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)

Stromal cell lines, designated MS-1, -2, -3, -4, -5, -6, and -7 were established by irradiating the adherent cells in long-term bone marrow cultures with 900-rad x-rays. Two of the cell lines, MS-1 and MS-5, have the capacity to support the growth of hemopoietic stem cells (spleen colony-forming cells and granulocyte-macrophage colony-forming cells) for greater than 2 months in vitro. These two cell lines were alkaline phosphatase-, peroxidase-, and factor VIII-negative and positive for periodic acid-Schiff and nonspecific esterase. Extracellular matrix proteins such as fibronectin, laminin, and collagen type I were produced by these two cell lines. Neither MS-1 cell- nor MS-5 cell-conditioned medium supported the growth of hemopoietic stem cells, and hemopoietic stem cells were found preferentially to be under and on MS-1 and MS-5 layers rather than in suspension. Close contact with the MS-1 cell layer or the MS-5 cell layer appears to be essential in maintaining hemopoiesis in vitro. Conditioned media from MS-1 cells and MS-5 cells stimulated granulocyte colony formation from murine bone marrow cells in semisolid culture.
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PMID:Reproducible establishment of hemopoietic supportive stromal cell lines from murine bone marrow. 278 73

A panel of eight antibodies was used by the alkaline-phosphatase/anti-alkaline phosphatase (APAAP) method to stain peripheral blood films, bone marrow smears, and cytocentrifuge preparations from 29 cases of acute myeloid leukemia. These findings were correlated with the French-American-British (FAB) classification. Leukemic cells from six cases of myeloblastic leukemia (FAB;M1) were predominantly labeled by the antimyeloperoxidase monoclonal antibody (MPO-7). Leukemic cells from the majority of eight cases of myeloblastic leukemia with maturation (FAB;M2) and progranulocytic leukemia (FAB;M3) stained with monoclonal antibodies MPO-7, NP57 (anti-elastase), and EBM11 (antimonocyte/macrophage). Leukemic cells from six cases of myelomonocytic (FAB;M4) and five cases of monocytic (FAB;M5) leukemia were most often labeled with antibodies MPO-7, NP57, and EBM11 as well as monoclonal antibodies Y1/82A (anti-monocyte) and KB90 (against the p150, 95 molecule, CD11c; a monocyte/granulocyte marker), but not with monoclonal antibody C17 (antiglycoprotein IIb/IIIa) and/or monoclonal antibody Y2/51 (antiglycoprotein IIIa). Erythroblasts from a single case of erythroleukemia (FAB;M6) were not labeled with any of the antibodies from this panel. Leukemic cells from two cases of acute megakaryocytic leukemia (FAB;M7) stained strongly with the monoclonal antiglycoprotein IIIa/IIb antibody (C17) and antiglycoprotein IIIa antibody (Y2/51). Staining by the APAAP method with this panel of antibodies was easy to perform, required no expensive instrumentation, and provided useful information in the classification of acute myeloid leukemia.
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PMID:Immunophenotyping of acute myeloid leukemia by immuno-alkaline phosphatase (APAAP) labeling with a panel of antibodies. 282 1

Infants with Down's syndrome have an increased incidence of acute nonlymphocytic leukemia (ANLL). They are also at risk of developing a transient myeloproliferative syndrome indistinguishable from ANLL except by its eventual clinical recovery. The authors studied five infants with Down's syndrome and leukocytosis with circulating blast forms in their peripheral blood with in vitro cultures of bone marrow colony forming units-granulocyte macrophage (CFU-GM), cytogenetics and peripheral blood neutrophil alkaline phosphatase (NAP) score. Three children developed ANLL, the other two had a transient myeloproliferative syndrome. The in vitro assay for CFU-GM showed abnormal results consistent with ANLL in the children who develop this disorder. Serial cytogenetic studies disclosed the appearance of an abnormal clone in one patient. A combination of clinical parameter in vitro colony studies and cytogenetic studies in these children was helpful in distinguishing ANLL from a myeloproliferative disorder. The NAP scores were not helpful.
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PMID:Infants with Down's syndrome. Use of cytogenetic studies and in vitro colony assay for granulocyte progenitor to distinguish acute nonlymphocytic leukemia from a transient myeloproliferative disorder. 295 84

