively). Fourteen hours after infection the median TNF activity (25th/75th percentiles) was 0.2 (0.1/1.9) U/mL for continuous infusion of quinupristin/dalfopristin and 0.1 (0.01/3.5) U/mL for short duration infusion, compared with 30 (4.6/180) U/mL for ceftriaxone (P = 0.02 for each comparison); 17 h after infection the TNF activity was 2.8 (0.2/11) U/mL (continuous infusion of quinupristin/dalfopristin) and 0.1 (0.04/6.1) U/mL (short duration infusion), compared with 48.6 (18/169) U/mL for ceftriaxone (P = 0.002 and 0.001). The concentration of neuron-specific enolase (NSE) 24 h after infection was significantly lower in animals treated with quinupristin/dalfopristin: 4.6 (3.3/5.7) microg/L (continuous infusion) and 3.6 (2.9/4.7) microg/L (short duration infusion) than in those treated with ceftriaxone (17.7 (8.8/78.2) microg/L) (P = 0.03 and 0.009 respectively). In conclusion, antibiotic treatment with quinupristin/dalfopristin attenuated the inflammatory response within the subarachnoid space after initiation of antibiotic therapy. The concentration of NSE in the CSF, taken as a measure of neuronal damage, was lower in quinupristin/dalfopristin-treated rabbits than in ceftriaxone-treated rabbits.

Animals↗
PubMed1985

Neuron-specific growth cone properties as seen in identified neurons of Helisoma.

By using cell-cultured identified neurons of the snail Helisoma, we demonstrate that the growth cones of different neurons are intrinsically different from one another in terms of their structure, behavior, and response to environmental signals. Structurally neuron 5 has a greater number of filopodia per growth cone, has shorter filopodia, and has a smaller interfilopodial distance than neuron 19. Behaviorally, the growth cones of neuron 5 advance over the substratum at a faster rate than those of neuron 19; and the growth cones of neuron 19, but not of neuron 5, respond to the presence of serotonin in their environment by retracting their filopodia. In addition to such intrinsic differences between the growth cones of different neurons, we also demonstrate that the separate growth cones of a single neuron, while having identical properties, can act independently of one another. Focal application of serotonin to a growth cone causes only a localized retraction of that growth cones' filopodia. Other growth cones that are attached to the same neuron but that are not exposed to serotonin retain their normal structural features.

Animals↗
PubMed1999

Quantitative comparison of growth-associated protein GAP-43, neuron-specific enolase, and protein gene product 9.5 as neuronal markers in mature human intestine.

This study was performed to compare GAP-43, PGP 9.5, synaptophysin, and NSE as neuronal markers in the human intestine. GAP-43-immunoreactive nerve fibers were abundant in all layers of the ileum and colon. GAP-43 partially co-localized partially with every neuropeptide (VIP, substance P, galanin, enkephalin) studied. All neuropeptide-immunoreactive fibers also showed GAP-43 reactivity. By blind visual estimation, the numbers of GAP-43-immunoreactive fibers in the lamina propria were greater than those of PGP 9.5, synaptophysin, or NSE. In the muscle layer, visual estimation indicated that the density of GAP-43-immunoreactive fiber profiles was slightly greater than that of the others. The number and intensity of GAP-43-, PGP 9.5-, and NSE-immunoreactive fibers were estimated in sections of normal human colon and ileum using computerized morphometry. In the colon, the numbers of GAP-43-immunoreactive nerve profiles per unit area and their size and intensity were significantly greater than the values for PGP and NSE. A similar trend was observed in the ileum. Neuronal somata lacked or showed only weak GAP-43 immunoreactivity, variable PGP 9.5 immunoreactivity, no synaptophysin immunoreactivity, and moderate to strong NSE immunoreactivity. We conclude that GAP-43 is the superior marker of nerve fibers in the human intestine, whereas NSE is the marker of choice for neuronal somata. (J Histochem Cytochem 47:1405-1415, 1999)

Biomarkers↗
PubMed1989

Neuron-specific enolase and thymidine kinase as an aid to the diagnosis and treatment monitoring of small cell lung cancer.

