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)

The levels of leukocyte alkaline phosphatase (LAP) messenger RNA (mRNA) are evaluated in B and T lymphocytes, monocytes, and polymorphonuclear cells (PMNs), and this transcript is found to be present only in PMNs. Precursors of the myelomonocytic pathway, represented by leukemic cells isolated from several cases of chronic myelogenous leukemia (CML) in its stable and blastic phase and acute myelogenous leukemia (AML), are devoid of LAP transcript. These data support the notion that LAP is a marker of the granulocyte terminal differentiation. Despite the absence of LAP mRNA in both the myeloid and the lymphoid precursors, nuclear run-on experiments show constitutive transcription of the LAP gene in leukemic cells obtained from AML, CML, as well as acute lymphoblastic leukemia (ALL) and B-cell chronic lymphocytic leukemia (B-CLL). In CML and in chronic myelo-monocytic leukemia (CMML) PMNs, granulocyte colony-stimulating factor (G-CSF) specifically accumulates LAP mRNA without showing a substantial increase in the rate of transcription of the LAP gene. Once increased by G-CSF, LAP mRNA is very stable, showing a half-life of more than 4 hours in the presence of actinomycin-D. G-CSF is suggested to play a pivotal role in the modulation of LAP transcript in PMNs.
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PMID:Expression of leukocyte alkaline phosphatase gene in normal and leukemic cells: regulation of the transcript by granulocyte colony-stimulating factor. 170 29

We report two cases of primary gastric mantle zone lymphoma. Histologic examination revealed numerous lymphoid vague nodules in the mucosa and submucosa of the resected stomach. The neoplastic cells in these nodules were slightly larger than small lymphocytes and had more or less cleaved nuclei. Immunostaining on paraffin-embedded sections showed that the neoplastic cells in the nodules of these cases were LN-1- and LN-2+ and had monotypic immunoglobulin (IgM-lambda and IgM-kappa, respectively). Immunostaining on frozen tissue specimens showed that the neoplastic cells or nodules were positive for surface IgM, surface IgD, alkaline phosphatase, and DRC-1. One third to two thirds of the cells were Leu-1+ (CD5+). These results indicated that these cases were primary gastric mantle zone lymphoma. More attention should be paid to primary gastric mantle zone lymphoma because this disease might be erroneously diagnosed as either pseudolymphoma or reactive lymphoid hyperplasia of the stomach.
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PMID:Primary gastric mantle zone lymphoma. A report of two cases. 171 Jan 4

We have shown previously that cytoplasmic extracts from actively dividing lymphoid cells are capable of inducing DNA synthesis in isolated nuclei. One of the factors involved in this activity, ADR, appears to be a greater than 90 kDa heat-labile protease. Cytoplasmic extracts prepared from nonproliferating lymphocytes express little to no ADR activity. However, ADR activity can be generated in these extracts by brief exposure to a membrane-enriched fraction of spontaneously proliferating, leukemic human T lymphoblastoid (MOLT-4) cells. This suggests that ADR activity is present in the resting cytoplasm in an inactive or precursor form. This in vitro generation of ADR activity can be inhibited in a dose-dependent manner by the isoquinolinesulfonamide derivative, H-7 (1-(5-isoquinoline-sulfonyl)-2-methylpiperazine dihydrochloride), an inhibitor of both cyclic adenosine monophosphate (cAMP)-dependent protein kinases and protein kinase C (PKC). However, more specific inhibitors of cAMP-dependent protein kinases, including N-[( 2-methylamino)ethyl]-5-isoquinolinesulfonamide dihydrochloride (H8) and N-(2-gua-nidinoethyl)-5-isoquinolinesulfonamide (HA-1004), had little to no effect on the in vitro generation of ADR activity. Furthermore, membranes from MOLT-4 cells depleted of PKC by long-term exposure (24 h) to phorbol esters and calcium ionophores were unable to induce ADR activity in resting peripheral blood lymphocytes extracts. The results of these studies suggest 1) ADR activity is present in resting cell cytoplasm in an inactive or precursor form; and 2) ADR activity can be induced in this resting cytoplasm through a mechanism involving a membrane-associated protein kinase, possibly PKC. The ability of alkaline phosphatase to deplete the activity of preformed ADR suggests the possibility that ADR itself is phosphoprotein.
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PMID:Induction of a cytoplasmic activator of DNA synthesis in lymphocytes is mediated through a membrane-associated protein kinase. 172 28