High doses of intravenous desferrioxamine infused over a short period of time induce a large faecal and urinary iron excretion but also produce retinal abnormalities that are characterised by decreased amplitude on electroretinography and defective dark adaptation. This regimen also results in high faecal iron, zinc, and copper excretion, and reduced granulocyte zinc concentrations and alkaline phosphatase activity. The retinal abnormalities may be related to the zinc and copper deficiency and/or iron depletion 'per se' which interferes negatively with critical iron dependent enzymes.
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PMID:Depletion of trace elements and acute ocular toxicity induced by desferrioxamine in patients with thalassaemia. 335 4

Mixed leukocyte suspensions were prepared from heparinized blood collected from healthy subjects and from patients with chronic myeloid leukemia (CML). In all the suspensions determinations were made for: zinc, by atomic absorption; granulocyte alkaline phosphatase (GAP), using the method with p-nitrophenylphosphatase; granulocyte LDH, by means of the enzymatic autoanalyser LKD 8,600. In the patients with CML, the values of zinc and of granulocyte alkaline phosphatase activity were very low while the granulocyte LDH values were higher than normal. The chromatogram of the granulocyte LDH isoenzymes on DEAE-Sephadex A50 minicolumn (0.5 X 12 cm) showed an "alpha type abnormality" revealed by the increased activity of the isoenzymes with high electrophoretic mobility LDH2 and LDH1 specific for tissues with intense oxidative phosphorylation. In the normal subjects the chromatogram of the leukocyte LDH isoenzymes showed a type M (skeletal muscle) prevalence denoting intense anaerobic glycolysis. Therefore the low zinc concentrations (0.55 micrograms mg N2 as compared with the normal 1.24 micrograms mg N2) in these patients cause the decrease of GAP activity by the lack of zinc in the active center of the enzyme and the decrease of cellular permeability thus allowing the extracellular release of granulocyte LDH.
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PMID:Study of the relationship between the granulocyte LDH, alkaline phosphatase and Zn at the level of the leukocyte in patients with chronic myeloid leukemia. 346 14

To test the biologic activity of 13-cis retinoic acid (13-CRA) in patients with myelodysplastic states (MDS), we administered 13-CRA orally (2.5 mg/kg/d initially, escalated to 4 mg/kg/d) for 8 weeks to 15 consecutive patients. Eight of 15 patients (53%) experienced an increase in peripheral granulocyte counts of greater than 20% (range, 22% to 700%). In five patients, the absolute increase in peripheral granulocyte count was greater than 500 cells/microL. Two of 15 patients experienced a decrease in the circulating granulocyte count of greater than or equal to 20%. Comparable values for peripheral platelet counts were 27% (4/15 patients) greater than 20% increase and 33% (5/15 patients) greater than 20% decrease. No patient experienced a major change in erythrocyte transfusion requirement while receiving 13-CRA in comparison with pretreatment status. Thirteen patients had morphologic and cytogenetic evaluation of marrow cells before 13-CRA treatment, and with one exception, marrow morphologic and cytogenetic abnormalities persisted following 13-CRA administration. The exception occurred in the patient with the most dramatic response, whose granulocyte count increased from 400 to 2,800 cells/microL along with a normalization of the leukocyte alkaline phosphatase score, a morphologic improvement in granulocyte maturation, and a disappearance of the initial chromosome abnormality. These changes did not persist after cessation of 13-CRA administration, but were reproduced following drug readministration. No patients experienced serious decrements in peripheral blood counts or leukemic transformation while receiving 13-CRA. All patients had mild to marked dermatologic toxicity (cheilosis, skin dryness). No other major toxicity was encountered. We conclude that 13-CRA may be safely administered and may increase peripheral granulocyte counts in a proportion of patients with MDS.
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PMID:13-cis retinoic acid treatment for myelodysplastic syndromes. 351 7

