Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.3.1 (alkaline phosphatase)
 47,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report two cases of Philadelphia (Ph1) chromosome positive acute mixed lineage leukemia (AMLL) with breakpoint cluster region (bcr) (M-BCR-1) rearrangement. A 31 year-old-man (case 1) and a 42 year-old-woman (case 2) were admitted to our hospital for further evaluation of leucocytosis with atypical blasts. Each case was diagnosed as having bilineal type of AMLL because: (1) blasts in each case consisted of larger myeloid cells positive for myeloperoxidase and small lymphoid cells positive for PAS, and blasts in case 2 were positive for TdT; (2) blasts in case 1 expressed B lymphoid associated antigen; (3) Southern analysis in each case showed clonal rearrangements of both the immunoglobulin heavy chain and the T cell receptor beta gene. These two cases demonstrated the Ph1 chromosome and rearrangement of the bcr (M-BCR-1) gene, but none of splenomegaly, basophilia, and additional chromosome abnormalities were observed. In addition, after achieving remissions, they didn't revert to chronic phase of chronic myelogenous leukemia (CML) and showed normal neutrophil alkaline phosphatase scores, and the Ph1 chromosome disappeared completely in case 1 and coexisted with the normal chromosome in case 2. These findings suggest that diagnosis of both cases should not be CML blast crisis (BC) but Ph1 positive acute leukemia, and Ph1 positive AMLL may be a distinct clinical entity to be distinguished from CML-BC.
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PMID:[Philadelphia chromosome positive acute mixed lineage leukemia with bcr (M-BCR-1) rearrangement]. 215 95

The distribution of cells expressing the integrins VLA-1 to 6 in human intestine was examined by alkaline phosphatase immunohistochemistry using monoclonal antibodies specific for the individual alpha-chains of the VLA heterodimer. VLA-2,3, and 6 were expressed on all epithelial cells in the small and large bowel. VLA-1 was expressed on crypt cells in the small and large bowel, but was only weakly expressed or was absent on villus epithelial cells in the small bowel and colonic surface epithelial cells. All epithelia were negative for VLA-4 and VLA-5. Intraepithelial lymphocytes were VLA-1+ and VLA-4+. VLA-1,3, and 5 were expressed uniformly by muscularis propria, muscularis mucosae, pericrypt cells, and smooth muscle fibres within the villi. By contrast, VLA-2 and 4 were present only in pericrypt cells and fibres within the villi; they were absent from the muscularis mucosae. VLA-1,3,5, and 6 were expressed by endothelium. Staining of muscle fibres and endothelium in the lamina propria made it difficult to determine the extent of VLA expression on lamina propria lymphocytes. However, VLA-1+ cells with lymphoid morphology were only rarely seen. All mononuclear cells in the lamina propria were VLA-4+.
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PMID:Expression of the VLA family of integrins in human intestine. 217 5

A review of immunohistology, involving the more commonly encountered fixation protocols and the use of proteolytic agents, was undertaken in an attempt to establish a method whereby cell surface immunoglobulins could be reliably demonstrated in routinely processed paraffin tissue sections. Immunoglobulin D (IgD) was selected as a suitable antigen for detection in reactive lymphoid tissues, since it is known to be present both on the cell surface and in the cytoplasm. Using the indirect immunoperoxidase technique and the alkaline phosphatase/anti-alkaline phosphatase technique as standard methods, only cytoplasmic IgD was identifiable in paraffin sections with monoclonal antibodies. However, using polyclonal antisera a technique was established in which membrane-bound IgD was also demonstrated in paraffin sections.
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PMID:Enhanced demonstration of cell surface immunoglobulins in paraffin-processed tissue. 220 75

