Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: HUMANGGP:012675 (S100)
 6,012 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. After long-term n-hexane exposure (2000 ppm, 12 h d-1, 6 d week-1, for 24 weeks), the content of neuron-specific enolase (gamma-enolase), creatine kinase-B and beta-S100 protein in the cortex, cerebellum, spinal cord and proximal and distal sciatic nerves of rats was determined by enzyme immunoassay. 2. The amounts of the three proteins decreased significantly in the distal segment of sciatic nerve, whereas they remained unchanged in the brain and proximal sciatic nerve. The quantitative decline in these marker proteins in the distal sciatic nerve could be related to neurophysiological deficits in the peripheral nerves. 3. This study indicates that the biochemical changes observed are consistent with the clinical and pathological findings of n-hexane neuropathy. These nerve-specific marker proteins can be used to assess solvent-related peripheral neurotoxicity.
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PMID:Chronic exposure to n-hexane induces changes in nerve-specific marker proteins in the distal peripheral nerve of the rat. 135 45

We report herein the clinical and pathological features of 20 patients with central neurocytomas. Investigations for various differentiation antigens and cell type-specific markers were performed by immunohistochemistry using paraffin-embedded tissue. In addition, the expression of L1 adhesion molecule and of the various N.CAM (neural cell adhesion molecule) isoforms were investigated by immunoblotting studies in two frozen specimens. Central neurocytomas are clinically characterized by their intraventricular localization, occurrence in young adults, and good prognosis. It rarely occurs in patients over 50, but such cases have a poor prognosis. Total surgical excision is the best treatment. Radiotherapy is appropriate if surgery is incomplete or contraindicated. Histologically, central neurocytomas display the following features: an oligo-like pattern, usually associated with large fibrillary rosettes or perivascular arrangement, and a rich endocrine-type vasculature. Central neurocytomas have a remarkably homogeneous antigenic profile. GFAP expression is only found in scattered reactive astrocytes, S100 protein in reactive astrocytes and rare tumor cells. Among the pan-neuroendocrine markers, central neurocytomas always express neuron-specific enolase; they frequently express synaptophysin but never chromogranin A. Synaptophysin is the most reliable immunohistological marker for central neurocytomas; however, immunoreactivity could be lost with long formalin fixation. In these cases, electron microscopy is used to support the neuronal nature of the tumor cells. The expression of L1 adhesion molecule and the isoform 180 of N.CAM, indicates that central neurocytomas are formed by cells committed to neuronal phenotype. Nevertheless, advanced neuronal differentiation may be absent, as suggested by the persistence of embryonic N.CAM, the nonexpression of neurofilament proteins, and the absence of mature synapses in numerous cases. Central neurocytomas and neuroblastomas share some biochemical properties, but their respective clinicopathological features and biological behavior are dramatically different.
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PMID:Central neurocytomas. Critical evaluation of a small-cell neuronal tumor. 137 Jul 56

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

Cytogenetic studies of pediatric tumors have revealed a number of reproducible karyotypic abnormalities, including del(p13) found in aniridia-Wilms' tumor association, t(8;14) in Burkitt's lymphoma, and t(11;22) in Ewing's sarcoma. To date, no consistent cytogenetic abnormality has been reported in association with hepatoblastoma. We report the case of a 7-month-old male infant with the undifferentiated small cell variant of hepatoblastoma. Immunohistochemistry revealed reactivity with antibodies to cytokeratin and vimentin throughout the tumor. Alpha-fetoprotein, neuron-specific enolase, and S100 stains were negative. Chromosomal analysis of metaphase cells from a culture of tumor tissue revealed a translocation of most of the long arm of chromosome 22 to the distal long arm of chromosome 10.
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PMID:Undifferentiated small cell hepatoblastoma with a unique chromosomal translocation: a case report. 138 17