The serum levels of neuron specific enolase (s-NSE) and thymidine kinase (s-TK) were studied in detail in patients with small cell lung cancer (SCLC) to evaluate as to whether their combined use may aid to diagnosis and follow-up of this particular tumor. Only s-NSE could differentiate between SCLC and non-small cell lung cancer (NSCLC) or benign pulmonary diseases (BPD) to some extent, pathologic serum concentrations occurring in 81%, 17%, and 0%, respectively. The comparable figures for s-TK were 62%, 24%, and 28%, respectively. Serum NSE decreased and increased paralleling tumor regression and progression, respectively, except when brain metastases were present. Alterations of s-TK, in contrast, did not usually mirror the course of disease. During initial chemotherapy (CT) a transitory increase of serum levels was observed for both NSE and TK. Monitoring, based on daily blood samples, showed comparable peaks only for s-TK during the following CT cycles, whereas s-NSE was within the normal range even when tumor mass was still present. Those subsequent s-TK peaks under CT may be due to tumor cell lysis as a result of CT indicating the efficacy of treatment by this way. Rapidly proliferating tissues such as bone marrow or bowel mucosa, however, have also to be considered as possible sources of s-TK.

Aged↗
PubMed2001

"Type III" cells of rat taste buds: immunohistochemical and ultrastructural studies of neuron-specific enolase, protein gene product 9.5, and serotonin.

Taste buds contain a variety of morphological and histochemical types of elongate cells. Serotonin, neuron-specific enolase (NSE), ubiquitin carboxyl terminal hydrolase (PGP 9.5), and neural cell adhesion molecule (N-CAM) all have been described as being present in the morphologically defined Type III taste cells in rats. In order to determine whether these substances coexist in a single cell, we undertook immunohistochemical and ultrastructural analysis of taste buds in rats. Double-label studies show that PGP 9.5 and NSE always colocalize. In contrast, PGP 9.5 and serotonin seldom colocalize. Further, whereas the serotonin-immunoreactive cells are always slender and elongate, the PGP 9.5/NSE population comprise two morphological types--one slender, the other broader and pyriform. Although gustducin-immunoreactive taste cells appear similar in overall shape to the pyriform PGP 9.5/NSE population, gustducin never colocalizes with PGP 9.5 or NSE. The serotonin-immunoreactive taste cells have an invaginated nucleus, synaptic contacts with nerve fibers, and taper apically to a single, large microvillus. These are all characteristics of Type III taste cells described previously in rabbits (Murray [1973] Ultrastructure of Sensory Organs I. Amsterdam: North Holland. p 1-81). PGP 9.5-immunoreactive taste cells exhibit two morphological varieties. One type is similar to the serotonin-immunoreactive population, containing an invaginated nucleus, synapses with nerve fibers, and a single large microvillus. The other type of PGP 9.5-immunoreactive taste cell has a large round nucleus and the apical end of the cell tapers to a tuft of short microvilli, which are characteristics of Type II taste cells. Thus, in rats, some Type III cells accumulate serotonin but do not express PGP 9.5, whereas others express PGP 9.5 but do not accumulate amines. Similarly, Type II taste cells come in at least two varieties: those immunoreactive for gustducin and those immunoreactive for PGP 9.5.

Animals↗
PubMed1991

Investigation on serum neurone-specific enolase in prostate cancer diagnosis and monitoring: comparative study of a multiple tumor marker assay.

