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)

The diagnosis of primitive hematologic malignancies in extramedullary sites (lymphoblastic lymphoma of T- or B-cell type and myeloid sarcoma) on paraffin-embedded tissue sections is difficult and often impossible because of the primitive morphology of the neoplastic cells. The authors studied 21 extramedullary tumors of lymphoid or myeloid blasts. They used a panel of 22 antibodies on frozen sections and 9 antibodies on paraffin sections to determine the spectrum of immunophenotypes and to develop a practical panel for diagnosis. All but two of the cases could be classified as lymphoid or myeloid using immunohistologic analysis. Thirteen cases were classified as lymphoblastic lymphoma/acute lymphoblastic leukemia (LBL/ALL); 10 were classified as precursor T (CD7+, CD3+/-, CD45+) and 3 as precursor B-cell (CD19+/-CD10+CD45-) type. Five cases were classified as myeloid sarcoma (CD13+ myeloperoxidase+, lysozyme+). Two LBL/ALL coexpressed either CD33 (1 case) or CD15 (1 case), and one myeloid sarcoma coexpressed TdT and CD7. One case appeared to be truly mixed lineage, coexpressing CD3 with myeloperoxidase and lysozyme, and two cases expressed no lineage-specific antigens. There were clinical differences between the three major tumor types, and within the category of T-precursor LBL/ALL, classification according to stage of thymocyte differentiation was associated with distinctive clinical features. In conclusion, the spectrum of immunophenotypes detected on frozen section was similar to that reported by flow cytometry on peripheral blood and bone marrow specimens. The most useful antigens on frozen sections were CD7 and CD3 (T cell), CD10 and CD19 (B cell), and CD13 (myeloid). TdT was coexpressed by one myeloid sarcoma and was undetectable in 40% of LBL/ALL. On paraffin sections, myeloperoxidase and lysozyme were reliable markers of myeloid lineage, but none of the markers used on paraffin sections distinguished between LBL/ALL of T- and B-precursor types. Both B-LBL/ALL and myeloid sarcomas were often CD45- on paraffin sections, which may be a obstacle in determining the diagnosis. These distinctions appear to have clinical relevance.
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PMID:Extramedullary tumors of lymphoid or myeloid blasts. The role of immunohistology in diagnosis and classification. 757 94

To date no hematopoietic progenitors of dendritic Langerhans' cells (DLC), which represent an highly efficient class of antigen presenting cells, have been identified or the cytokines they elaborate have been defined. Here we describe an acute leukemia patient whose blasts (90-96% in peripheral blood and bone marrow) had a phenotype consistent with putative progenitors of DLC. The patient was treated with ara-C and VP-16 but did not achieve remission. The blasts had lobulated nuclei, no cytoplasmic vacuolation or Auer rods and were weakly positive for acid phosphatase and non-specific esterase and negative for PAS, granzyme A, dipeptidyl aminopeptidase IV, ATPase/ADPase and lysozyme production. The blasts were positive for CD1a, CD4, CD16, CD35, HLADR, HLADQ, CD11b, CD11c, CD14, CD33, CD34, CD11a, CD71, CD19, CD25, IL-2R beta and negative for CD2, CD7, CD8, CD10, CD22, CD56, CD57, surface or cytoplasmic CD3, TCR delta and TCR beta, HTLV-1p19 and P-glycoprotein. On liquid culture with or without 5 x 10(-9) M 12-O-tetradecanoylphorbol-13-acetate (TPA) for 3 days, the blasts formed aggregates of proliferating and elongating cells on the wall of the flasks with a decline in CD34, numerous dendritic processes appeared on the cells and there was strong positivity for ATPase/ADPase, but no other changes in phenotype. No macrophages were observed, indicating derivation from separate DLCs. Cytogenetic analysis showed chromosomal abnormalities and electron microscopy showed Birbeck granules. Southern blotting of DNA showed rearrangement of one allele for both JH and TCR beta but no HTLV-1 related sequences. Culture supernatants from blasts cultured with or without TPA showed the production of large amounts of IL-8, IL-6, TNF-alpha, MIP-1 alpha, IL-10 and interferon gamma and modest amounts of IL-1 alpha, GM-CSF and stem cell factor. The presence not only of CD1a, HLADR, HLADQ and many other characteristics including Birbeck granules, but also differentiation along the lines of DLC with appearance of dendritic processes on the cells and expression of ATPase/ADPase activity, indicate that the leukemic blasts in our patient represented a leukemic counterpart of normal progenitors of DLC and the leukemia a new entity which could possibly be classified as AML-M8. Lastly, many pro-inflammatory cytokines produced by DLC could contribute to inflammation and IL-10 to immunosuppression.
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PMID:Phenotype, genotype and cytokine production in acute leukemia involving progenitors of dendritic Langerhans' cells. 791 55

