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)

Paraffin sections of granulocytic sarcomas (GS) (n = 30) were immunohistochemically evaluated for CD3, CD15 (LeuM1), CD20 (L26), CD31, CD34, CD43, CD45, CD68 (KP1), lysozyme, myeloperoxidase (BM1), CD45RO (UCHL1), and LN5 with an avidin-biotin amplification system and a peroxidase-based color development system with DAB as a chromogen. CD45 positivity was present in all lymphomas and 24 of 25 granulocytic sarcomas. Lysozyme and CD43 labeled 26 of 29 granulocytic sarcomas, showing intense cytoplasmic staining. LN5 (membrane-staining) and CD68 (subtle cytoplasmic caplike staining) were found in 20 of 30 cases, often only focally. BM1 and CD15 mainly labeled maturing granulocytes and mostly were negative in primitive myeloid cells. Myeloid progenitor cell antigens CD31 and CD34 were seen in 7 and 12 of 30 cases, respectively. They seemed to recognize different subsets of myeloid leukemia infiltrates (16 cases positive for at least one); the use of CD31 and CD34 for defining these subsets should be evaluated further. Features suggesting a dual phenotype--T-cell and myeloid (positive for CD3, CD68, and lysozyme)--were documented in two cases. In contrast, lymphoblastic lymphomas (n = 4) were positive for CD3 and CD43 but negative for CD68, lysozyme, CD31, CD34, LN5, and myeloperoxidase. Lymphocytic lymphomas (n = 10) were positive for CD20 and CD43 but negative for all other markers. Small, round-cell tumors (n = 15) were negative for all markers. If T-cell and B-cell differentiation can be excluded with other markers, CD43+ is a sensitive marker for myeloid differentiation. Our results show that several markers are useful in the identification of myeloid leukemia infiltrates and in distinguishing them from lymphoblastic and lymphocytic lymphomas and small round-cell tumors in formaldehyde-fixed, paraffin-embedded tissue.
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PMID:Immunohistochemical evaluation of myeloid leukemia infiltrates (granulocytic sarcomas) in formaldehyde-fixed, paraffin-embedded tissue. 803 68

The morphology of anaplastic large-cell lymphoma (ALCL) is associated with a clinical syndrome of peripheral lymphadenopathy (> 80%) and frequent extranodal disease (> 40%) in children and young adults (median age < 40 yrs.). Skin lesions occur in more than 20% of patients; other extranodal sites are bone, soft tissue, gastro-intestinal tract, lung, and pleura. Marrow involvement is infrequent (< 10%). Features that distinguish ALCL from Hodgkin's disease (HD) are noncontiguous nodal disease (> 50%), infrequent mediastinal mass (< 20%), and frequent inguinal lymphadenopathy (> 40%). Most patients present with stage III/IV disease. Stage is highly predictive of achieving complete remission, disease-free survival, and overall survival. Localized skin lesions have an excellent prognosis and occasional spontaneous regressions are noted. Distinctive histopathologic features of ALCL are partial lymph node involvement with sinus infiltration, sparing of B-cell regions, and tumor cell pleomorphism. Other features are high mitotic rate, necrosis, fibrosis, and plasma cell infiltrates. Morphologic variants of ALCL resemble carcinoma, syncytial variant of nodular sclerosing HD, true histiocytic lymphoma or interdigitating cell sarcoma, and mycosis fungoides. ALCL can be distinguished from these morphologically similar disorders by immunophenotype (CD30+, CD45+, CD15-, EMA+, BNH9+, keratin-, lysozyme-). A recurrent cytogenetic translocation, t(2;5) (p23; q35), has been observed among morphologic variants, including a small-cell-predominant variant and tumor cell line which contains a spectrum of small cerebriform and large anaplastic CD30+ cells. 70% of ALCL cases are of T-cell lineage, 15% B, 5% T/B, and 10% undefined.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Primary Ki-1-positive anaplastic large-cell lymphoma: a distinct clinicopathologic entity. 817 12