Mac387 monoclonal antibody (MAb) recognizes two calcium binding, myeloid-associated proteins, now termed calgranulins, expressed at high levels by neutrophils and monocytes. Calgranulins are related to migration inhibitory factor (MIF) and are lost in a few days from monocytes differentiated in vitro. This marker is therefore potentially useful to analyze macrophage heterogeneity and turnover in tissue sections. In this study, we developed an immunohistochemical multimarker technique, including calgranulin demonstration, suitable for analyzing different inflammatory cells on paraffin-embedded material. The technique was carried out in subsequent steps demonstrating (a) naphthol AS-D chloroacetate esterase (CAE); (b) S100 immunoreactivity using a rabbit antibody in peroxidase-antiperoxidase (PAP) staining; and (c) Mac387 immunoreactivity using the alkaline phosphatase-anti-alkaline phosphatase (APAAP) technique. CAE staining was introduced in this method to distinguish Mac387+/CAE- macrophages from Mac387+/CAE+ neutrophils, and Mac387-/CAE+ mast cells. S100 protein is strongly expressed within lymphoid tissues by dendritic accessory cells and was then applied to distinguish these cells from S100-macrophages. We have also verified the possibility of reducing the staining time for this time-consuming procedure by use of microwave irradiation. The technique was applied to a representative variety of normal and pathological samples to assess its usefulness for study of cell heterogeneity. Our results showed the multimarker technique to be highly informative in the study of inflammatory lesions (e.g., rheumatoid arthritis, sarcoid and cat-scratch granulomas, dermathopathic lymphadenopathy), and is of wide potential value as an aid to histopathological diagnosis of several diseases.
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PMID:Multimarker immunohistochemical staining of calgranulins, chloroacetate esterase, and S100 for simultaneous demonstration of inflammatory cells on paraffin sections. 221 22

Stromal cell numbers from subjects with no haematological disease and those with acute myeloid leukaemia (AML), chronic granulocytic leukaemia (CGL), acute lymphatic leukaemia (ALL) and non-Hodgkin's lymphoma (NHL) were compared to determine their role in malignancy. Frozen sections of trephine biopsy specimens from iliac crests were stained for endogenous alkaline phosphatase activity, endogenous acid phosphatase activity, and, using immunocytochemical methods, for endothelial cells (anti-factor-VIII related antigen) and macrophages and related cells (EBM/11). In granulocytic malignancies, whether acute or chronic, alkaline phosphatase positive reticulum cells (AL-RC) and vascular endothelial cells were generally increased. In lymphoid malignancies, the numbers of AL-RC were generally reduced. Numbers of vascular endothelial cells seemed to be normal in ALL but reduced in foci of NHL. Macrophages are numerous in normal marrow, and their numbers seemed to be normal in granulocytic lesions but were more variable and sometimes reduced in ALL and NHL. Lymphoid malignancies, therefore, have a destructive effect on some stromal elements; granulocytic malignancies are associated with normal or increased numbers of stromal cells. A possible consequence of depleted stromal cells might be slower reconstitution of normal haemopoiesis after treatment. The large numbers in granulocytic malignancies raises the possibility of synergistic stimulation between stromal and neoplastic cells.
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PMID:Bone marrow stromal cell changes in haematological malignancies. 226 66

bcl-2 is a marker for the translocation t(14;18)(q32;q21) indicative of follicular B-cell lymphoma. We studied 115 cases of lymphoproliferative disease with the polymerase chain reaction for bcl-2 oncogene using biotin and radiolabeled probes to the major breakpoint and minor cluster regions. Twenty-three percent of B-cell lymphomas were positive for bcl-2. These included 12 of 20 cases of nodular follicular center cell lymphoma (nine small cleaved cell, one mixed small and large cell, and two large cell types). bcl-2 translocation was detected in only three of 45 cases of diffuse B-cell lymphoma, and cases of AIDS-related malignant lymphoma, monocytoid B-cell lymphoma, and mantle zone lymphoma were all negative. Nonneoplastic lymphoid proliferations were negative for bcl-2 including nine cases of abnormal follicular hyperplasia from patients with acquired immunodeficiency syndrome (AIDS) and AIDS-related complex. Cases of T-cell lymphoma and five cases of Hodgkin's disease were also negative. The polymerase chain reaction for bcl-2 is a rapid, sensitive technique in the evaluation of follicular B-cell proliferations, and the use of biotinylated probes and the alkaline phosphatase reaction eliminates the requirement for radioactive reagents.
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PMID:Polymerase chain reaction for bcl-2 in diagnostic lymph node biopsies. 226 90

To study the reactivity of nasal-associated lymphoid tissue (NALT) and its position in the mucosal immune system, rats were intranasally challenged with 200 micrograms TNP-LPS. Priming had occurred 15 days previous to the challenge with the same antigen and dose, either intranasally, intratracheally, subcutaneously in the cheek or intraperitoneally. The number of anti-TNP antibody-forming cells (AFC) was determined in various tissues using the conjugate TNP/alkaline phosphatase. Generally, anti-TNP AFC were predominantly found in the posterior cervical lymph nodes, while NALT contained hardly any such AFC. The highest response in the posterior cervical lymph nodes occurred on day 5, after subcutaneous priming and intranasal boosting. This also evoked peak responses in several other tissues. The highest response in spleen and lung occurred on day 7 after intraperitoneal priming and intranasal boosting. Irrespective of the immunization route, IgA was the least produced isotype in the spleen as compared to antigen-specific IgG and IgM. In the posterior cervical lymph nodes, besides specific IgG and IgM, a considerable proportion of specific IgA was produced. All four immunization routes yielded anti-TNP antibodies in serum. As for the non-lymphoid cells, the intratracheal-intranasal immunization protocol induced an increase in pulmonary macrophages on days 3 and 5. The immunological role of lung macrophages is discussed.
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PMID:Anti-TNP-forming cells in rats after different routes of priming with TNP-LPS followed by intranasal boosting with the same antigen. 228 97

