Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.1.3.1 (alkaline phosphatase)
47,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have established a cell line (KU-SN) from a peripheral neuroectodermal tumor originating in the left scapula of a 4-year-old girl. The original tumor was immunoreactive with antibodies for neurofilament proteins, neuron-specific enolase, vimentin, S100 protein, and beta 2-microglobulin. Dense core granules, 50-150 nm in diameter, were identified by electron microscopy. The cell line was established from tumor cells in metastatic lung fluid. KU-SN cells were immunoreactive with the antibodies for neurofilament proteins, vimentin, neuron-specific enolase, S100 protein, glial fibrillary acidic protein, cytokeratin, and carcinoembryonic antigen. Besides these neuronal features, KU-SN cells express type 2 collagen and insulin-like growth factor 1 receptor. The addition of insulin-like growth factor 1 (100 ng/ml) increased the growth rate of KU-SN cells 2.1-fold over control. Some cells were positive for Alcian blue and alkaline phosphatase staining. Cytogenetic analysis of KU-SN cells disclosed a reciprocal chromosomal translocation [t(11,22)]. Northern blot analysis of KU-SN cells demonstrated amplified expression of the c-myc gene but not the N-myc gene. When tumor cells were transplanted into nude mice, cartilage was formed. The cartilage was immunoreactive with the antibody for HLA-ABC, indicating that it was derived from the tumor cells, not from mouse tissue. Chondrocytic differentiation was not observed in xenografts of Ewing's sarcoma cell lines SK-ES or RD-ES or the peripheral neuroectodermal tumor cell line SK-N-MC. These results indicate that KU-SN cells represent primitive neural crest cells having the potential for chondrocytic differentiation.
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PMID:Chondrocytic differentiation of peripheral neuroectodermal tumor cell line in nude mouse xenograft. 137 22

Seventy-seven cases of meningioma (15 with single or multiple recurrences), selected on the basis of their histologic subtypes, and nine cases of neurilemoma were analyzed immunohistochemically for the presence of the five classes of intermediate filament proteins, neuron-specific enolase (NSE), protein S-100, epithelial membrane antigen (EMA), and HNK-1 (Leu-7). Most antibodies were studied with the alkaline phosphatase-antialkaline phosphatase method. The peroxidase-anti-peroxidase and avidin-biotin-complex methods were used for Leu-7 and NSE, respectively. Meningiomas were subdivided into groups showing cytokeratin or protein S-100 positivity. Coexpression of these two markers was rare (5%) and occurred in meningotheliomatous meningiomas only. Only in these cases was cytokeratin expression more frequent than in meningiomas taken together (33% versus 20%). In contrast, protein S-100 expression was less frequent (46% versus 60% on average). In fibrous meningiomas, both cytokeratins and NSE were expressed less frequently than on average (11% versus 20%, 67% versus 88%, respectively). Protein S-100 occurred in a higher percentage of cases. Transitional meningiomas did not show cytokeratin expression. Protein S-100 occurred in a higher percentage of cases. Transitional meningiomas did not show cytokeratin expression. Protein S-100 was expressed slightly more often than in the other subtypes. Psam-momatous meningiomas coexpressed more markers than any other subtype. Hemangioblastic and hemangiopericytic forms did not stain for EMA, but otherwise showed a staining profile similar to that of meningiomas. HNK-1 was expressed in 29% of meningiomas, particularly among tumors with anaplastic histologic features. There was no marker that retrospectively indicated impending recurrences.
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PMID:Immunohistochemical profile of meningiomas and their histological subtypes. 169 24

A comparative study of immunohistochemical staining for neuron-specific enolase (NSE), protein-gene product 9.5 (PGP 9.5) and S-100 was made in 71 undifferentiated round cell tumours from 65 children using formalin-fixed tissues and a standard alkaline phosphatase-anti-alkaline phosphatase method. All of 29 neuroblastomas marked for NSE and 27 for PGP 9.5; staining was diffuse and usually strong in all tumour elements, irrespective of the degree of differentiation. Patterns of staining remained consistent in primary, recurrent and metastatic tumours and were not modified by previous chemotherapy. S-100 staining was weak and confined to cell processes and schwannian elements in less than half of the tumours studied. Two primitive neuroectodermal tumours both stained strongly for NSE and PGP 9.5. Staining for NSE was observed in single maturing cells in 3/12 rhabdomyosarcomas and in tubular elements in 2/4 Wilms' tumours; primitive rhabdomyoblasts and undifferentiated renal blastema were negative; seven lymphomas were negative. Six of 17 skeletal Ewing's sarcomas showed light to moderate cytoplasmic staining for NSE and PGP 9.5. The site, histology and clinical course of these marker-positive Ewing's sarcomas showed no distinctive features. Staining for PGP 9.5 is a useful additional marker for neural differentiation in round cell tumours.
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PMID:A comparative study of immunohistochemical staining for neuron-specific enolase, protein gene product 9.5 and S-100 protein in neuroblastoma, Ewing's sarcoma and other round cell tumours in children. 216 56

