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)

Intracytoplasmic lysozyme (muramidase) may be readily identified in paraffin sections of tissues fixed in formalin or Zenker's acetic acid and in smears of peripheral blood or bone marrow using an immunoperoxidase technique. Sites of intracellular lysozyme in normal human tissues and in various specimens from patients with myeloproliferative and lymphoproliferative disorders, hairy cell leukemia, granulomatous diseases, toxoplasmic lymphadenitis, and other pathologic processes were defined by this method. Intracellular lysozyme was demonstrated in mature and immature neutrophilic and eosinophilic myeloid cells, in monocytic cells, and in some types of histiocytes and had a limited distribution in normal tissues. The neoplastic cells of hairy cell leukemia were devoid of intracytoplasmic lysozyme. Identification of intracellular lysozyme, as determined by the immunoperoxidase technique, was compared with various cytochemical methods, particularly chloroacetate esterase and alpha-naphthyl butyrate esterase studies, for detection and characterization of myeloid cells, monocytes, and histiocytes.
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PMID:Profile of intracytoplasmic lysozyme in normal tissues, myeloproliferative disorders, hairy cell leukemia, and other pathologic processes. An immunoperoxidase study of paraffin sections and smears. 33 90

Surface marker studies were performed on "hairy cells" from 7 patients with hairy cell leukemia (HCL). Using sensitive analytic techniques including specific antisera and Fluorescence Activated Cell Sorter (FACS-1), further definition of the abnormal cell was achieved. Four different antisera were used in infestigating the cell surface characteristics of these patients: anti-p23,30, an antiserum reactive with B cells and a subset of monocytes, anti-311, which reacts only with T cells, pepsin digested anti-F(ab')2 which reacts with B cells only and pepsin digested anti-lysozyme reactive with monocytes and myeloid cells, but not with B or T cells. In all cases strong reactivity was observed with anti-p23,30 and anti-F(ab')2, but no reactivity with anti-311. Five out of the seven cases were reactive with anti-lysozyme in a pattern similar to normal monocytes. Furthermore, when cells were separated according to binding to anti-p23,30, anti-F(ab')2 and anti-lysozyme and in two cases, according to cell size, the majority of reactivity and large cells were "hairy" when examined under microscopy. In contrast, the small and nonreactive (dull cells) appeared as normal mature lymphocytes. Thus, our data supports the view that HCL cells bear in most cases B cell and monocytic membrane markers.
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PMID:Cell-surface characteristics of hairy cell leukemia in seven patients. 37 55

Enzymaticaly homogeneous fractions of lymphocytes, monocytes, and neutrophils were isolated by zonal centrifugation from peripheral blood of a patient with hairy cell leukemia, or leukemic reticuloendotheliosis, LRE,(with leukopenia, neutropenia, lymphocytosis, and massive splenomegaly). To detect enzymatic deficiencies, the cells were analyzed quantitatively for six leukocytic enzymes on three occasions: 1) before splenectomy, 2) 5 days after splenectomy, and 3) 6 weeks after splenectomy. Before splenectomy, the patient's cells showed moderate deficiency of beta-glucuronidase in lymphocytes and monocytes; server to modorate deficiency of lysozyme and myeloperoxidase in monocytes and granulocytes; and complete absence of neutral protease and alkaline phosphates in neutrophils. Full restoration of neutral protease and a three-fold rise in alkaline phosphatase activities occurred in the patient's neutrophils 5 days after splenectomy. Lysozyme and myeloperoxidase returned to normal in both monocytes and neutrophils of the patient. Six weeks following splenectomy, the alkaline phosphatase activity again disappeared from patient's neutrophils, although neutral protease remained normal. The patient's lymphocytes were unresponsive to PHA and PW mitogen before splenectomy but became responsive 6 weeks postoperatively. Monocytic transfomation into macrophges was supressed before and after splenectomy. The findings indicate that developmenally, in lymphocytic leukemia, a biochemical defect involves the patient's monocytes and neutrophils much more severely than it affects the leukemic lymphocytes. Functionally, the results partly explain the susceptibility of LRE patients to microbial infections.
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PMID:Absence of neutral protease and alkaline phosphatase in neutrophils of a case of hairy cell leukemia. 43 13