A quadruple tumor marker serotest assay (neurone-specific enolase, NSE, prostate-specific antigen, PSA, prostatic acid phosphatase, PAP, and carcino-embryonic antigen, CEA) was performed on sera from both 63 patients with untreated prostate cancer and 135 patients treated with orchiectomy, flutamide, diethylstilbestrol (DES), cyproterone acetate (CPA), and Estracyt. In untreated patients with local tumor elevated blood NSE concentrations were found more frequently (10/35, 28.6%) than in untreated subjects with disseminated disease (3/28, 10.7%). Elevated NSE values were measured more frequently in nonresponders to therapy 10/46 (21.7%), than in responders during prostate cancer partial remission (2/89, 2.2%). In none of NSE-positive neoplasms a small cell prostate cancer has been histologically detected. Many of NSE-positive tumors are also closely associated with elevated blood CEA values. The applied anticancer drugs were inefficient in the normalization of neither one from the pair of elevated NSE and CEA concentrations (regardless of the numerical values of the other two markers, PSA and PAP), but their values were found to decline occasionally only after surgical treatment. In patients with raised PSA, PAP, and CEA levels but with a normal NSE value, the application of the same treatment strategies was in the most of subjects sufficient to provoke either temporary or even lasting tumor response to therapy. Hence, it appears that the assessment of the NSE serotest, despite its minimal value in the overall tumor staging and monitoring, might furnish the decision-making step related to the treatment of aggressive prostate cancer with an additional and powerful tool.

APUD Cells↗
PubMed1984

Immunohistochemical detection of chromogranin and neuron-specific enolase in pancreatic endocrine neoplasms.

Twenty pancreatic endocrine tumors and one duodenal somatostatinoma were stained with polyclonal antisera against eight hormones, neuron-specific (NSE), and with a monoclonal antibody against the endocrine granule protein chromogranin. Silver staining was performed on all tumors with the Grimelius method. All the tumors and all cells in the normal pancreatic islet showed NSE immunoreactivity. Chromogranin immunoreactivity was found predominantly in the glucagon cells of normal islets, in one glucagonoma, four gastrinomas and in 10 tumors associated with multiple hormonal production, but not in five insulinomas or in one somatostatinoma. Grimelius reactivity was identical to chromogranin immunoreactivity in all cases except that more cells in the tumors and in the normal islets were positive for chromogranin. Both chromogranin and NSE were detected in a metastasized pancreatic endocrine tumor which had metastasized to a peripancreatic lymph node. The metastatic tumor failed to stain with antisera to all eight hormones. These results indicate that chromogranin and NSE are excellent general markers for pancreatic endocrine tumors and that the Grimelius stain and other related argyrophilic reactions may involve binding to chromogranin.

Antibodies, Monoclonal↗
PubMed2006

Elevated serum levels of S-100beta protein and neuron-specific enolase are associated with brain injury in patients with severe sepsis and septic shock.

OBJECTIVE: We investigated whether serum levels of neuron-specific enolase (NSE) and S-100beta protein could be used to evaluate cerebral injury and to predict outcome in severe sepsis and severe septic shock. DESIGN: Prospective study. SETTING: University hospital. PATIENTS AND MEASUREMENTS: In 170 consecutively enrolled patients with severe sepsis and septic shock, serum S-100beta and NSE were measured daily during four consecutive days after intensive care unit admission. Admission Glasgow Coma Scale before sedation and daily Sequential Organ Failure Assessment scores were recorded in all patients. Acute encephalopathy was defined as either a state of agitation, confusion, irritability, and convulsions (type A) or characterized by somnolence, stupor, and coma (type B) and persistently observed during 72 hrs after withdrawing sedation. When clinically indicated, contrast computed tomography or magnetic resonance imaging were performed to evaluate brain injury. MAIN RESULTS: S-100beta and NSE increased in, respectively, 72 (42%) and 90 (53%) patients. High biomarker levels were associated with the maximum Sequential Organ Failure Assessment scores (p = .001), and the highest values were found in patients who died early, within 4 days of inclusion (p = .005). Low consciousness encephalopathy type B was more frequently observed in patients with elevated S-100beta (p = .004). S-100beta levels of >or=4 microg/L were associated with severe brain ischemia or hemorrhage, and values of <2 microg/L were found in patients with diffuse cerebral embolic infarction lesions. High S-100beta levels were associated with higher intensive care unit mortality (p = .04) and represented the strongest independent predictor of intensive care unit survival, whereas NSE and the Glasgow Coma Scale failed to predict fatal outcome. CONCLUSIONS: S-100beta and NSE are frequently increased and associated with brain injury in patients with severe sepsis and septic shock. S-100beta levels more closely reflected severe encephalopathy and type of brain lesions than NSE and the Glasgow Coma Scale.