In this study of 40 cases of basaloid squamous cell carcinoma, 83% arose in the pyriform sinus, base of tongue, tonsil, and larynx. The 35 men and five women ranged in age from 27 to 88 years (median 62). In patients for whom social habits were recorded, 24 of 26 patients were smokers and 22 of 25 drank ethanol. Most presented with stage III or IV disease. Twenty-seven patients had regional metastases at the time of presentation and 15 developed distant metastases. Seventeen patients died with disease (median survival 18 months). The tumors were composed of moderately pleomorphic basaloid cells forming nests, cords, and frequent cribriform patterns. Squamous dysplasia of surface mucosa, focal squamous differentiation within invasive basaloid squamous cell carcinoma, or foci of conventional squamous cell carcinoma were present, alone or in combination. All studied neoplasms were immunohistochemically positive for keratins with the 34 beta E12 antibody. Approximately 80% were immunoreactive using AE1/AE3 or CAM 5.2. Epithelial membrane antigen, carcinoembryonic antigen, and S100 protein were found in 83%, 53%, and 39%, respectively, of the cases. Diffuse, weak immunoreactivity for neuron-specific enolase was seen in 75% of tumors. Synaptophysin, chromogranin, muscle-specific actin, and glial fibrillary acidic protein were absent. Basaloid squamous cell carcinoma has been confused with adenoid cystic carcinoma and small cell undifferentiated carcinoma, but is usually distinguishable in routine hematoxylin and eosin-stained sections, or, in rare problematic cases, with the aid of immunohistochemical studies. Distinction is warranted because the biologic behavior of basaloid squamous cell carcinoma differs from that of both of these lesions.
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PMID:Basaloid squamous cell carcinoma of the head and neck. A clinicopathologic and immunohistochemical study of 40 cases. 138 69

To provide baseline information on the immunoarchitecture of normal bone marrow, we studied cryostat-cut, frozen, and paraffin-embedded, fixed tissue sections prepared from 21 core biopsies of normal bone marrow obtained during bone marrow harvests for transplantation. A large panel of antibodies was applied that included, for frozen tissue, Leu-6 (CD1), T11 (CD2), Leu-3a (CD4), Leu-1 (CD5), Leu-2a (CD8), J5 (CD10), My7 (CD13), Leu-11 (CD16), B4 (CD19), B1 (CD20), B2 (CD21), Tac (CD25), My9 (CD33), T200 (CD45), NKH-1 (CD56), kappa and lambda chains, beta F1, Ki-67, HLA-DR, TQ1, and keratin, and for fixed tissue, leukocyte common antigen (CD45), L26 (CD20), LN1 (CDw75), LN2 (CD74), LN3, LN4, LN5, MB1 (CD45R), MB2, MT1 (CD43), MT2 (CD45R), UCHL1 (CD45R0), BM1, Ki-1 (CD30), Leu-M1 (CD15), lysozyme, KP1 (CD68), actin, S100, neuron-specific enolase, vimentin, and keratin. On fresh-frozen sections CD19 and CD2 were the most reliable and sensitive markers for B and T cells, staining 5% and 9% of marrow cells, respectively. Immunoglobulins generally showed heavy background staining, which frequently precluded an accurate assessment. The CD4 to CD8 ratio in the bone marrow was reversed from that of peripheral blood. On fixed tissues, leukocyte common antigen was found in 14% of the marrow cells, corresponding roughly to the lymphocyte population. L26, a pan-B-cell marker, stained 3% of the marrow cells. Among the other B-cell markers, LN1 and MB2 stained a large number of cells (40% to 70%), indicating reactivity with cells of the myeloid or erythroid series in addition to lymphocytes. Among the T-cell markers, UCHL1 and MT1 stained 66% and 50% of the cells, respectively, which could be explained by their cross-reactivity with myeloid cells. Nonspecific myelomonocytic markers (Leu-M1, KP1, and lysozyme) also showed reactivity in a high percentage of cells. No particular architectural distribution patterns of B or T lymphocytes were noted in either frozen or fixed bone marrow specimens. The results of this study provide normal baseline data for the immunohistologic application of hematopoietic and lymphoid markers on frozen or fixed bone marrow biopsy specimens.
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PMID:Immunoarchitecture of normal human bone marrow: a study of frozen and fixed tissue sections. 159 93