Three hundred twenty-five previously untreated patients with chronic lymphocytic leukemia were analyzed to identify significant prognostic factors for survival. Univariate analysis identified the following characteristics associated with survival: (1) clinical characteristics: age, race, sex, performance status, lymphadenopathy, and hepatosplenomegaly; (2) hematologic parameters: WBC count, absolute lymphocyte and granulocyte counts, hemoglobin level, and platelet count; and (3) biochemical parameters: serum albumin, calcium, uric acid, lactate dehydrogenase, alkaline phosphatase, BUN, and creatinine. Multivariate regression analysis in a randomly selected training subset of 217 patients demonstrated that the combination of uric acid, alkaline phosphatase, lactate dehydrogenase, external lymphadenopathy, and age had the strongest predictive relation to survival time. The resulting model was validated in the remaining independent subset of 108 patients and led to classification of patients into low, intermediate, and high-risk groups with five-year survival rates of 75%, 59%, and 14%, respectively, and with distinctively different annual mortality rates (P less than .01). Both the regression model and Rai staging were highly effective in identifying risk groups among the entire patient population (P less than 0.001). Overall the regression model was superior to Rai staging in defining prognostic risk groups. In addition, it was able to separate patients into significantly different risk categories within each Rai stage, thus improving on the prognostic prediction of individual patients with chronic lymphocytic leukemia.
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PMID:Prognosis of chronic lymphocytic leukemia: a multivariate regression analysis of 325 untreated patients. 381 21

Leukocyte alkaline phosphatase (LAP) is a granulocyte enzyme whose level of expression is markedly altered in various disease states. We have characterized LAP from normal cells and leukemic cells with a high level of LAP activity in order to determine whether increased enzyme levels are caused by increased levels of the same enzyme or induction of a different alkaline phosphatase. Leukocyte alkaline phosphatase was purified from normal granulocytes and from leukemic cells of a patient with chronic granulocytic leukemia (CGL) in blast phase with an elevated LAP level. LAP was partially purified utilizing diethylaminoethyl (DEAE)-cellulose ion exchange chromatography, gel filtration, and preparative electrophoresis. The sample prepared from normal granulocytes contained a single protein with LAP activity having a molecular weight of 61,000 as determined by SDS gel electrophoresis. The sample from the CGL blast-phase cells, however, demonstrated two proteins with alkaline phosphatase activity, one with a molecular weight of 61,000 (LAPs) and one with a molecular weight of 45,000 (LAPf). Differential heat inactivation and distinct isoelectric points of the two isozymes suggest that they are different proteins. We interpret our data to suggest two closely related LAP alleles whose expression is controlled independently. This may represent either genetic heterogeneity or induction of "tumor marker" gene expression.
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PMID:Evidence for two isozymes of leukocyte alkaline phosphatase in leukemic leukocytes. 385 98

Normal human granulocytes obtained by Ficoll-Hypaque sedimentation were subjected to mild hypotonic shock and disruption by shear. The homogenate was fractionated by differential centrifugation and equilibrium ultracentrifugation to yield a plasma membrane preparation constituting 1% of the total cellular protein and enriched fifteen- and six-fold in alkaline phosphatase and Mg2+-adenosine triphosphatase activities, respectively. Granulocytes obtained from patients with chronic myeloid leukemia (CML) were identically processed. The protein constituents of both the normal and CML granulocyte plasma membranes were resolved by two-dimensional polyacrylamide gel electrophoresis. Comparison of the stained gels revealed CML-associated quantitative changes in four out of the fifteen protein spots examined. Thus, this analysis has permitted identification of those protein moieties that deserve attention for further isolation and purification.
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PMID:Plasma membranes from normal and chronic myeloid leukemic granulocytes: isolation and two-dimensional polyacrylamide gel electrophoretic analysis. 385 66

A 38-year-old woman developed chronic myeloid leukaemia after 2 years of lithium carbonate therapy. A peculiar feature of her leukaemia, as well as of the 5 patients previously reported in whom CML has developed in the course of lithium therapy, was the unusually high degree of granulocyte maturation manifested in normal leucocyte alkaline phosphatase (LAP) score and, in 1 case, selective increase of transcobalamin III. Although a cause and effect relation between lithium therapy and CML has not yet been established, in view of the stimulatory effect of lithium on granulocyte proliferation, such treatment should be avoided in patients with established myeloproliferative disorders, or in patients at high risk of developing leukaemia.
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PMID:Increased leucocyte alkaline phosphatase and transcobalamin III in chronic myeloid leukaemia associated with lithium therapy. 385 3


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