Adolescent↗
PubMed1999

Kinetics of serum neuron-specific enolase and prolactin in patients after single epileptic seizures.

PURPOSE: To investigate and compare the temporal profile of serial levels of neuron-specific enolase (NSE) and prolactin in serum from patients after single epileptic seizures. METHODS: Measurement of NSE and prolactin by sensitive immunoassays in 21 patients with complex partial seizure (CPSs: n = 11) and secondarily generalized tonic-clonic seizures (SGTCSs; n = 10) during continuous video-EEG monitoring at four different time points (1, 3, 6, and 24 h after ictal event). Statistical analysis was performed by using a repeated-measures analysis of variance (ANOVA) model. RESULTS: Mean+/-SD values for NSE levels (ng/ml) were 12.5 +/-4.4 (1 h), 10.8+/-3.8 (3 h), 11.1+/-4.9 (6 h), and 8.2+/-1.9 (24 h). The corresponding prolactin levels (mU/L) were 1,311+/-1,034, 232+/-158, 237+/-175, and 251+/-98. There was a significant decrease of NSE and prolactin levels over time (p < 0.001). The pair-wise comparison of NSE levels showed significant differences between the time points 1 vs. 24 h (p < 0.001), 3 vs. 24 h (p = 0.007), and 6 vs. 24 h (p = 0.009). In contrast, serum prolactin levels showed a significant difference between 1 vs. 3 h (p < 0.001) only. Most of the NSE levels remained normal after CPSs and SGTCSs. At 1 h after the seizure, only 33% of the subjects had increased NSE, whereas abnormal prolactin levels occurred with a sensitivity of 80%. CONCLUSIONS: In contrast to prolactin, serum NSE is not a sensitive marker of individual seizures. Only some individuals showed an increase of NSE beyond the prolactin-sensitive time frame after a single seizure, and mean NSE levels were not significantly increased compared with those of normal controls.

Adult↗
PubMed1996

Serum neuron-specific enolase as a prognostic marker for irreversible brain damage in comatose cardiac arrest survivors.

OBJECTIVE: To assess the use of serum neuron-specific enolase (S-NSE) level as a noninvasive predictor of CNS injury irreversibility in comatose cardiac arrest survivors. METHODS: An observational, prospective clinical study was performed in a community hospital ED and intensive care unit. All cardiac arrest survivors (n = 52) with impaired neurologic status admitted between February 1994 and May 1995 were followed until return of consciousness (1) or death due to CNS failure (0). Serum samples for S-NSE determination (ng/mL) using the radioimmunoassay technique were obtained 24 hours after cardiac arrest. Data were analyzed using stepwise logistic regression with dichotomized predictors to validate the correlation between S-NSE (X) and outcome (Y), where X = 0 if < or = median and 1 if > median S-NSE level. Adjustment was made for the following variables: glucose level on admission, total epinephrine dose used before return of spontaneous circulation, and best Glasgow Coma Scale score on admission. These data were all available in 34 cases. In 16 cases, CSF enzymes at 48 hours postarrest were obtained and compared with S-NSE. RESULTS: The logistic equation determining the influence of S-NSE (X) on outcome (Y) was: Y = 0.606-1.785X (odds ratio = 6; p = 0.020). There was no confounding effect of the other variables related to survival. The mean S-NSE value for all the patients was 34 (7.9-188). All the patients recovering consciousness (n = 15) had an S-NSE mean +/- SEM value of 17.5 +/- 2.4, with a maximum of 47. CONCLUSION: These data support the conclusion that measurement of S-NSE at 24 hours post-cardiac arrest may supplement clinical assessment of hypoxic-ischemic encephalopathy after cardiac arrest.

