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)

A grave prognosis is usually associated with leukemic skin infiltrates (leukemia cutis). However, some leukemic skin infiltrates are clinically similar to reactive non-leukemic infiltrates in patients with leukemia; thus it is of great importance to distinguish them. Fifty-four cases which were thought clinically to be leukemia cutis underwent immunophenotyping with a panel of nine T, B, monocytic, and macrophage markers using paraffin sections. Immunohistochemistry helped identify 44 cases with leukemia cutis and 10 with reactive infiltrates. In all cases of leukemia cutis, the staining patterns of skin infiltrates were concordant with cell type in the bone marrow. Furthermore, the panel of markers was usually helpful in distinguishing reactive from leukemia infiltrates, especially in cases with chronic lymphatic leukemia. Immunohistochemistry is a valuable adjunct in histopathologic differentiation of skin infiltrates in most cases of leukemia. With formalin-fixed, paraffin-embedded biopsies, we recommend that CD45 (LCA), CD45RO (UCHL-1), CD3, CD20 (L-26), CD43 (Leu-22), CD68 (KP-1), lysozyme, and chloroacetate esterase be considered in cases of systemic leukemia with cutaneous papules and nodules that prove difficult to interpret with routine section.
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PMID:Value of immunohistochemistry in the diagnosis of leukemia cutis: study of 54 cases using paraffin-section markers. 138 98

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

The term "plasmacytoid T-zone cells" has been used to describe distinctive cells that occur in clusters in the paracortex of some reactive lymph nodes. Recently, tumorous proliferations of these cells have been described in several patients with myelomonocytic leukemias. Neither the nature of these cells nor their relationship to myeloid leukemia has been conclusively established. We report the case of a 64-year-old woman with chronic myelomonocytic leukemia who developed lymphadenopathy that proved to be due to tumorous accumulation of plasmacytoid T-zone cells in the interfollicular regions of the lymph nodes. She underwent splenectomy because of symptomatic splenomegaly; the resected spleen also contained aggregates of plasmacytoid T-zone cells, in addition to extramedullary hematopoiesis. On treatment with busulphan and prednisone, the lymphadenopathy resolved and did not recur. The patient died 7 years later with blast transformation of her myelomonocytic leukemia and no recurrence of lymphadenopathy. The aggregates of plasmacytoid T-zone cells were architecturally and cytologically distinct from the leukemic infiltrates of myeloid cells in the spleen, and there was no evidence of differentiation of these cells into myeloid or monocytic cells. A panel of monoclonal antibodies on paraffin sections revealed no lineage-specific T- or B-cell markers (UCHL1-, L26-), and the plasmacytoid cells were positive for CD68 (KP1) and L60 (CD43), as well as faintly positive for 4KB5 (CD45RA) and MB1 (CD45R). They did not stain with antibodies to myeloid lineage antigens CD15, lysozyme, or myeloperoxidase. The combination of clinical, morphologic, and immunologic features of plasmacytoid T-zone cells in this case suggests that these cells may be of monocytic lineage but are not direct precursors of mature monocytic or granulocytic cells, and may not be part of the neoplastic clone in patients with myelomonocytic leukemia.
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PMID:Plasmacytoid T-zone cell proliferation in a patient with chronic myelomonocytic leukemia. Histologic and immunohistologic characterization. 184 25