We report the establishment of a novel cell line from a pediatric patient with recurrent non-Hodgkin's lymphoma. This cell line, termed USP-91, showed both T-lymphoid cell as well as myeloid (ie, nonlymphoid) cell characteristics using a comprehensive multiparameter approach. The initial growth of this cell line was dependent on the presence of the murine stromal cell line, 14F1.1. Subsequently, a phenotypically stable, stroma-independent cell line was established. Although the recurrent biopsy material and the derivative cell line, USP-91, were clonally-derived from T-lineage lymphoid cells, as evidenced by the same rearrangement of the T-cell receptor-beta locus, USP-91 coexpressed both the T-cell antigens CD7, CD3, and CD4, and the myeloid antigens CD13, CD33, CD11b, and CD34. The myeloid features of USP-91 were most consistent with monocytic differentiation as these cells expressed alpha-napthol acetate esterase, lysozyme, alpha-1-antitrypsin, alpha-1-antichymotrypsin, as well as the cell surface receptor for macrophage colony-stimulating factor. In addition, incubation in the presence of phorbol esters induced USP-91 to exhibit morphologic and functional properties of mature mononuclear phagocytes. The expression of this bilineage phenotype suggests that USP-91 represents the malignant transformation of a progenitor cell capable of either myelomonocytic or T-lymphoid differentiation.
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PMID:Establishment and characterization of a human mixed-lineage, T-lymphoid/myeloid cell line (USP-91). 840 Feb 35

A peculiar case of cutaneous granulocytic sarcoma without leukemic manifestation (so-called aleukemic leukemia cutis) that developed in the skin of the back of a 69-year-old man is reported. A skin biopsy specimen showed atypical cells with a prominent nucleolus proliferating around dermal blood vessels and along adnexa without epidermotropism. Atypical cells similar to those of the skin had infiltrated diffusely into the interfollicular area of an inguinal lymph node. Flow cytometric and immunohistochemical studies with a panel of monoclonal antibodies revealed neoplastic cells that had a biphasic phenotype of myeloid and T cell precursors. They expressed CD13, CD15, CD33, lysozyme, CD3epsilon, CD4, CD7 and terminal deoxynucleotidyl transferase (TdT). Gene analysis showed no rearrangement of the immunoglobulin heavy chain or T cell receptor beta and gamma genes. Ultrastructurally, the tumor cells exhibited a few intracytoplasmic electron-dense granules and well-developed rough endoplasmic reticulum with an occasional whorling arrangement. The initial diagnosis was immunoblastic large cell lymphoma, and the patient was treated with six courses of ProMACE-CytaBOM. In spite of the high-grade cytological characteristics of this tumor, the patient has been free of disease for 5 years.
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PMID:Cutaneous granulocytic sarcoma mimicking immunoblastic large cell lymphoma. 1036 56

The MLL gene is fused with the cAMP-responsive element binding protein-binding protein (CBP) gene in t(11;16)(q23;p13), which has been reported to be associated with therapy-related acute leukemia. We established a novel myeloid cell line, SN-1, from a patient with T-cell acute lymphoblastic leukemia with t(11;16)(q23;p13) having in-frame MLL-CBP fusion transcripts. The majority of the SN-1 cells were positive for myeloperoxidase when examined using an electron microscope and expressed CD13, CD33, CD56, and HLA-DR antigens, but not CD7, CD10, CD19, CD34, or CD41 antigens, suggesting that these cells are of myeloid origin. SN-1 cells underwent functional and morphological differentiation when treated with actinomycin D or sodium butyrate, but not with all-trans-retinoic acid (ATRA) or 1alpha,25-dihydroxyvitamin D3 (VD3). Exposure of SN-1 cells to ATRA hardly affected cell growth and differentiation, whereas the growth of HL-60 and NB4 cells treated with ATRA was effectively inhibited, and differentiation into mature granulocytes was induced. SN-1 cells were relatively insensitive to VD3 with respect to inhibiting the cell growth and inducing the ability to reduce nitroblue tetrazolium, lysozyme activity, and morphological differentiation, although the expression of CD11b was slightly induced by VD3. These results suggest that the cell line was impaired in the signal transduction systems of ATRA and VD3. This cell line should be useful for the study of the role of CBP as a transcriptional regulator in leukemia differentiation and for the functional analysis of the MLL-CBP fusion gene, which will provide new insights into leukemogenesis caused by 11q23 translocations.
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PMID:SN-1, a novel leukemic cell line with t(11;16)(q23;p13): myeloid characteristics and resistance to retinoids and vitamin D3. 1070 36

