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:1.11.1.7 (peroxidase)
65,474 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Polar solvents induce terminal differentiation in the human promyelocytic leukemia cell line HL-60. The present studies describe the functional changes that accompany the morphologic progression from promyelocytes to bands and poly-morphonuclear leukocytes (PMN) over 9 d of culture in 1.3 percent dimethylsulfoxide (DMSO). As the HL-60 cells mature, the rate of O(2-) production increase 18-fold, with a progressive shortening of the lag time required for activation. Hexosemonophosphate shunt activity rises concomitantly. Ingestin of paraffin oil droplets opsonized with complement or Ig increases 10-fold over 9 d in DMSO. Latex ingestion per cell by each morphologic type does not change significantly, but total latex ingestion by groups of cells increases with the rise in the proportion of mature cells with greater ingestion capacities. Degranulation, as measured by release of beta-glucuronidase, lysozyme, and peroxidase, reaches maximum after 3-6 d in DMSO, then declines. HL-60 cells contain no detectable lactoferrin, suggesting that their secondary granules are absent or defective. However, they kill staphylococci by day 6 in DMSO. Morphologically immature cells (days 1-3 in DMSO) are capable of O(2-) generation, hexosemonophosphate shunt activity, ingestion, degranulation, and bacterial killing. Maximal performance of each function by cells incubated in DMSO for longer periods of time is 50-100 percent that of normal PMN. DMSO- induced differentiation of HL-60 cells is a promising model for myeloid development.
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PMID:Functional changes in human leukemic cell line HL-60. A model for myeloid differentiation. 22 36

Ten cases of acute granulocytic leukemia with blast cells containing Auer bodies (ABs) have been studied by electron microscopy after cytochemical demonstration of myeloperoxidase. The cytochemical dense reaction product has been used as a dark field to visualize unreactive protein of ABs which may then be easily identified by its negative contrast. This method has allowed us to identify three types of ABs which differ in their substructure. In type I, (five patients with promyelocytic leukemia), our study confirmed that all of the ABs consisted of a hexagonal arrangement of hollow tubes. Cells from four cases of acute myeloblastic leukemia displayed type II ABs, in which a unique pattern of protein associated in a regular linear arrangement with well defined periodicity was identified. Type III appeared characteristic of a subclass of acute myeloblastic leukemia in which large inclusions with Chediak-Higashi-like granules containing numerous micro-ABs were seen. The configuration, size, and organization of the protein in the crystal were distinct from those seen in the two other types of ABs. These features suggest that the nature of the protein in ABs may be heterogeneous.
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PMID:Three types of Auer bodies in acute leukemia. Visualization of their protein by negative contrast after peroxidase cytochemistry. 22 15

We studied the effect of hematopoietic growth factors (granulocyte-macrophage colony-stimulating factor [GM-CSF], granulocyte [G]-CSF, interleukin (IL)-1, IL-3, IL-5, IL-6, and macrophage [M]-CSF) on differentiation and functional activity of human eosinophilic HL-60 cells (Eos-HL-60) and compared them with effects on parental HL-60 promyelocytic leukemia cells. Purified biosynthetic GM-CSF and IL-5 enhanced cell proliferation and induced eosinophilic differentiation in the eosinophilic subline in both liquid and agar cultures. IL-3 and IL-6 stimulated cell proliferation but had no effect on cell differentiation, whereas IL-1 and G-CSF affected neither differentiation nor proliferation of Eos-HL-60 cells under the conditions tested. GM-CSF-, IL-3-, and IL-5-treated Eos-HL-60 cells showed increased O2- production in response to phorbol esters (PMA), enhanced phagocytosis of Candida albicans, and release of the enzymes arylsulfatase, beta-glucuronidase and eosinophil peroxidase (EPO). The degranulation of eosinophils induced by GM-CSF, IL-5, and IL-3 may have relevance to the potential clinical toxicity of these hematopoietins, which also stimulate eosinophilopoiesis. G-CSF had no effect on enzyme release, oxidative metabolism, or phagocytic capacity of Eos-HL-60 cells. IL-5 did not affect proliferation, differentiation, or enzyme release in promyelocytic HL-60 cells. These results indicate the specificity of IL-5 for the eosinophil lineage, confirm the effects of GM-CSF and IL-3 on eosinophilopoiesis and mature eosinophil function in a model system, and indicate the absence of G-CSF and IL-1 stimulation of eosinophils. The Eos-HL-60 line is a useful model for studying human eosinophil responses to cytokines.
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PMID:Differentiation and functional activity of human eosinophilic cells from an eosinophil HL-60 subline: response to recombinant hematopoietic growth factors. 137 88

