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
Query: EC:3.2.1.17 (
lysozyme
)
21,489
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Cytochemical and immunological studies were performed on "hairy" cells from 5 patients. The results, primarily the detection of surface immunoglobulins after incubation in immunoglobulin-free medium support the hypothesis that hairy cells are B-cells. Further parameters for B-cell lineage are the failing suppression of unspecific esterases by NaF, the presence of tartrate-resistant acid phosphatase and the absence of phagocytic capacity and glass adherence (skin window). A
lysozyme
could not be demonstrated. Of two patients with prolymphocytic leukemia one was characterized as T- and one as B-cell leukemia. Therefore, the prolymphocytic leukemia has to be discussed as intermediate form of
ALL
and CLL. In both patients the therapeutic results were discouraging with cytostatics (e. g. chlorambucil), splenectomy is considered as the treatment of choice.
...
PMID:[Prolymphocytic and hairy cell leukemias as special forms of chronic lymphatic leukemia]. 29 12
Surface marker analysis with rosette tests and a large panel of xenoantisera and monoclonal antibodies was done on the malignant cells of 55 patients with acute myeloid leukemia (AML). The diagnosis was made on morphological and cytochemical grounds, and the leukemias were classified according to the quantified FAB criteria. The marker tests included the E- and EA-rosette test, immunofluorescence with rabbit-polyclonal antisera against human Ig, kappa, and lambda light chains, thymocytes, granulocytes, erythrocytes, platelets,
lysozyme
, (leukemic) myeloblasts, the common
ALL
antigen, SB cell-line cells (anti-Ia), and a mouse anti-Ia serum. The monoclonal mouse antibodies applied were anti-T-cell antibody (3A1), two anti-granulocyte-monocyte antibodies (OKM1 and B2.12), four antigranulocyte antibodies (MI/N1, UJ 308, B4.3, and B13.9), an antiplatelet antibody (C17.28), anti-HLA heavy chains (w6/32.HLK), anti-Ia antigen (OKI1), and OKT10. AML cells from many patients lacked the expression of myeloid markers, and we found that a correlation existed between the relative maturity of the leukemia subtype and the extent of positivity for these markers. Surface marker analysis discriminated poorly between the "myeloid" and "monocytoid" subtypes; OKT10 and the "T-cell marker" 3A1 were often expressed on AML cells. In two cases of AML, there was an unexpected expression of platelet antigens with the monoclonal antiplatelet antibody. One of them, classified as M1, was ultrastructurally a megakaryoblastic proliferation with a positive reaction for platelet peroxidase. Only with the help of computerized analysis, was it possible to prove a clear correlation between the surface marker profile and the FAB classification.
...
PMID:A comparison of surface marker analysis and FAB classification in acute myeloid leukemia. 657 76
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.
...
PMID:Extramedullary tumors of lymphoid or myeloid blasts. The role of immunohistology in diagnosis and classification. 757 94
The value of immunohistochemical staining in the subtyping of acute leukemia was investigated on 36 routinely processed (formalin-fixed and paraffin-embedded) trephine biopsy specimens from the iliac crest containing diffuse infiltrates of acute myelogenous leukemia (AML; n = 23) and acute lymphoblastic leukemia (
ALL
; n = 13). These were stained with a broad panel of antibodies (n = 23) against various leukocyte antigens, among them 11 macrophage-associated antibodies (MAAs): Ki-M1p, MAC387, HAM56, LN5, KP1 (CD68), PG-M1 (CD68), Ki-M4p, DAKO-DRC (CD35), and antibodies against
lysozyme
, alpha 1-antichymotrypsin, and S100 protein. The French-American-British (FAB) classification subtypes of the AML cases, as determined by enzyme-cytochemical and/or immunocytological investigation of bone marrow smears, were as follows: M1 = 6, M2 = 5, M4 = 7, M5 = 3, and AML (not classified) = 2. The 13 cases of
ALL
were classified as follows: c-ALL (pre-B-ALL) = 7, B-ALL = 3, T-ALL = 2, and
ALL
(not classified) = 1. All the MAAs except LN5, Ki-M4p, and DAKO-DRC stained blast cells in AML. However, the number of stained blast cells varied considerably within and between the individual subtypes (M4/5 > M2/1). Using Fisher's exact test a significant difference in frequency of blast cell staining between AML and
ALL
was found for four MAAs (anti-
lysozyme
, MAC387, Ki-M1p, and KP1) and two of the three myeloid cell markers applied (Ki-My2p and anti-neutrophil elastase). Of these six antibodies, the combination of anti-
lysozyme
and KP1 can be recommended for use in routine diagnostics for the differentiation of AML from
ALL
on the basis of immunohistochemical staining because both of these antibodies were found to stain a relatively large percentage of cases of AML but none of
ALL
. However, none of the MAAs were found to discriminate reliably between the FAB M4/5 and M1/2 subtypes of AML.