Adolescent↗
PubMed1991

Immunohistochemical demonstration of neurone specific enolase in bone marrow infiltrated by neuroblastoma.

One hundred and two bone marrow samples were analysed by histological and immunohistochemical methods for neurone specific enolase (NSE). The biopsies were performed to determine the extent of bone marrow disease in 84 neuroblastomas, nine embryonal rhabdomyosarcomas, five Ewing's sarcomas, two cases of Hodgkin's disease and two lymphoblastic lymphomas. Twenty seven (32%) of neuroblastoma bone marrows showed metastases by conventional histological techniques and 33 (39%) after immunohistochemical staining with NSE. Five embryonal rhabdomyosarcomas, five Ewing's sarcomas, and two lymphoblastic lymphomas showed bone marrow metastases. Only one of these cases was reactive for NSE. NSE represents a very sensitive immunomarker for the follow up of neuroblastoma and improves detection of bone marrow invasion by neuroblastoma.

Biomarkers, Tumor↗
PubMed1990

Localization of chromogranins, non-neuron-specific enolase, and different forms of somatostatins in the submandibular salivary glands of mice.

The localizations of chromogranins A, B, and C, neuron-specific enolase (NSE, gamma gamma-type) and non-NSE (alpha alpha-type), and different forms of somatostatins were immunocytochemically identified. The localizations were compared with those of epidermal growth factor (EGF) and nerve growth factor (NGF) in the submandibular salivary glands (SMG) of male mice at five to six weeks of age, with use of a variety of antibodies and the peroxidase-antiperoxidase (PAP) and avidin-biotin complex (ABC) detection methods. In the SMG of male mice, the major chromogranin present was chromogranin A, whereas chromogranins B and C were not detected at these ages by either method. Chromogranin A-like immunoreactivity was located in the granular convoluted tubule (GCT) cells of the SMG, whereas non-NSE immunoreactivity was observed throughout the duct system and in some acinar-associated cells. NSE was not detected in any part of the SMG. The distribution of chromogranin A and somatostatins in the GCT cells was similar to that of EGF and NGF. Our results strongly suggest that chromogranin A and somatostatins, but not chromogranin B or C, may be useful as a means of differentiation of the cells in the duct system of the SMG responsible for the production of biologically-active factors.

Animals↗
PubMedDate not supplied

Neuron-specific enolase in the diagnosis and therapy monitoring of lung cancer: a comparison with CEA, TPA, ferritin and calcitonin.

The significance of neuron-specific enolase (NSE) in the diagnosis and treatment monitoring of lung cancer was investigated in comparison with such established tumour markers as carcinoembryonic antigen (CEA), tissue polypeptide antigen (TPA), ferritin and calcitonin. We determined the serum concentrations of these tumour markers in 25 patients with small cell lung cancer (SCLC), 30 patients with non small cell lung cancer (NSCLC), and 38 patients with benign pulmonary diseases (BPD). In 14 patients with lung cancer, it was possible to follow up the behaviour of the tumour markers under treatment for up to 16 months. Calcitonin proved to have a surprisingly low sensitivity for SCLC. The utility of TPA and of ferritin was restricted, although the sensitivity was comparably high, by the high rate of false positive results. For NSCLC, CEA proved to be the best tumour marker. At present, NSE appears to be the tumour marker with the greatest specificity and sensitivity for SCLC. Its determination in the diagnosis, treatment and follow-up of SCLC makes good sense.

Adult↗