Leukemic cells from acute promyelocytic leukemia containing pseudo-Chediak-Higashi (P-CH) granules in a 38-year-woman were studied with ultrastructural and cytochemical techniques to evaluate the origin and nature of the granules. Wright-Giemsa stain revealed giant granules to be azurophilic. Cytochemical stain revealed p-CH granules ot the basic of their peroxidase and glycoprotein content. Electron microscopy revealed numerous giant granules formed by fusion of azurophilic granules these morphological, different type granules were classified into four types, 1) circular granule with homogeneous matrix, 2) circular granule with heterogeneous change by autolysis, 3) Auer body-like granule with crystalline arrangement, 4) vacuolar formation. The results demonstrate that the Auer body-like granule of P-CH granules in leukemic cells is a morphologically variant type of the classical Auer body observed in common acute myeloid leukemia.
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PMID:[Studies on pseudo-Chediak-Higashi granules formation in acute promyelocytic leukemia]. 140 62

The mechanism by which a clone of HL-60 human promyelocytic leukemia cells designated Tf-Gel-1 expresses reduced levels of the transferrin receptor (TfR) was investigated. Tf-Gel-1 was developed by continuous exposure of HL-60 cells to human iron-saturated transferrin covalently linked to the plant toxin gelonin (Tf-Gel); this variant was five- to sixfold more resistant to Tf-Gel than parental HL-60 cells. The amount of cell surface, as well as of solubilized, TfR and the cycling pools of TfR in Tf-Gel-1 cells, as measured by the binding of [125I]Tf, were all decreased to 20-30% of the levels present in parental cells. The growth of Tf-Gel-1 cells was independent of exogenous Fe3+ and was comparable to that of parental HL-60 cells. Despite the lower levels of TfRs, the Tf-Gel-1 clone retained the capacity to alter receptor expression, depending upon the phase of growth and the intracellular iron concentration, and to down-regulate TfRs in response to inducers of differentiation. Southern hybridization of cellular DNA with TfR cDNA did not reveal differences between parental and Tf-Gel-1 cells in the level and arrangement of the TfR gene. Basal and inducible (repressible) levels of TfR mRNA from Tf-Gel-1 cells, as measured by northern hybridization of cellular RNA with TfR cDNA, were comparable to those of parental cells. Metabolic labeling of cells with [35S]methionine, followed by immunoprecipitation of TfRs, demonstrated that the amount of radioactivity incorporated into TfRs in Tf-Gel-1 cells was reduced to a degree that approximated the decrease in [125I]Tf binding. Cell surface TfRs prepared from exponentially growing parental cells labeled with 125I by the solid-phase lactoperoxidase-glucose oxidase method existed as a doublet, with one form being phosphorylated and the other not phosphorylated. In contrast, Tf-Gel-1 cells not only contained diminished amounts of TfRs but also contained only the phosphorylated form of TfRs in the surface membrane. The decrease in the surface membrane concentration of the TfR in Tf-Gel-1 cells was specific for this glycoprotein, since the levels of other cell surface antigens, such as CD13, CD15 and CD45, were normal in Tf-Gel-1 cells. A reduction in the incorporation of [3H]mannose into the acid-insoluble fraction of cells and an increase in sensitivity to ricin suggested that Tf-Gel-1 cells possessed an aberration in carbohydrate metabolism.
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PMID:Characterization of the defect in a variant of HL-60 promyelocytic leukemia cells with reduced transferrin receptor expression. 154 69

Human neutrophil elastase (NE), a 29-Kd potent serine protease stored in azurophilic granules of mature neutrophils, is coded for by the NE gene, a single copy gene with 5 exons spanning a 6-kb segment of chromosome 11 at q14. With the knowledge that the NE gene expression is limited to early myeloid cell differentiation, mechanisms modulating expression of the NE gene were evaluated in the HL-60 promyelocytic leukemia cell line, a model of early bone marrow precursor cells. Consistent with the presence of NE messenger RNA (mRNA) transcripts in undifferentiated HL-60 cells, nuclear transcription run-on analyses showed that HL-60 cells actively transcribed the NE gene. However, the transcription rate of the NE gene was relatively low, only 40% of the myeloperoxidase gene, a gene expressed in parallel with NE. When induced toward the mononuclear phagocytic lineage with phorbol 12-myristate 13-acetate (PMA), HL-60 cells exhibited marked suppression of NE gene transcription, declining to 17% of the resting rate within 2 days. Induction toward mononuclear phagocytic lineage differentiation caused no change in NE mRNA transcript half-life (T1/2), but mRNA levels decreased markedly over time, with levels undetectable 1.5 days after PMA stimulation. In contrast, when induced toward the myelocytic lineage with dimethyl sulfoxide, the rate of NE gene transcription increased 1.9-fold within 5 days. Interestingly, the mRNA transcript levels increased 2.5-fold by 5 days despite the fact that induction toward myelocytic lineage differentiation was accompanied by a marked reduction of NE mRNA transcript T1/2. Together, these observations suggest that the NE gene expression during bone marrow differentiation is modulated mainly at the transcriptional level, with some posttranscriptional modulation contributing, particularly during myelocytic lineage differentiation.
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PMID:Transcriptional and posttranscriptional modulation of human neutrophil elastase gene expression. 158 20

