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:3.2.1.17 (lysozyme)
21,489 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sections of primary lung carcinomas, lung metastases, mesotheliomas, and lung metastases of some rare mesenchymal tumors were incubated with different cytokeratin (CK), vimentin, desmin, and tissue polypeptide antigen (TPA) antibodies and with antibodies reactive with different hormones (ACTH, PTH, alpha-HCG, Calcitonin CT), CEA, carcinoma-associated antigen (CA1), secretory component (SC), neuron-specific enolase (NSE), alpha-1-antitrypsin (alpha-1-AT), lysozyme (lyso), and S-100 protein (S 100). CK antibodies derived from a 49 kD (reactive with simple epithelia [SE]) and a 67 kD CK polypeptide fraction (reaction with complex epithelia [CE] were useful differentiation markers for the four major groups of lung carcinomas. In one half of small cell carcinomas a positive reaction with NSE antibodies was found. S 100 and SC were good markers for papillary and bronchioloalveolar adenocarcinomas, whereas CEA was less important because of its reactivity with different types of lung carcinomas. To discern clear cell carcinomas of lung and renal origin a positive reaction with vimentin antibodies (some renal but not lung types) and with CA1 (no renal but all lung types) seemed to be useful. All hormone antibodies were of no importance as markers for difficult differential diagnosis, because positive reactivities were found in cases from every major carcinoma group. In addition, a Ca2+-activated adenosine triphosphatase (ATPase) was found in mesotheliomas but not in papillary adenocarcinomas.
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PMID:Immunohistochemical and histochemical markers of primary lung cancer, lung metastases, and pleural mesotheliomas. 243 80

Ten cases of "undifferentiated" large-cell tumors were ultrastructurally characterized by cells with abundant filiform cytoplasmic projections without intercellular junctions. These cases were studied by means of the avidin-biotin-peroxidase complex (ABC) technique applied to formalin-fixed, paraffin-embedded sections using antibodies against high- and low-molecular weight keratins (Ker), vimentin (Vi), epithelial membrane antigen (EMA), S-100 protein, leucocyte common antigen (LCA), kappa (K) and lambda (L) light chains, Leu-M1, lysozyme (Ly), alpha-1 antitrypsin (A1AT) and alpha-1 antichymotrypsin (A1ACT). All 10 cases were negative for Ker and EMA but positive for Vi. S-100 was present only in scattered dendritic cells. LCA was identified in seven cases. In the three LCA-negative cases, two stained for Leu-M1, and one of these also showed intracytoplasmic L; one was negative for all markers but Vi. None of the tumors showed any significant staining for Ly, A1AT, or A1ACT. Our findings indicate that these tumors are nonepithelial and nonneuroectodermal, and that they are best classified as non-Hodgkin's lymphomas. The possibility that some of the filiform large-cell lymphomas may be derived from dendritic reticular cells cannot be excluded.
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PMID:Filiform large-cell lymphomas. An ultrastructural and immunohistochemical study. 243 14

The histogenesis of alveolar soft part sarcoma (ASPS) has been investigated since its description. Twenty ASPS cases were analyzed for immunohistochemical content, with emphasis directed toward the paraganglial, Schwann cell, and muscle theories of histogenesis. In addition, the cases were examined for possible prognostic clinical features. The clinical characteristics of the patients were similar to those reported previously concerning average age (23 years); male:female ratio (1:1); and predominant primary site (lower extremity, nine cases). Despite a local recurrence rate of 20% and a metastatic rate of 68% (including four at presentation), the natural history was often indolent and relapse commonly occurred very late. The average follow-up period was 10.1 years. While the overall 5-year survival was 67%, only seven of 18 patients were alive without disease at last follow-up (1.7-32 years), and one patient died of tumor after a 28-year disease-free interval. Neither tumor size nor site appeared to affect prognosis. The tumors were analyzed immunohistochemically for neurofilament, S-100 protein, met-enkephalin, leu-enkephalin, acetylcholinesterase, alpha 1-antichymotrypsin, Factor VIII-related antigen, serotonin, lysozyme, neuron-specific enolase, myoglobin, cytokeratins, desmin, and vimentin. Except for weak vimentin immunoreactivity, no other antigenic expression was detected despite multiple repeated experiments with several antibodies. S-100 protein which is present in virtually all granular cell tumors was absent in the cases of ASPS. The lack of detectable expression of neurofilament, met-enkephalin and leu-enkephalin, and neuron-specific enolase is interpreted as evidence against the paraganglial theory of histogenesis. Similarly, the repeated absence of the muscle proteins, desmin and myoglobin, in contrast to a previous report, is interpreted as evidence against a myogenic origin.
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PMID:Alveolar soft part sarcoma. A clinicopathologic and immunohistochemical study. 243 29