Thirteen cases of juvenile xanthogranuloma (JXG) and 13 cases of adult-type xanthogranuloma (AXG) were compared at the light and immunohistochemical levels. Histologically, four main cell types (vacuolated, xanthomatized, spindle-shaped, and "oncocytic") were seen in variable proportions (from monomorphous to mixed variants) with different types of giant cells (nonspecific, foreign body, Touton, and "ground-glass"). Giant cells were more prominent in AXG than in JXG; oncocytic cells (characterized by an eosinophilic, slightly granular cytoplasm similar to thyroid oncocytic cells) and mostly periodic acid-Schiff (PAS) negative giant cells with a ground-glass appearance (6 of 26) were not observed in classic JXG (i.e., occurring in children < 2 years old). Immunohistochemically, JXG and AXG gave similar results: most xanthogranuloma cells labeled strongly with KiM1P and vimentin, while HHF35 and HAM56 stained less intensively. Factor-XIIIa (FXIIIa), KP1 (CD68), and HAM56 stained mostly in the periphery of the lesions. Some markers gave variable results: peanut agglutinin (PA), 60%; alpha-1-antitrypsin, 50%; lysozyme, 25%; LN3 (HLA-DR), < 10% of cells positive. Others were negative: S-100, MAC387 (L1 antigen), LeuM1 (CD15), desmin, smooth muscle-specific actin, and QBEND10 (CD34). This profile helps to delineate xanthogranuloma from histological stimulants such as dermatofibroma (which is FXIIIa+, LN3+, KP1-, and PA-) and multicentric reticulohistiocytosis (which is FXIIIa-, KP1+, PA-, and HHF35-).
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PMID:Juvenile and adult xanthogranuloma. A histological and immunohistochemical comparison. 829 51

We had 18 patients (15 males and 3 females) with lethal midline granuloma (polymorphic reticulosis) in the period from 1981 to 1990. This number was about 5.6% of the total number of patients with malignant head and neck tumors that we encountered during this period. An average of 9.1 months separated the first appearance of disease and the beginning of treatment. Most of the 18 patients underwent both radiation therapy and chemotherapy (COP, CHOP, MACOP-B), but, since their disease had reached an advanced stage, 3 underwent radiation therapy only, 3 underwent chemotherapy only, and 1 received no radical therapy at all. Of the 18 patients, 13 died of the disease. In of 6 of these, the disease was confined to the local lesion. The 5-year cumulative survival rate was 15.7% (Kaplan-Meier). Fourteen autopsy studies revealed that tumor cells had invaded the liver (92.8%), lung (92.8%) and spleen (71.4%) and in all cases it was in leukemic patterns. Fifteen cases were studied for tumor surface marker phenotype, but none was found to be positive for L26, CD43, Leu M1 (CD15), or MAC 387. Five cases were positive for UCHL-1 (CD45RO) and 10 cases were positive for lysozyme. All cases were positive for Ki-1 (CD30).
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PMID:[Cases of lethal midline granuloma (polymorphic reticulosis) at our department in a recent 10-year period]. 834 94

In an attempt to correlate the morphologic and immunophenotypic findings in extramedullary myeloid cell tumors (EMT), we studied 28 cases with a large panel of antibodies using paraffin section immunohistochemistry. A previous or concurrent diagnosis of acute myelogenous leukemia or chronic myelogenous leukemia was made in 25 cases. Six EMT were morphologically classified as well differentiated (WD-EMT), 17 as poorly differentiated (PD-EMT), and five as blastic EMT. The WD-EMT were easily recognized morphologically and displayed a relatively mature myeloid phenotype, with elastase, CD15, and CD68 positivity in all cases. On the other hand, the five blastic-EMT displayed no morphologic evidence of myeloid derivation, were completely negative for CD15, and were weakly positive for elastase in only one case. The PD-EMT, with a morphologic appearance that resembles large cell non-Hodgkin's lymphoma, variably expressed CD15 and elastase. CD68 and lysozyme were present in the majority of PD-EMT, with some variability, but were negative in most blastic-EMT. CD45 (LCA) was detected in 75% of all EMT and CD34 was positive in 36%; neither antigen was significantly associated with a specific morphology. CD30 reactivity was not evident in any case, but slight positive staining was seen with CD20 (L26) in one WD-EMT. CD43 (Leu 22) was the only antibody that was positive in 100% of cases; staining was always intense and widespread. Antimyeloperoxidase (MPO) was positive in all cases but two, both with a blastic morphology. We conclude that (a) an immunohistochemical panel including CD20, CD43, CD68, and MPO can successfully identify the vast majority (96%) of EMT in paraffin sections, and (b) there is an association between morphology and phenotype in these lesions.
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PMID:Extramedullary myeloid cell tumors. An immunohistochemical and morphologic study of 28 cases. 837 41