The immunoprofiles of 121 germ cell and trophoblastic neoplasms were defined, using a battery of antibodies against cytokeratin (CK), vimentin (VIM), epithelial membrane antigen (EMA), placental alkaline phosphatase (PLAP), S-100 protein, leukocyte common antigen (LCA), UCHL-1, LN-2, carcinoembryonic antigen (CEA), neuron-specific enolase (NSE), chromogranin A, Leu-7, alpha-fetoprotein (AFP), alpha-1-antitrypsin (AAT), and the beta subunit of human chorionic gonadotropin (BHCG). In addition to 85 neoplasms of testicular origin, the cases included eight ovarian germ cell tumors and 28 extragonadal neoplasms. All tissues had been subjected to formalin fixation and paraffin embedding. Similar immunoreactivity patterns were seen in gonadal and extragonadal neoplasms, gestational and nongestational choriocarcinomas, components of mixed germ cell tumors and their pure counterparts, and metastatic and primary lesions. Placental alkaline phosphatase was a sensitive marker of germ cell differentiation, and expression of this marker in the absence of EMA appeared to be a staining pattern unique to germ cell tumors. Both LCA and S100 were absent in neoplastic germ cells, and thus were useful in differentiating these tumors from malignant lymphoma and malignant melanoma, respectively. Cytokeratin was helpful in distinguishing seminomas/dysgerminomas from nonseminomatous germ cell tumors, although 10% of seminomas showed focal or diffuse cytokeratin reactivity. Finally, 75% of all germ cell neoplasms displayed NSE, calling the specificity of this determinant into question.
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PMID:Immunohistochemistry of germ cell and trophoblastic neoplasms. 245 24

The pre-treatment serum levels of neuron-specific enolase (NSE), phosphohexose isomerase (PHI) and circulating immune complexes (CC) as tumour markers were compared to measurements of standard haematology and biochemical indices in 73 patients with lung cancer, as an aid to differentiation of tumour type, estimating disease extent, predicting response to therapy and prognosis. Elevated NSE greater than or equal to 12.5 ng ml-1, PHI greater than or equal to 55 mgl-1 levels were observed in 55% of cases for NSE, 90% for PHI and 49% for CC. NSE was significantly elevated in 61% (25/41) of patients with SCLC (P less than 0.005) compared to 41% (13/32) with NSCLC. CC levels were significantly raised in 72% (23/32) of patients with NSCLC (P less than 0.05) compared to 32% with SCLC. The levels of NSE and PHI were not related to tumour stage but CC was significantly raised in limited compared to extensive disease in SCLC (P less than 0.05). Serum albumin was significantly lower in NSCLC compared to SCLC, and median values of alkaline phosphatase, gamma-glutamyltranspeptidase and aminoaspartate transferase were significantly higher in patients with extensive disease. The pre-treatment serum values of NSE, PHI, and CC did not predict the response to therapy or prognosis in the 73 patients with lung cancer. The most important prognostic factor was the number of abnormal routine laboratory parameters (greater than 4) in this group of patients.
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PMID:The value of tumour markers in lung cancer. 290 54

The complex vasculature of the human nasal mucosa plays an important role in the protection of the lower respiratory airways. It has to react to different external and internal stimuli and is under control of the autonomic nervous system. The aim of our study was to detect the precise localisation of neural structures in human nasal mucosa vessels under physiological conditions. Silver impregnation and histochemical staining techniques only allowed a partial aspect of autonomic innervation. Modern immunostaining methods with antibodies to neuron-specific enolase (NSE) and S-100 protein proved to be better for the demonstration of nerve structures. Tissue samples were taken from inferior turbinates received at mucotomy in 42 patients. After fixation the samples were embedded in paraffin wax and cut into serial sections. Additionally frozen sections were performed. The immunocomplexes were visualised by the avidin-biotin-complex (ABC) or by the alkaline phosphatase anti-alkaline phosphatase (APAAP) technique. A high density of S-100 and NSE immunoreactivity of neuronal and glial components of autonomic innervation could be demonstrated in the vessels of human nasal turbinates. Branching off relatively thick nerve bundles of the lamina propria fibres extended to the adventitia of the arteries near the periost and formed a periarterial nerve plexus. Fibres of this plexus supplied the smooth muscle tissue of the tunica media. Around veins only a few single nerve fibres could be demonstrated. By using immunocytochemical techniques it is possible to correlate the localisation of the classical neurotransmitters and multiple vasoactive neuropeptides with the corresponding innervation structures of the complex vasculature in human nasal mucosa.
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PMID:[Immunohistochemical study of the neuroanatomy of the nasal turbinate in man. Innervation pattern of the blood vessels]. 814 55