A case of Hodgkin's disease (HD) in a patient with long-standing hairy cell leukemia (HCL) is reported. The diagnosis of HCL was confirmed by clinical features (chronic illness with marked splenomegaly) and hematopathologic findings (increase of characteristic hairy cells with tartrate-resistant acid phosphatase activity in peripheral blood and bone marrow). Cervical lymphadenopathy first appeared 6 years after the diagnosis of HCL, and histologic features of the node were characteristic of HD. As it was possible that the neoplastic cells of both lesions might have originated from a single clone, their phenotypic features were defined. The hairy cells were found to bear surface immunoglobulin, receptors for complement components, leukocyte common antigen, and antigen defined by LN-1 monoclonal antibody, whereas lymph node lesion was characterized as HD because the Reed-Sternberg-like cells were positive for Leu M1 antigen, lysozyme, alpha-1-antitrypsin, and nonspecific cross-reacting antigen. Since there was no evidence indicating a common clonal origin, it is more likely to consider that both lesions are derived from different clones.
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PMID:Hodgkin's disease in hairy cell leukemia. Phenotypic characterization of neoplastic cells. 365 3

A 28-year-old woman developed leukopenia and slight cervical lymphadenopathy. Bone marrow aspiration and special stains established the diagnosis of acute monocytic leukemia. Following chemotherapy a complete hematologic remission was elicited. Seven months later, she consulted an ophthalmologist because of bilateral conjunctival lesions. Ophthalmologic examination showed subconjunctival, perilimbal grayish-pink infiltrates. A conjunctival biopsy disclosed sheets of mononuclear cells consistent with acute monocytic leukemia. Four months later, she developed cutaneous lesions in the face and chest wall. Subsequent biopsies of conjunctiva and skin and immunohistochemical demonstration of muramidase in the tumor cells supported the diagnosis of monocytic leukemia. Electron microscopic studies were particularly valuable and disclosed that more than 80% of the leukemic cells contained two types of cytoplasmic complexes of rough endoplasmic reticulum that displayed both tubular and helical configurations. These complexes differed morphologically from the ribosome-lamellar complexes observed in hairy cell leukemia and other hematologic disorders.
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PMID:Acute monocytic leukemia recurring as bilateral perilimbal infiltrates. Immunohistochemical and ultrastructural confirmation. 386 54

Cell surface marker analyses conducted on human peripheral blood lymphoid cells have proven extremely useful in the diagnosis of immunodeficiency and the diagnosis and staging of malignancies. In this paper we have focused on the ratio of helper to suppressor cells in patients with the acquired immune deficiency syndrome and in patients with malignancy. In thirty-three patients with the acquired immune deficiency syndrome, the majority showed an inverted helper:suppressor ratio, elevated serum thymosin alpha 1, and elevated serum lysozyme levels. The inverted ratio was due to a deficiency in T-helper cells. The inverted helper:suppressor ratio was associated with functional suppressor cell activity that was seen in 12 out of 21 patients examined. Patients' lymphocytes were found to suppress the PHA, pokeweed mitogen, and concanavalin-A responses of normal subjects' lymphocytes. The suppression also correlated with impaired lymphocyte proliferative responses among the patients' cells themselves. Because of these findings, the helper:suppressor ratio was studied in patients with solid tumors, lymphoma, acute leukemia, chronic lymphocytic leukemia, and hairy cell leukemia. Approximately 30% of these patients have an inverted helper:suppressor ratio. However, in ten out of 30 patients with chronic lymphocytic leukemia and in three out of 45 patients with lymphoma, the helper:suppressor ratio was elevated, being greater than 3.0. The significance of these findings is as yet to be explored, but it is suggested that an inverted helper:suppressor ratio in patients with malignancy may relate to an advanced stage of disease or a poor prognosis. Documentation of this point will require further study.
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PMID:Leukocyte subset analysis and related immunological findings in acquired immunodeficiency disease syndrome (AIDS) and malignancies. 623 50