Two cases of true histiocytic lymphoma of the small intestine occurred in middle-aged patients, manifesting as tumors causing intestinal obstruction. One of the patients died of uncontrollable local and metastatic disease, 16 months after surgery and polychemotherapy, and the other patient is alive 12 months after surgery and chemotherapy. The histologic characteristics of the tumor cells, namely complex nuclear outlines and abundant variably eosinophilic cytoplasm, suggested histiocytic differentiation. Both cases had negative results for B-cell and T-cell markers but stained for the histiocytic markers lysozyme, CD68, and HLA-DR and had positive results for S-100 protein and vimentin. Acetone-fixed frozen sections of one case showed positive results for several histiocytic markers, including CD11c, CD14, CD33, CD68, and BerMac3 (unclustered monoclonal antibody). CD4, a T-cell antigen present in a subset of histiomonocytic cells, had positive results in the cytoplasm. The tumor cells had negative results for CD1a, CD15, and CD30. Immunoglobulin and T-cell receptor gene probes showed germline configuration in one case studied. These results indicate the tumors are true histiocytic lymphomas, which have immunophenotypic features of both ordinary histiocytes and interdigitating reticulum cells.
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PMID:True histiocytic lymphoma of small intestine. Analysis of two S-100 protein-positive cases with features of interdigitating reticulum cell sarcoma. 837 37

True histiocytic lymphoma (THL), as it is currently defined, is a rare entity. We report 12 cases of THL seen at Stanford over the last ten years. By definition, the neoplastic cells in each case showed histological and immunological evidence of histiocytic differentiation. Seven females and five males ranged in age from 9 to 67 years. Sites of involvement included lymph node, soft tissue, bone, stomach, small intestine, mediastinum, kidney, breast and salivary gland. Lymph nodes showed diffuse architectural effacement and/or a paracortical pattern of involvement. The infiltrates involved other tissues in a diffuse pattern. Cytologically the cells were characterized by abundant eosinophilic cytoplasm and enlarged, indented eccentrically placed nuclei containing prominent nucleoli. In all cases the cytological features were sufficiently atypical to indicate a neoplastic infiltrate. Paraffin section immunophenotyping demonstrated reactivity of the atypical cells for CD15, 43, 45RO, 45RB, 68, lysozyme and/or S100. In frozen sections, the atypical cells demonstrated reactivity for CD4 (cytoplasmic), 11c, 14, 15, and/or 68. Genotypic studies were performed on 3 cases, one of which showed rearrangements of immunoglobulin heavy and light chain genes. Follow-up was available on eleven patients, six of whom died of disease 0.5 to 36 months following diagnosis.
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PMID:True histiocytic lymphoma: a study of 12 cases based on current definition. 858 Aug 33

An immunohistochemical study of renal tubule cell differentiation in hydrops fetalis was performed using antibodies against lysozyme, CD15, keratin, epithelial membrane antigen and Leu-7, and formalin-fixed, paraffin-embedded sections of tissue that was obtained at autopsy. In 3 cases among 17 cases of hydrops fetalis (17.6%) there was a marked decrease in the number of cells stained positively for lysozyme, suggesting abnormal differentiation of the cells of the proximal convoluted tubules. This is the first report concerning the abnormalities of the renal tubular epithelium in hydrops fetalis.
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PMID:Renal tubular abnormalities in hydrops fetalis: a histological and immunohistochemical study. 913 3