The influence of pretreatment serum neuron-specific enolase (S-NSE) in addition to more conventional prognostic factors on survival duration in small-cell lung cancer (SCLC) was investigated in 770 patients from nine centres in six countries. The other variables included stage of disease, performance status (PS), age, sex, serum lactate dehydrogenase (S-LDH), serum alkaline phosphatase (S-AP), and serum carcinoembryonic antigen (S-CEA). Increased values of S-NSE (> 12.5 micrograms-1 l) were observed in 81% of the patients, whereas S-LDH, S-AP and S-CEA were elevated in only half of the patients or less. Multivariable analysis by Cox's proportional hazard model disclosed S-NSE as the most powerful prognostic factor followed by poor PS and extensive stage disease. If PS was ignored, S-LDH came up as a significant prognostic factor. S-AP, S-CEA, age and sex had no significant influence on the prognosis. The three prognostic factors, S-NSE, PS and stage of disease, enabled establishment of a prognostic index (PI) based on a simple algorithm PI = zNSE + z(stage) + 2zPS. This segregated the patients into four groups with clearly different prognosis. The median survival and 95% confidence intervals of the four groups were: 468 days (540-408), 362 days (405-328), 256 days (270-241) and 125 days (179-58). Based on the present results we recommend S-NSE and PS, in addition to stage, for prognostic stratification in treatment trials on SCLC.
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PMID:Serum neuron-specific enolase (S-NSE) and the prognosis in small-cell lung cancer (SCLC): a combined multivariable analysis on data from nine centres. 869 66

Four examples of spermatocytic seminoma with a predominant anaplastic component occurred in men 33 to 43 years of age, without histories of cyptorchidism. The seminomas presented with painless testicular masses recognized 3 to 18 months before orchiectomy. Preoperative serum measurements of human chorionic gonadotropin and alpha-fetoprotein were negative. All tumors contained areas (10% to 30% of the tumor) in which the three cell types characteristic of conventional spermatocytic seminoma could be identified under light microscopy. The predominant anaplastic component also contained the three cell types, but the nuclei had prominent nucleoli with granular and filamentous chromatin. In addition, sheets of cells with vesicular nuclei and prominent nucleoli superficially resembling embryonal carcinoma were found. There were numerous large mononuclear and multinucleated giant cells with bizarre nuclei and prominent nucleoli, but no sarcomatous elements. Many normal and abnormal mitotic figures were present. Tunical and vascular invasion and extensive necrosis were constant features. Immunohistochemistry documented p53 protein overexpression in two tumors, but neoplastic cells were negative with immunostains for placenta-like alkaline phosphatase, leukocyte common antigen, neuron-specific enolase, alpha-fetoprotein, human chorionic gonadotropin, vimentin, and cytokeratins. Ultrastructural examination of the anaplastic component showed large rope-like nucleoli, but the cytoplasmic features were similar to those of conventional spermatocytic seminoma. Despite the presence of a major anaplastic component, no patient has developed metastasis. Larger series and longer follow-up are needed to understand the natural history of these neoplasms.
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PMID:Anaplastic variant of spermatocytic seminoma. 869 7

Dimorphous cancer of the lung with predominantly peripheral localization was diagnosed in 9 (1.2%) out of 716 patients operated for lung tumor in 1986-1995. The blood-serum levels of neuron-specific enolase, tissue polypeptide antigen, carcinoembryonic antigen, alpha-fetoptotein, CA 19-9 and CA-125 carbohydrate antigens and total activity of alkaline phosphatase were assayed in all the patients before surgery. The study showed an 1.5-times increase in CEA concentration in 5 cases, with primary tumor size being 5 cm and more.
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PMID:[Dimorphous cancer of the lung]. 921 24

Most granular cell tumours (GCTs) are benign proliferations of purported Schwannian derivation, showing immunoreactivity for Schwann cell-related antigens. Due to incomplete agreement on the precise nature of GCTs (reactive vs neoplastic), we performed an immunohistochemical study with the alkaline phosphatase/anti-alkaline phosphatase (APAAP) technique on 30 GCTs. The aim was to evaluate their growth patterns and the possible relationships of granular cells with other nerve sheath-related cell types (i.e., Schwann and perineurial cells, and dendritic cells displaying CD34/vimentin immunoreactivity). An expansive growth pattern was detected in five cases, a pseudoinfiltrative growth pattern in nine cases and a mixture of the above in the remaining 16 cases. Besides immunoreactivity for S-100 protein, neuron-specific enolase, vimentin, CD57, CD68, MAC 387, alpha-1-antitrypsin and alpha-1-antichymotrypsin in granular cells, we documented intimate architectural relationships between granular cells, Schwann and perineurial cells, and a third type of CD34/vimentin-positive nerve sheath-related cell in most GCTs. These results suggest that GCTs are heterogeneous lesions. Some of them show a pseudoinfiltrative growth pattern and retain close relationships with the normal components of the nerve sheath. In other lesions, granular cells grow in an expansive fashion and constitute the predominant cell component of the tumour. These architectural and immunophenotypic differences may reflect a different nature of GCTs: they may initially represent reactive or hamartomatous lesions that subsequently acquire truly neoplastic potential.
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PMID:Cellular heterogeneity of granular cell tumours: a clue to their nature? 1089 May 60


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