...
PMID:Assessment of the value of immunohistochemistry in the subtyping of acute leukemia on routinely processed bone marrow biopsy specimens with particular reference to macrophage-associated antibodies. 805 22
Urokinase-type plasminogen activator receptor (UPA-R-CD87) is a GPI-anchored membrane protein which promotes the generation of plasmin on the surface of many cell types, probably facilitating cellular extravasation and tissue invasion. A flow cytometric quantitative analysis of expression levels for UPA-R was performed on fresh blast cells from patients with acute myeloid leukaemia (AML, n = 74), acute lymphoblastic leukaemia (
ALL
, n = 24), and biphenotypic leukaemia (BAL, n = 3) using two CD87 monoclonal antibodies (McAbs) (3B10 and VIM5). Peripheral blood and bone marrow (BM) cells from 15 healthy adults served as controls. Using 3B10 McAb, UPA-R was expressed (>99%) by blood monocytes, neutrophils, and BM myelomonocytic precursors in controls, whereas resting T and B lymphocytes, and CD34+ cells were UPA-R negative. We also attempted to clarify whether UPA-R has a role in mediating neutrophil functions. Oriented locomotion induced by different chemotaxins and
lysozyme
release by granules stimulated with fMLP or PMA were significantly decreased when UPA-R was neutralized by CD87 McAb. In contrast, the anti-UPA-R McAb had no effect on superoxide anion generation of normal neutrophils. Blasts from AML showed a heterogenous pattern of expression for the UPA-R McAbs, with reactivity strictly dependent on FAB subtype. The highest UPA-R expression was seen in the M5 group: all patients tested (n = 20) showed strong positivity for the UPA-R McAb whereas only 12% (3/24) of
ALL
patients were CD87 positive, and 2/3 of BAL patients showed a dim expression for CD87. The number of receptors expressed by blast cells in 6/74 (8.1%) AML patients was higher than those of normal samples: in addition, since co-expression of UPA-R and CD34 was not found in normal haemopoietic cells, it may be postulated that CD87 can be used alone (when overexpressed) or in combination with CD34 for the detection of minimal residual disease. Results also indicated that patients with UPA-receptors >12 x 10(3) ABC/cell, irrespective of FAB subtype, had a greater tendency for cutaneous and tissue infiltration and a higher frequency of chromosome abnormalities, thus suggesting the concept that cellular UPA-R content positively correlates with the invasive potential of AML cells. The combination of higher UPA-R positivity, abnormalities of chromosome 11, and M5 FAB morphology may identify a peculiar subset of AML, characterized by a more aggressive clinical course.
...
PMID:Expression and functional role of urokinase-type plasminogen activator receptor in normal and acute leukaemic cells. 979 97
Thirty-two cases of granulocytic sarcoma (GS) are reported in this paper. Age range was from 16 - 70 years. GS was accompanied by AML in 13 cases,
ALL
(My+) in one case, CML in 11 cases and MDS in two cases. GS was diagnosed simultaneously with leukemia in five cases and preceded the leukemia in eight. Lymph node and soft tissue were the most commonly detected localizations. Seven cases had first been diagnosed as NHL. Histopathologically blastic, immature and mature variants were found in 11, nine and 11 cases respectively and overall survival was shortest in the blastic type. Myeloperoxidase and
lysozyme
were found to be positive in 30 and 24 cases respectively. Therapy was radiation in five cases and surgery in three. Systemic chemotherapy was given to the cases. The clinical outcome of the patients after the diagnosis of GS was poor. GS is a unique entity; prognosis is poor but it is important to detect the signaling pathways associated with migration of myeloid cells to the extra-medullary tissues. The critical factors for detecting this interesting tumor are to be aware of this disease, cooperation between clinician and pathologist and the application of special stains to detect the myeloid origin.
...
PMID:Granulocytic sarcoma: 32 cases and review of the literature. 1716 97