N-acetylmuramyl-L-alanine amidase (NAMLAA) specifically degrades peptidoglycan, which is a major component of bacterial cell walls with strong inflammatory properties. For instance, peptidoglycan is capable of stimulating peripheral blood cells to release pro-inflammatory cytokines and is capable of inducing chronic arthritis in an animal model. In a previous study we found that degradation of peptidoglycan by purified NAMLAA reduced its inflammatory effects. To determine where NAMLAA is located in tissues, monoclonal antibodies against purified NAMLAA were produced for use in immunohistochemistry, immunoelectron microscopy, flow cytometric analysis, and Western blotting. The immunohistochemical studies showed NAMLAA-positive cells in human spleen, liver, arthritic synovial tissues, and lymph nodes. In flow cytometric studies of blood and bone marrow, neutrophilic and eosinophilic granulocytes proved to be positive. Monocytes were negative, although they do contain lysozyme, the other important peptidoglycan-degrading enzyme. However, mature macrophages obtained by bronchoalveolar lavage and subsequent selection based on autofluorescence did possess NAMLAA. In immunocytochemical staining of blood smears, thrombocytes were also positive for NAMLAA. Western blot analysis and immunoelectron microscopy of neutrophils and eosinophils showed that NAMLAA is located in azurophilic granules of neutrophils and in secretory vesicles and crystalloid-containing granules of eosinophils. Flow cytometric analysis of blood and bone marrow from different French-American-British-classified acute myeloid leukemia (AML) patients showed that AML-M2 myeloblasts were the first in the granulocyte maturation lineage that were positive for NAMLAA. The more immature AML, such as AML-M0 and AML-M1, did not express NAMLAA. CD15- and CD13-negative megakaryoblasts, corresponding to AML-M7, were also positive for NAMLAA. The expression pattern of NAMLAA in the myeloid lineage suggests that the monoclonal antibody AAA4, recognizing NAMLAA, is useful for discrimination between AML in the monocyte lineage and in the granulocyte lineage.
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PMID:Expression and intracellular localization of the human N-acetylmuramyl-L-alanine amidase, a bacterial cell wall-degrading enzyme. 924 59

Reed-Sternberg (R-S) and dendritic interdigitating (DI) cells share many features in nodular sclerosing Hodgkin's disease (NSHD). Such features include commonalities of location (paracortex), histochemistry (paranuclear acid phosphatase and nonspecific esterase activity), and immunohistochemical reactivity (positivity for Mr 70,000 antigen). Because of these similarities, it is hypothesized that there may be a common precursor for R-S and DI cells. To investigate this possibility, paraffin-embedded material from five (5) archival cases of NSHD were reacted in immunohistochemical procedures with antibodies to detect the following antigens: CD15, CD30, S-100 protein, CD68 and IL-9, respectively. Double immunostaining for lysozyme or CD45RB (leukocyte common antigen) or S-100 protein and one of the aforementioned was carried out on representative slides from selected cases. Both relatively large dendriform cells and a population of small mononuclear cells with monocytic karyomorphism showed immunoreactivity for S-100 protein. Similarly, IL-9 antigen which is characteristically found in R-S cells in NSHD was strongly expressed in a population of CD45RB- monocytoid cells. Coexpression of lysozyme antigen in some of the CD30+ R-S cells and Hodgkin's cells is also consistent with a monocytic/histiocytic lineage. Finally, CD30 antigen occasionally could be traced from monocytoid cells, where it was found in a pancytoplasmic distribution to histiocytic cells with a pancytoplasmic and sometimes also paranuclear (Golgizone) pattern of immunoreactivity, to R-S cells with paranuclear and plasmalemmal immunopositivity. In sum, the results of these studies support the contention that there are monocytoid precursors for R-S, Hodgkin's, and DI cells in NSHD and suggest a role for IL-9 in the development of R-S cells from tissue monocytes and monocytoid histiocytes.
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PMID:Histogenesis of Reed-Sternberg and dendritic interdigitating cells in nodular sclerosing Hodgkin's disease. Immunohistochemical evidence for monocytoid precursors. 930 71


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