We report a case of intracystic papillary carcinoma of the male breast in a 70-year-old male Caucasian. Grossly, the tumor was a cystic lesion measuring 6 cm in diameter. It contained hemorrhagic fluid and a mural nodule with filiform projections. PAS stain with and without digestion revealed small clumps of diastase-resistant material in the cytoplasm of the neoplastic cells. Grimelius stain was positive. Immunoperoxidase stains were negative for neuron-specific enolase, S100 protein, cromogranin and synaptophysin and were positive for carcinoembryonic antigen and epithelial membrane antigen. On ultrastructural examination the neoplastic cells showed membrane-bound, dense-core secretory granules. We believe that this neoplasm, despite negative neuroendocrine markers, is a variant of mammary adenocarcinoma with endocrine differentiation, partly because of the positive Grimelius stain and partly because of the presence of electron-dense granules, which according to some authors represent lactational differentiation.
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PMID:Intracystic papillary carcinoma of the male breast. A case report (histochemical, immunohistochemical and ultrastructural study). 160 58

The immunohistochemical expression of neuron-specific enolase (gamma/gamma) (NSE) was studied comparatively with S100 protein in a group of Langerhans-cell-type ("X") (n = 8) and non-Langerhans-cell-type ("non X") (n = 24) cutaneous histiocytoses. NSE was expressed by the majority (70-90%) of histiocytic cells in all cases of Langerhans-cell histiocytoses, whereas it was absent from non-Langerhans-cell histiocytoses. S100 protein was expressed by the majority of Langerhans-cell histiocytosis cells but also by a small percentage (1-5%) of cells in non Langerhans-cell histiocytoses. These results show that NSE is almost as sensitive as, but more specific than, S100 protein in discriminating Langerhans-cell from non-Langerhans cell cutaneous histiocytoses, and that it consequently represents a useful adjunct in the immunohistochemical diagnosis of histiocytic skin diseases.
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PMID:Neuron-specific enolase is a marker of cutaneous Langerhans' cell histiocytosis ("X")-a comparative study with S100 protein. 164 31

Immunocytochemistry was used to examine 18 cases of rat fibrous histiocytic tumours (11 malignant; seven benign). The diagnosis was made by light microscopic criteria and all cases were categorized as pleomorphic-storiform. A selection of polyclonal antibodies to histiocytic, muscle, neural and mesenchymal antigens was used. Fifteen tumours were positive with alpha 1-antitrypsin, four with alpha 1-chymotrypsin, ten with muramidase, five with desmin, 15 with neuron-specific enolase, 14 with S100, one with glial fibrillary acid protein and 12 with vimentin. Many tumours expressed several antigens, highlighting the confusion which has arisen with regard to the histiogenesis of fibrous histiocytic tumours in man, and supporting the concept of differentiation from a primitive mesenchymal common precursor able to differentiate in several directions.
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PMID:An immunohistochemical study of spontaneous histiocytic tumours in the rat. 165 Aug 3

We present a case of multiple benign spindle cell tumors of the jejunum in a patient with von Recklinghausen's neurofibromatosis and describe the light-microscopic, immunohistochemical, and ultrastructural features of these lesions. Two small spindle cell nodules were located in the region of Auerbach's myenteric plexus and a third larger tumor produced a subserosal mass. The immunohistochemical profile of these tumors revealed that they were actin and S100-protein negative but positive for neuron-specific enolase. At the ultrastructural level, the tumors recapitulated features of Auerbach's plexus. These lesions are similar to previously described gastrointestinal autonomic nerve tumors, and we propose that this may be the site of origin of enteric stromal tumors in von Recklinghausen's neurofibromatosis.
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PMID:Auerbach's myenteric plexus. A possible site of origin for gastrointestinal stromal tumors in von Recklinghausen's neurofibromatosis. 169 3


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