Seven cardiac myxomas were studied by immunoperoxidase and immunofluorescence in formalin fixed and paraffin embedded tissues. Specific antisera to factor VIII related antigens, vimentin, myosin of smooth muscle, actin, desmin, alpha-1-antitrypsin, muramidase, fibrin and prekeratin antigens were used. All myxoma cells reacted positively with antibodies to vimentin and showed no staining reaction with antibodies to alpha-1-antitrypsin, muramidase, myosin, or prekeratin. Factor VIII related antigen was found only in endothelial cells and not in myxoma cells proper. Fibrin was found in patchy areas within the stroma. Antisera to actin and desmin failed to react with formalin fixed tissue. Our results suggest that the main cellular component of cardiac myxoma is a primitive mesenchymal cell without immunohistochemical evidence of more specific differentiation.
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PMID:Cardiac myxoma. A retrospective immunohistochemical study. 243 71

Clinical, microscopic, and immunohistochemical characteristics of 17 jaw sarcomas are reported. Histologic subtypes included chondroblastic (five), fibroblastic (five), osteoblastic (three), telangiectatic (one), parosteal (two), and chondrosarcoma (one). Reactivity for all antigenic markers in decalcified tissue was judged to be comparable to nondecalcified tissue. All neoplasms were nonreactive for muramidase and leukocyte common antigen. alpha-1 Antichymotrypsin and HLA-DR immunoreactivity was found focally. Positive S-100 staining was found predominantly in chondrocytes. All tumors were positive for vimentin. Cells in focal zones of cartilage were positive for keratin. No distinctive pattern emerged relative to clinical recurrence and histologic subtype or immunotype. Leukocyte common antigen determinations were useful because they distinguished between neoplastic and inflammatory cells. S-100 protein stains helped in the subclassification of chondroblastic osteosarcoma, and vimentin stains confirmed mesenchymal origin. Cross-reactive staining of cartilage with keratin antibodies was regarded as a possible diagnostic pitfall.
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PMID:Osteosarcomas and chondrosarcomas of the jaws: immunohistochemical correlations. 244 91

Variant expressions of modified myoepithelial cells in salivary pleomorphic adenomas are described as determined by immunohistochemical techniques which visualized the distributions of S-100 protein, intermediate-sized filament proteins (keratin, vimentin, and desmin), and contractile proteins (myosin and actin), as well as lysozyme and lactoferrin. Immunohistochemical staining patterns of S-100 protein were basically used to classify modified myoepithelial cells, along with histologic criteria. Histochemical modifications of myoepithelial cells in pleomorphic adenoma of salivary glands could be divided into a) reactive, b) transformed, and c) neoplastic myoepithelial cells. Reactive myoepithelial cells were stromal-like cells which displayed an intense S-100 protein reaction. Transformed myoepithelial cells were negative or slightly positive for S-100 protein; they were located in the outer zone of tubular or duct-like structures and were spindle-shaped. The inner round cells of tubular and ductal structures, which could be ductal origin, gave intense keratin staining, as well as marked reactions for lysozyme and lactoferrin. Neoplastic myoepithelial cells were plasmatoid or fibrous types of cells and contained abundant S-100 protein and vimentin. These cells were termed "myoepithelioma" as in classical diagnosis.
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PMID:Various expressions of modified myoepithelial cells in salivary pleomorphic adenoma. Immunohistochemical studies. 244 94

Twenty chordomas from 20 patients, including 17 nonchondroid and three chondroid types, were studied with a variety of antibodies directed against cytokeratin (AE-1/3), epithelial membrane antigen, carcinoembryonic antigen, S100 protein, vimentin, alpha 1-antichymotrypsin, and lysozyme. All 17 nonchondroid chordomas stained for cytokeratin, and most (16) stained for epithelial membrane antigen. In contrast, two chondroid chordomas failed to stain for either cytokeratin or epithelial membrane antigen, while one of them did stain for both antigens. Sixteen of the 20 chordomas (80%) stained for S100 protein, including all three chondroid chordomas. Vimentin was found in six (30%), and alpha 1-antichymotrypsin in 16 chordomas (80%). Carcinoembryonic antigen and lysozyme were each found in two specimens (10%). While these findings basically agree with the immunohistochemical studies of other investigators, there are a few discrepancies. Most significant is the lack of epithelial markers in two of three chondroid chordomas located at the base of the skull. Possible reasons for the discrepancies are discussed.
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PMID:Chordoma. An immunohistochemical study of 20 cases. 245