A patient with resistant acute promyelocytic leukemia was treated with all-trans-retinoic acid (45 mg/m2 per day for 42 days) and obtained complete remission at day 14. Analysis of the neutrophils from the patient at day 7 demonstrated that they were indistinguishable from neutrophils from normal individuals as far as this is assessed by presently available functional tests. Furthermore, the degree of peroxidase positivity of neutrophils obtained from the patient was similar to control values. Thus, taken together with the hematologic features, all-trans-retinoic acid induces leukemic promyelocytes to become functionally normal neutrophils. This therapy is particularly suitable in obtaining complete remission in patients with acute promyelocytic leukemia with neutropenia with or without previous chemotherapy.
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PMID:All-trans-retinoic acid induced enrichment of functionally normal neutrophils in vivo in a patient with acute promyelocytic leukemia. 837 99

Cytochemical studies including peroxidase, sudan black B and esterases were used for staining peripheral blood and bone marrow smears from 42 patients with acute promyelocytic leukemia. The most sensitive methods were sudan black B (mean 98%, range 81-100%) and peroxidase (mean 92% range 70-100%). Naphthol AS-D chloroacetate esterase activity was less sensitive and was positive in only 49.4 per cent (range 2-100%). All of the population of leukemic cells contained less than 3 per cent of alpha-naphthyl acetate esterase staining. For stability tests of the storage specimens compared to fresh stains, there was no difference in naphthol AS-D chloroacetate esterase (mean 45% vs 49% P greater than 0.7) and sudan black B (mean 74% vs 98% P greater than 0.3), but the enzyme activity was significantly decreased in peroxidase staining (mean 42% vs 92% P greater than 0.05). When the patients were divided into 2 groups according to the degree of AS-D chloroacetate esterase activity, those with lower activity had a higher number of white blood cells, promyelocytes and shorter survival compared to those with higher activity. Therefore, naphthol AS-D chloroacetate esterase may be useful as a prognostic index.
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PMID:Cytochemical stainings in acute promyelocytic leukemia: chloroacetate esterase reaction as a prognostic index. 164 35

Metabolism of hydrazine derivatives, procarbazine and iproniazid, to reactive free radical intermediates has been studied using spin-trapping techniques in intact human promyelocytic leukemia (HL60) and mouse hepatic cell lines. While HL60 cells have been shown to contain both myeloperoxidase and cytochrome P-450 enzymes, the hepatic cell line shows only cytochrome P-450 activity. Both peroxidases and cytochrome P-450 have been reported to catalyze biotransformation of hydrazines. Procarbazine and iproniazid were rapidly metabolized in these cell lines to methyl and isopropyl radicals, respectively. However, in HL60 cells, procarbazine was metabolized by myeloperoxidase while iproniazid was metabolized mostly by the cytochrome P-450 system. In the hepatic cells, both of these compounds were metabolized by the P-450 system.
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PMID:Cytochrome P-450- and peroxidase-dependent activation of procarbazine and iproniazid in mammalian cells. 166 71

Human granulocyte colony-stimulating factor (G-CSF) receptors on human acute leukemia cells were investigated using human G-CSF iodolabeled by the lactoperoxidase method. Among various human leukemic cell lines, only cells of myelogenous lineage including HL-60, THP-1 and U937 had one type of high-affinity receptor for G-CSF, as shown by Scatchard analysis. Fresh leukemia cells from 19 patients with acute myelogenous leukemia (AML) were then studied. Specific receptors for G-CSF were demonstrated on blast cells in all 19 cases, the mean number of G-CSF receptors per AML cell ranging from 95 to 1436. G-CSF receptors on AML cells appeared to be a single affinity type, although some variations were observed. The mean number of G-CSF receptors on leukemic cells from patients with either FAB M3 or FAB M2 was greater than that of cells from patients with M1 (p less than 0.01, p less than 0.10, respectively). Moreover, the mean number of receptors for G-CSF on CD13- and CD34-positive AML cells was higher than that on CD13-negative and CD34-positive AML cells (p less than 0.01), and the mean number of G-CSF receptors on CD7-positive AML cells was lower than that for CD7-negative AML cells (p less than 0.10). Since the FAB classification and surface phenotypes reflect maturation stages, our findings indicate that the distribution of G-CSF receptors, even on AML cells, may be related to the maturation process.
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PMID:Human granulocyte colony-stimulating factor receptors in acute myelogenous leukemia. 170 27


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