In evaluating histologically malignant infiltrates in the skin, it is often challenging to distinguish granulocytic sarcoma (GS) from selected cases of peripheral T-cell lymphoma (PTCL). These lesions have clinical features in common, in addition to shared histologic attributes. These include similarity in dermal distribution and growth pattern, nuclear characteristics, propensity to recruit other inflammatory cell types, and production of matrical sclerosis. In order to determine if immunohistology could contribute to differential diagnosis in this setting, we analyzed 15 cases of mucocutaneous GS, and compared them with 11 cases of well-documented PTCL. Antibodies in the CD15, CD20, CD34, CD43, CD45, CD45RO, and CD68 groups were used, as well as anti-myeloperoxidase (anti-MPX), anti-lysozyme (anti-LYSO), Mac387, and MB2. Anti-LYSO and anti-MPX were sensitive and specific markers of GS, labeling 93% and 80% of GS cases, respectively, and no cases of PTCL. Anti-CD15 and MB2 were also specific for GS, but each labeled only 60% of GS cases. CD34, CD68, and Mac 387 were specific but insensitive markers of GS. CD43 and CD45 were not particularly useful discriminants, with each being seen in 93% of GS cases, but also 64% and 100% of cases of PTCL, respectively. CD45RO was specific for PTCL; it was present in 82% of PTCL cases and no GS cases. Thus, conjoint reactivity for CD43, CD45, MPX, and LYSO characterizes GS, and differs from the pattern of PTCL, which is characterized by reactivity for CD45 and CD45RO, occasional reactivity for CD43, and lack of other specified markers.
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PMID:Granulocytic sarcoma: an immunohistologic comparison with peripheral T-cell lymphoma in paraffin sections. 796 23

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

A case of cutaneous B-cell lymphoma is described. The patient was treated only by surgical excision of the skin tumors five times during a period of about two years from February of 1984 to October of 1986. After the last surgical excision, a continuous disease-free period was achieved. Biopsy samples showed dense lymphocytic infiltrations with discrete masses in the dermis and subcutis; one of them showed a storiform pattern. At the time, the infiltrating cells were composed of medium and large lymphoid cells and spindle-shaped cells. The medium and large lymphoid cells were positive for CD20, CD22 and HLA-DR and negative for CD3, CD4, CD5, CD8, CD43, and kappa and lambda light chain. The spindle-shaped cells were negative for CD20, CD43, kappa and lambda light chain, lysozyme, and S-100 protein.
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PMID:A case of cutaneous B-cell lymphoma with a storiform stromal reaction. 834 May 35

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

We report two cases of extramedullary myeloid cell tumor that arose in patients with chronic myelomonocytic leukemia. In both cases, the tumors were difficult to recognize histologically because the neoplasms lacked cytological evidence of granulocyte maturation, such as cytoplasmic granulation or eosinophilic myelocytes, and the Leder stains for chloroacetate esterase were negative. Immunohistochemical studies were necessary to establish the correct diagnosis. The neoplastic cells in both tumors expressed myeloperoxidase, lysozyme, and CD43 and were negative for B-cell, T-cell, and other nonhematopoietic antigens tested. We report these cases to emphasize that extramedullary myeloid cell tumors may rarely precede transformation to acute myeloid leukemia in patients with chronic myelomonocytic leukemia. Extramedullary myeloid cell tumors of monocytic lineage may be difficult to recognize in routine and Leder-stained sections, and immunohistochemical studies may be essential for establishing the diagnosis.
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PMID:Extramedullary myeloid cell tumors arising in the setting of chronic myelomonocytic leukemia. A report of two cases. 855 47

We report herein a case of extramedullary myeloid tumor arising bilaterally in the testes of a 66-year-old man, who had previously been diagnosed with myelodysplastic syndrome. Light microscopy of the testicular neoplasm demonstrated a tumor composed of large, slightly polygonal cells with pale blue to weakly eosinophilic cytoplasm. The tumor cells were immunoreactive for CD45, myeloperoxidase, lysozyme, CD43, and MB2. Many of the cells also expressed chloroacetate esterase. Peripheral blood and bone marrow findings were consistent with chronic myelomonocytic leukemia (FAB-CMML), particularly in the most recent material, which showed clear cellular dysplasia and an increase in the percentage of blasts in the bone marrow (15% to 20% of all nucleated cells). This case of extramedullary myeloid tumor is unusual in view of the patient's age and the testicular location. It emphasizes the importance of including extramedullary myeloid tumor in the differential diagnosis of histologically undifferentiated large-cell tumors, as well as a need to use a broad panel of immunohistochemical stains in such cases.
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PMID:Testicular extramedullary myeloid cell tumor in a patient with myelodysplastic syndrome. 861 53


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