In a study of 55 patients with either acute lymphoid leukemia (ALL; 25 cases) or acute myeloid leukemia (AML; 30 cases), paraffin-embedded bone marrow particle sections were examined with a panel of monoclonal and polyclonal antibodies reactive toward lymphoid and myeloid-associated antigens, using the alkaline phosphatase-anti-alkaline phosphatase (APAAP) technique. All cases were previously classified according to the French-American-British (FAB) Co-operative Group, and cases of ALL were immunophenotyped by flow cytometry. Results indicated that myeloid-associated antibodies (Mac 387, KP 1 [CD68], antielastase, antilactoferrin, and antilysozyme) did not react with any case of ALL, M1-AML, or M6-AML, whereas at least one of these antibodies reacted with 20 of 21 (95%) cases of M2, M3, M4, and M5-AML. Anti-glycophorin C marked cases of M6-AML, whereas anti-CD3 labeled T-cell ALL. None of the antibodies tested specifically identified cases of B-cell ALL. The authors conclude that use of a selected panel of antibodies on paraffin-embedded bone marrow particle sections may be of value in the diagnosis and immunophenotypic classification of many cases of acute leukemias.
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PMID:Immunophenotyping of acute leukemias using paraffin-embedded tissue sections. 232 81

The major initial clinical, hematological and cytogenetical features of a series of 80 patients with blastic crisis (BC) in chronic myelocytic leukemia with positive Philadelphia chromosome (Ph) were evaluated, and also were their outcome and response to therapy. Mean age of patients was 45 years (SD: 14.3). Ten patients fulfilled the criteria for initial BC, and 14 had extramedullary blastic infiltration. In one third there was an acceleration phase before the development of BC. The mean leukocyte count was 69 (SD 75) X 10(9)/l. In 40% there was anemia with hemoglobin less than 90 g/l, and 37.5% had thrombopenia with less than 100 X 10(9) cells/l. In most patients, serum lactic dehydrogenase activity was increased, and in one fourth the index of granulocyte alkaline phosphatase was high. In 9 patients, blast cells had a lymphoid phenotype and in 47 (59%) cytogenetic abnormalities in addition to Ph chromosome were found, usually consisting of 8 trisomy, duplication of Ph chromosome, and the presence of a 17q isochromosome. The median survival of the series was 4.8 months. When analyzed as a time-dependent variable, the achievement of a favorable therapeutic response (found in 26% of patients) was associated with a longer survival.
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PMID:[Blast crisis of chronic myeloid leukemia with positive Philadelphia chromosome: course and clinico-hematologic profile in 80 patients]. 238 91

Defining cell lineage in the non-Hodgkin's lymphomas (NHL) is challenging for the immunopathologist. Cell surface marker techniques have made a major contribution to the understanding of the biology and classification of lymphoproliferative disorders by permitting the determination of the lymphoid (B- or T-cell) or monocytic lineage of the tumors. Because lymphoma cells often simulate the morphologic features and cell surface phenotype of their normal lymphocytic counterparts, it is difficult to discriminate normal from neoplastic lymphocytes. The authors have used representative monoclonal antibodies (MAb) to cell surface antigens to assess tumor cell surface antigens associated with various lymphoreticular cell lineages. Heteroantisera to the human malignancy-associated nucleolar antigen (HMNA) was utilized as a marker for neoplastic lymphoid cells as previously described. The use of double immunoenzymatic staining with both peroxidase and alkaline phosphatase allow us simultaneously to determine lymphoid lineage and malignancy on human lymphoma cells. In 101 cases of various cell types of NHL, the anti-HMNA antiserum reacted with nucleoli in the morphologically neoplastic lymphoma cells, but not with normal-appearing lymphoid and other cell types present in the lesions. Control specimens from normal and hyperplastic lymphoid tissue also failed to react with anti-HMNA antibodies.
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PMID:Double immunoenzymatic labeling of lymphomatous tissues for both immunologic phenotype and a malignancy-associated nucleolar antigen. 242 82


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