Neoplastic cells from 13 cases of hairy cell leukemia were investigated for immunoglobulin production and lysozyme activity by an electron-immunoperoxidase technique. In 10 cases cytoplasmic immunoglobulins were found, but lysozyme activity was absent in all cases. Immunoglobulins were detected in the perinuclear space and endoplasmic reticulum and at the surface of hairy cells. Of the cases in which immunoglobulins were detected in hairy cells, nine were positive with IgM antiserum and one with IgG antiserum. The immunoglobulins were monoclonal in all cases; six were positive with lambda antiserum and three with kappa antiserum. The class and type of surface immunoglobulins were identical to those of cytoplasmic immunoglobulins in the hairy cells. These results support the conclusion that hairy cells are commonly derived from immunoglobulin-producing B cells at an earlier stage of differentiation than plasma cells.
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PMID:Ultrastructural localization of immunoglobulins in hairy cell leukemia. 643 66

Hairy cell leukaemia (leukaemic reticuloendotheliosis) appears to be a homogeneous and well defined disease on the basis of clinical presentation, light and electron microscopic features and cytochemical characteristics, but the study of immunological markers of hairy cells (HC) from many patients reveals apparent heterogeneity. The most common phenotype associates B-cell and monocytic properties: HC usually express monoclonal surface (and in certain cases cytoplasmic) immunoglobulins, receptors for IgM and IgG Fc, and mouse erythrocytes, and la-like antigens. Additionally, they are capable of phagocytosis, glass adherence, lysozyme and peroxidase synthesis. However, most of these features are not constant and cases have been reported in which HC fail to express one or more of these properties. In certain cases HC even display a T-cell phenotype, while, in others, features of both T and B cells are expressed. Moreover, in two recently studied patients, the phenotype of HC in the blood differed from that in the spleen (B + T in the blood and B in the spleen). These surprising discrepancies led us to hypothesize that HC from the same individual might be able to express different phenotypes following an appropriate stimulus. We therefore studied immunological parameters of HC stimulated by mitogens and the results indeed showed that after stimulation by phytohaemagglutinin (PHA) the cells switched from B to T or B + T phenotypes.
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PMID:Phenotypic changes of phytohaemagglutinin-stimulated hairy cells. 696 66

To date, the diagnosis of mast cell disease (MCD) relied on routine plus histochemical stains. Its differential diagnosis, however, includes a variety of other hematopoietic and particularly B-cell lymphoid neoplasms that are best identified in paraffin sections using immunostains. To determine the paraffin-section immunoreactivity of MCD, 20 specimens from 14 patients with MCD and 1 bone marrow sample (from a patient with probable MCD) that showed equivocal metachromasia, were stained with antitryptase, CD68 (KP-1), CD20 (L26), antilysozyme, and antimyeloperoxidase antibodies. Ten hairy cell leukemias (HCLs), six lymphomas of parafollicular and/or monocytoid B-cell (MBCLs) and low-grade mucosa-associated lymphoid tissue (MALT) types, six granulocytic sarcomas, and five acute myeloid leukemias with monocytic differentiation (M4 and M5 types) were also stained. Tryptase positivity was identified in all of the MCD cases. The staining was moderate to strong in 20 of the 21 specimens, including the probable MCD case. No other neoplasms tested were tryptase positive. CD68 showed similar to even stronger staining in all of the specimens of MCD, HCL, granulocytic sarcoma, and acute myeloid leukemia (M4 and M5 types) tested and in five of the six MBCL and/or MALT-type lymphomas. Weak-to-moderate lysozyme staining seemed to be present in at least 7 of the MCD specimens, whereas there was a lack of staining for myeloperoxidase in 12 specimens, and 7 specimens were nonevaluable (1 case was not tested). Myeloperoxidase was identified in all of the granulocytic sarcomas and acute myeloid leukemias (M4 and M5 types) but not in any HCLs, MBCLs, or low-grade lymphomas of MALT type. CD20 was negative in all of the MCD and myelomonocytic neoplasms but positive in all of the HCLs, MBCLs, and low-grade B-cell lymphomas of MALT type. MCD, therefore, has a characteristic tryptase-positive, CD68-positive, and CD20-negative phenotype in paraffin sections. This distinguishes MCD from the hematopoietic and/or lymphoid disorders that it most closely resembles.
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PMID:Immunohistochemical characterization of mast cell disease in paraffin sections using tryptase, CD68, myeloperoxidase, lysozyme, and CD20 antibodies. 890 35