The nature of the stromal cells in formalin-fixed paraffin-embedded material from 23 cerebellar haemangioblastomas was investigated using antisera to intermediate filaments (glial fibrillary acidic protein, vimentin and desmin), histiocytic markers (alpha 1-antitrypsin, alpha 1-antichymotrypsin and lysozyme), glycolytic enzymes (alpha and gamma enolase and aldolase C4) and the endothelial markers, factor VIII related antigen and Ulex europaeus I lectin. Most stromal cells stained positively for vimentin and the glycolytic enzymes. Occasional process-bearing cells within the stroma stained strongly for glial fibrillary acidic protein, alpha 1-antitrypsin and alpha 1-antichymotrypsin. No stromal cell staining for desmin, lysozyme or the endothelial markers was observed, although the latter stained the vascular endothelium within all neoplasms. The findings do not support previous suggestions of an endothelial or histiocytic origin for the stromal cells. They appear to be a heterogeneous population including entrapped reactive astrocytes and locally-derived non-angiogenic cells of neuroectodermal (pial) origin.
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PMID:Stromal cells in cerebellar haemangioblastomas: an immunocytochemical study. 245 34

Renal disease is a common cause of morbidity and mortality in patients with plasma cell dyscrasia (PCD). We have conducted a systematic study of the formalin-fixed, paraffin-embedded renal tissues from 53 patients with plasma cell dyscrasia, 24 of whom had Bence Jones cast nephropathy (with large casts, often associated with giant cells and polymorphonuclear leukocytes). A battery of 5 immunocytochemical and lectin markers for various segments of the nephron was used [Tetragonolobus lotus, Arachis hypogaea (AH), Tamm-Horsfall protein (THP), epithelial membrane antigen (EMA), and cytokeratin (AE1/AE3)]. In particular, we sought to determine the nature of the intratubular multinucleated giant cells in Bence Jones myeloma cast nephropathy with a variety of epithelial and hematopoietic cell markers. Although tubular epithelial cells stain with their respective markers (whether inflamed, thinned, detached, or adjacent to and lining casts), true intratubular giant cells in PCD were never positive for these tubular markers. In approximately one-third of the cases studied, intratubular and extratubular giant cells stained for several of the seven hematopoietic cell markers employed [i.e., alpha 1-antitrypsin (A1AT), alpha 1-antichymotrypsin (A1ACT), vimentin, and lysozyme], suggesting that giant cells are of hematopoietic origin. The majority of the casts are present in the distal nephron, although some casts were noted in more proximal sites of the nephron. Some larger casts did not stain for THP; smaller casts often showed lamination or stratification of THP staining. Finally, in one-half of the cases, Tamm Horsfall protein (THP) and other distal tubular markers (AH, EMA, AE1/AE3) were found in Bowman's space, almost always in association with interstitial deposits of THP; these markers were virtually never noted in Bowman's spaces of PCD patients without numerous large casts. This suggests that there are communications between distal and proximal nephron, most likely by intraluminal reflux but possibly also through breaks in the tubules and via the interstitium.
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PMID:Myeloma cast nephropathy: immunohistochemical and lectin studies. 246 87

Small cell carcinoma of the ovary is a rare, poorly understood aggressive tumor of young women, associated with paraendocrine hypercalcemia in two-thirds of the cases. Immunohistochemical staining of 15 small cell carcinomas, one-third of which were associated with hypercalcemia, 15 adult granulosa cell tumors, 15 juvenile granulosa cell tumors, and 5 Sertoli cell tumors, was performed with the use of antibodies against cytokeratins (AE-1/AE-3, CAM 5.2, 902), epithelial tumor-associated antigens (B72.3, epithelial membrane antigen [EMA]), vimentin, S-100, neuron-specific enolase (NSE), lysozyme, parathyroid hormone, and chromogranin-A in an attempt to define histogenetically this tumor type. One-third of the small cell carcinomas were positive for EMA, whereas all of them were negative for B72.3 and S-100. In contrast, one-third of the granulosa cell tumors were positive for S-100 and all of them were negative for EMA and B72.3. One of five Sertoli cell tumors were positive for EMA and two were positive for B72.3, but all were negative for S-100. Differences existed in the frequency, intensity, and/or pattern of staining for cytokeratin, vimentin, lysozyme, and NSE among the various tumor types. A single small cell carcinoma from a patient with hypercalcemia stained focally for parathyroid hormone, whereas all 30 granulosa cell tumors and 4 of 5 Sertoli cell tumors were nonreactive. Chromogranin-A staining was noted in four of five small cell carcinomas, none of ten granulosa cell tumors, and two of five Sertoli cell tumors. These immunohistochemical findings, as well as previous light and electron microscopic data, do not clearly indicate any specific cell as the cell of origin of the ovarian small cell carcinoma.
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PMID:Ovarian small cell carcinoma. Histogenetic considerations based on immunohistochemical and other findings. 247 44


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