Chronic graft-versus-host reaction (GVHR) due to male specific (H-Y) antigen was induced by the injection of syngeneic (DA x Lewis) F1 female cells into (DA x Lewis)F1 male rats. Chronic host-versus-graft reaction (HVGR) based on major histocompatibility complex (MHC) (RT1a) occurred when host Lewis (RT1(1)) rats were transplanted (DA x Lewis)F1 donor cells (RT1a & RT1I). Chronic GVHR and HVGR were activated at fixed periods. The first attacks of the GVHR and HVGR were recognized 50-80 days after cell transplantation, but the most intensive attacks of both responses were observed 120-175 days after cell transplantation. During the most intensive attacks, two rats died from either GVHR or HVGR. Rat immunoglobulin assays measured by radial immunodiffusion (RID) showed that serum IgG2b rose to 10.600-11.500 mg/ml in the rats that had the advanced GVHR or HVGR. The tissue mast cells derived from the loose lymphoid tissues of the medullary and subcapsular sinuses have proliferated in the mesenteric lymph nodes of the rats. IgM and IgG1 binding Fc receptors expressed on the mast cells were demonstrated indirectly using alkaline phosphatase conjugated ant-rat IgM and anti-rat IgG1.
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PMID:Increased serum IgG2b and IgM & IgG1 Fc receptors expressed on tissue mast cells in experimental GVHR and HVGR rat models. 179 38

The association of alkaline phosphatase (ALPase) with the cytoskeleton in lymphoid cells was investigated. Extracting cells with non-ionic detergents such as Triton, we determined that ALPase is present in the cytoskeletal fraction in fully differentiated B lymphocytes, X63 myeloma cells and Sp2/O hybridoma cells. During the course of B-lymphocyte activation, the ALPase shifted from a soluble to a Triton-insoluble form. Changes in the phosphorylation of Triton-insoluble proteins with molecular weights of 120, 100, 90, 75, 34 and 31 kDa were detected, coinciding with the appearance of the ALPase in this fraction. The possible role of ALPase in the differentiation of B cells is discussed.
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PMID:Translocation of alkaline phosphatase during the activation of B cells. 186 87

Recent evidence suggests that nodular lymphocyte predominance Hodgkin's disease (NLPHD) is a distinct entity that may be related to progressively transformed germinal centers, abnormal B-lymphoid hyperplasia, and low-grade B-cell lymphoma. bcl-2 is a marker for the translocation t(14;18)(q32;q21), which occurs in most follicular-derived B-cell lymphomas. Eleven cases of NLPHD and 19 cases of Hodgkin's disease of nodular sclerosis (NSHD) and mixed cellularity (MCHD) type were analyzed for immunoglobulin JH gene rearrangement. bcl-2 translocation was determined with Southern blot analysis and the polymerase chain reaction using biotin labeled probes to the major breakpoint region and the alkaline phosphatase reaction. All cases of NLPHD were negative for JH gene rearrangement and bcl-2 translocation. Cases of NSHD and MCHD were similarly negative for bcl-2, although three cases exhibited clonal JH gene rearrangements. These results confirm that a clonal B-cell population is not detected in NLPHD. Cases of NLPHD differ from most low-grade follicular B-cell lymphomas in that they lack bcl-2 gene rearrangement and t(14;18) translocation at the major breakpoint region.
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PMID:Absence of bcl-2 major breakpoint region and JH gene rearrangement in lymphocyte predominance Hodgkin's disease. Results of Southern blot analysis and polymerase chain reaction. 189 39

The determination of immunoglobulin light chain restriction using monoclonal and polyclonal antibodies is a rapid method for the detection of a neoplastic B-cell-population. Cytocentrifuge preparates of mononuclear blood cells from 42 patients with chronic B-lymphoid leukaemia and of lymph node aspirates from 24 patients with B-non-Hodgkin's lymphoma were examined using the alkaline phosphatase-antialkaline phosphatase (APAAP) method. Monoclonal antibodies from different commercial sources and rabbit polyclonal antibodies were used in this study. Staining with polyclonal antibodies demonstrated light chain restriction in 65 cases. The leukaemic cells of a patient with hairy cell leukaemia did not express light chain immunoglobulins. Monoclonal antibodies from two manufacturers demonstrated monotypic staining for light chains in all cases with light chain immunoglobulins. Monoclonal antibodies from four manufactures failed to show monotypic light chains in 5, 21, 25 and 28 of the 65 cases. All investigated antibodies detected a similar percentage of light chain-positive lymphocytes in 10 healthy persons. We conclude that not all investigated monoclonal antibodies are suitable for detection of light chain restriction in B-non-Hodgkin's lymphomas and chronic B-lymphoid leukaemias. However, using selected monoclonal antibodies or rabbit polyclonal antibodies the APAAP method is very sensitive for detection of light chain restriction in these disorders.
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PMID:Detection of light chain restriction in chronic B-lymphoid leukaemia and B-non-Hodgkin's lymphoma. 190 3