A 75-year-old man was admitted because of right knee joint pain in December 1999. He had suffered from acute myelocytic leukemia (AML: M0) in November 1994 and achieved the first complete remission (CR) then. His AML relapsed in August 1996, but fortunately he achieved a second CR. Radiographical bone examination revealed osteolytic lesions in his right knee and bone scintigraphy showed uptake in the right knee and the middle part of the left femur. MRI also revealed a low attenuation signal in the left femur. He had no abnormal findings in peripheral blood or bone marrow. Histological examination of the biopsied bone tissue showed a diffuse proliferation of round cells with medium-sized or large nuclei. These cells were histochemistrically negative for myeloperoxidase and naphtol-ASD-chloroacetate esterase, and were also negative for lysozyme, cytokeratin 7, 9, 20, EMA, CEA, CD3, CD79a on immunohistochemistry, but were positive for CD43, CD56. In immunophenotypic analysis of these cells by flow cytometry, CD7, CD13, CD33, CD41, CD56 were revealed to be strongly positive. On the basis of these findings we diagnosed these tumors as granulocytic sarcomas (GS), extramedullary recurrence of AML M7. Although radiation (36Gy) to these tumors brought a temporary relief of the pain, he died of systemic relapse of AML in February 2001. When presented CD7+ AML M0 had been diagnosed, but GS cells were also positive for CD 56 and CD41. Although CD56 had not been examined initially, he might have been had myeloid/NK cell precursor acute leukemia and CD41 might be acquired later in the course of the disease. It is known that AML M0, M7 and myeloid/NK cell precursor acute leukemia have poor prognoses, nevertheless he survived for 6 years. It may be that intensive and repeated chemotherapy for AML can obtain excellent outcome in the elderly cases in good systemic condition and with favourable prognostic factors.
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PMID:[Acute myelocytic leukemia (M0) in an elderly patient with relapsed granulocytic sarcoma (M7) of bone during the second period of complete remission 5 years after onset]. 1270 54

Immature-type CD56(+) natural killer (NK)-cell neoplasms are classified as either myeloid/NK-cell precursor acute leukemia or blastic NK-cell lymphoma. We identified two cases of immature-type CD56(+) NK-cell neoplasms that were not categorizable as either of these entities. The first case involved a 74-year-old woman presenting with skin eruptions and pancytopenia due to bone marrow necrosis. Skin biopsy specimen revealed CD4(+), CD7(-), CD34(-), CD43(+), CD56(+), CD68(+), muramidase (lysozyme)(+), and myeloperoxidase (MPO)(-), and immunophenotyping of peripheral blood showed CD4(+), CD7(-), CD13(+), CD33(+), CD34(-), CD43(+), CD56(+), cytoplasmic (cy)CD68(+), CD123(+), and HLA-DR(+). The second case involved a 62-year-old man who had bilateral optic nerve tumor and presented with malignant cells in peripheral blood. Cell surface markers of malignant cells showed CD4(+), CD7(-), CD13(+), CD33(+), CD34(-), CD43(+), CD56(+), cyCD68(+), and HLA-DR(+). The phenotypes of tumor cells in both cases were compatible with blastic NK-cell lymphoma, except for the expression of myeloid antigen. Clinical presentations of these cases showed characteristics of both blastic NK-cell lymphoma and myeloid/NK-cell precursor acute leukemia.
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PMID:Uncommon cases of immature-type CD56+ natural killer (NK)-cell neoplasms, characterized by expression of myeloid antigen of blastic NK-cell lymphoma. 1910 30

An 87-year-old woman not known to have either a lymphoma or leukemia developed a left multinodular, fish-flesh superior epibulbar and forniceal mass. A biopsy disclosed a blastic tumor with scattered multinucleated immature megakaryoblasts. Immunophenotyping of bone marrow cells revealed strong positivity for CD7, CD31, CD43, CD45, CD61, and CD117; CD71, myeloperoxidase, and lysozyme were also positive in scattered cells. Forty percent of the neoplastic cells were Ki-67 positive. Cytogenetic studies indicated a trisomy 8 (associated with worse prognosis) and a t(12; 17) translocation. Desmin, smooth muscle actin, pancytokeratin, CAM 5.2, adipophilin, tryptase, S100, SOX10, MART1, and E-cadherin were negative, ruling out a nonhematopoietic tumor. The conjunctival lesion was diagnosed as a myeloid sarcoma with megakaryoblastic differentiation, a rare variant. It probably arose from a myelodysplastic syndrome. This is the first case of its type to develop in the conjunctiva.
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PMID:Myeloid Sarcoma with Megakaryoblastic Differentiation Arising in the Conjunctiva. 3067 74

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