The aim of the present study was to compare the immunofluorescence technique (IF) with the immunoenzymatic (IE) alkaline phosphatase-antialkaline phosphatase method for the evaluation of the presence of lymphoid antigens (Ag) in 46 cases of acute myeloid leukemia (AML). The first technique allows detection of Ag expressed on the cytoplasmic membrane of living cells, whilst the second shows the presence of intracytoplasmic Ag on fixed cells. In general, the percentages of lymphoid Ag expression on AML cells are relatively low with both IE (15.2%) and IF (17.4%). We found a good correlation between the two methods for CD2 (4/4), CD7 (4/5), CD20 (1/1) and CD4 (2/2). The Ag CD19, CD21 and CD8 were negative in all cases, both with IE and with IF. CD3 (2 cases) and CD22 (1 case) were only evident with IE. CD10 was seen in 1 case with IF, whilst it was found more frequently with IE. For this reason, demonstration of CD10 with IF is more specific for the classification of acute leukemia.
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PMID:Incidence of lymphoid markers in acute myeloid leukemia. Alkaline phosphatase-antialkaline phosphatase versus immunofluorescence. 195 Mar 56

2-Mercaptobenzimidazole (2-MBI), used in rubber processing, is a suspect carcinogen structurally related to ethylene thiourea. The inhalation toxicity of 2-MBI was evaluated in male and female F344/N rats exposed 6 hr/day, 5 days/week to respirable aerosols generated by spray atomization of aqueous suspensions of the 2-MBI powder and subsequent drying of the resulting aerosols. Twelve exposures at target concentrations of 0, 6.3, 12.5, 25.0, 50.0, or 100 mg/m3 of 2-MBI produced a dose-related reduction in body weight gains, thyroid follicular cell hyperplasia, adrenal cortex fatty change, and pituitary atrophy. Sub-chronic exposures were conducted at target concentrations of 0, 3.1, 6.2, 12.5, 25.0, and 50.0 mg/m3 of 2-MBI. Rats at greater than or equal to 25 mg/m3 displayed hunched posture, hypoactivity, and reduced body weight gain, with compound related mortality at the highest exposure level. Anemia; increased SGPT, SGOT, alkaline phosphatase, sorbitol dehydrogenase, BUN, and cholesterol; and reduced free fatty acid were seen in rats at greater than or equal to 25 mg/m3. Increased thyroid weight and thyroid follicular cell hyperplasia were noted in both sexes at greater than or equal to 6.2 mg/m3, with reduced triiodothyronine and thyroxine levels in both sexes at greater than or equal to 12.5 mg/m3. Thyroid follicular cell hyperplasia was also seen in rats at 3.1 mg/m3. Thymus weights were significantly reduced in both sexes at all exposure levels with liver weight increases at greater than or equal to 6.2 mg/m3. Exposure-related histopathologic changes included pituitary cytoplasmic vacuolization, adrenal cortex necrosis, lymphoid depletion, thymic atrophy, liver cell hypertrophy, renal mineralization and tubular atrophy, and hypocellularity of the bone marrow.
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PMID:Prechronic inhalation toxicity studies of 2-mercaptobenzimidazole (2-MBI) in F344/N rats. 201 41

Reactive leukocytosis has been reported in patients with non-Hodgkin's lymphoma of different histologic types. On the other hand, the blastic crisis of chronic myelocytic leukemia (CML) can sometimes be localized outside the bone marrow and simulate lymphoma, particularly when the blasts are of lymphoid lineage and the blastic crisis is the presenting feature of the disease. We report two patients in whom the differential diagnosis between lymphoblastic lymphoma with reactive leukocytosis and blastic crisis of CML outside the bone marrow was raised. They were two males aged 32 and 22 years, respectively, with lymphadenopathy (and one with splenomegaly), who were initially diagnosed of T lymphoblastic lymphoma. In both cases, leukocytosis was detected with myelemia and dysgranulopoiesis in the onset in one of them and when lymphadenopathy reappeared after remission in the other one. In addition, one patient had marked eosinophilia. In the bone marrow there was marked granulopoietic hyperplasia, with a reduction of fatty cells, and the granulocyte alkaline phosphatase index was reduced. However, the cytogenetic study did not disclose the existence of Philadelphia (Ph) chromosome, and bcr/abl molecular rearrangement was also not observed in the molecular study of both cases. We discuss the basic aspects of differential diagnosis between T lymphoblastic lymphoma with leukemoid reaction and T lymphoid lymphadenopathic blastic crisis of Ph-negative, bcr/abl-negative CML.
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PMID:[T lymphoblastic leukemia with leukemoid reaction or the extramedullary blast crisis of Philadelphia chromosome-negative chronic myeloid leukemia? Comments apropos 2 cases]. 209 54


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