Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Changes in the production of reactive oxygen species and total superoxide dismutase activity have been observed during differentiation of some hematopoietic cells. We therefore investigated whether the steady-state level and rate of transcription of superoxide dismutase-1 (SOD-1) mRNA change during terminal differentiation of the human leukemia cell lines THP-1, HEL, and HL-60 into macrophages and/or granulocytes, respectively. Macrophage differentiation is accompanied by a gradual decrease in both the transcription rate (10x) and the steady-state level (6x) of SOD-1 mRNA. No decrease was observed after treatment with the diacylglycerol analog 1,2 dioctanol-rac-glycerol (di-C8), which like phorbol 12-myristate 13-acetate also activates protein kinase C but does not induce differentiation at the concentration used. The same decrease in SOD-1 mRNA level was observed when HL-60 cells were induced to differentiate into granulocytes by treatment with dimethylsulfoxide. These data suggest that a decrease in SOD-1 mRNA to almost undetectable levels accompanies differentiation of macrophages and granulocytes.
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PMID:Loss of copper-zinc superoxide dismutase gene expression in differentiated cells of myelo-monocytic origin. 279 Feb 4

Herbimycin A, a benzoquinonoid ansamycin antibiotic, is found to reduce intracellular phosphorylation by tyrosine protein kinase. The human chronic myelogenous leukemia cell line K562 expresses a structurally altered c-abl protein with tyrosine kinase activity. When K562 cells are induced to undergo erythroid differentiation by hemin, reduction in the intracellular level of tyrosine phosphorylation occurs. In order to understand the relationship between induction of differentiation and reduction of tyrosine phosphorylation by the c-abl gene product, the effect that herbimycin A, a selective inhibitor of intracellular tyrosine kinase activity, exerts on the differentiation of K562 cells was examined. Reduction of tyrosine phosphorylation in K562 cells by herbimycin A was observed within 1 h. Noncytotoxic concentrations of herbimycin A induced erythroid differentiation of K562 cells but not of murine erythroleukemia 745A cells. The other human myeloid leukemia cell lines (HL-60, THP-1, and U937) tested were not induced to undergo cell differentiation by this antibiotic. Herbimycin A and the other well-known inducers such as hemin, butyric acid, Adriamycin, and 1-beta-D-arabinofuranosylcytosine had additive or more than additive effects on induction of erythroid differentiation of K562 cells. With respect to inhibition of cell growth, the sensitivity of K562 cells to herbimycin A was highest in the human leukemia cell lines we tested. Noncytotoxic concentrations of herbimycin enhanced the antiproliferative effect of Adriamycin or 1-beta-D-arabinofuranosylcytosine on K562 cells. Combination therapy with herbimycin A and its derivatives may be considered for use in the treatment of some types of leukemia where tyrosine kinase activities are implicated as determinants of the oncogenic state.
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PMID:Induction of erythroid differentiation of K562 human leukemic cells by herbimycin A, an inhibitor of tyrosine kinase activity. 291 Apr 52

The human leukemia cell lines HL-60, KG-1, KLM-2, ML-3, THP-1, and U-937 were treated with the phorbol ester 12-O-tetradecanoylphorbol 13-acetate (TPA). TPA partially or completely inhibited the proliferative activity of the cell cultures. The number of cells with the ability to reduce nitroblue tetrazolium increased in the TPA-treated cell lines HL-60, ML-3, THP-1, and U-937, whereas the cell lines KG-1 and KLM-2 remained nitroblue tetrazolium negative. Except for KG-1 and KLM-2, all TPA-treated cell lines showed varying degrees of strong adherence to plastic surface. The carboxylic esterase, acid phosphatase, hexosaminidase, and lactate dehydrogenase isoenzyme profiles from these cell lines were analyzed by isoelectric focusing on horizontal polyacrylamide gels. The new or stronger expression of an esterase isoenzyme which is specific for monocytes-macrophages was induced in HL-60, ML-3, THP-1, and U-937 but not in KG-1 or KLM-2. The new expression of the tartrate-resistant acid phosphatase isoenzyme was induced in ML-3, THP-1, and U-937. The number of esterase and acid phosphatase isoenzymes and the staining intensity of isoenzymes characteristic for myeloid cells were increased by TPA in all cell lines. The loss of the hexosaminidase I isoenzyme which is a marker of immature hematopoietic cells was noted in KG-1, ML-3, THP-1, and U-937. TPA triggered an increase in number and staining intensity of the lactate dehydrogenase isoenzymes in all cell lines. Some isoenzymatic changes (e.g., monocyte-specific esterase, tartrate-resistant acid phosphatase, hexosaminidase I) appear to correlate with TPA-induced differentiation while other alterations in the isoenzyme patterns do not (e.g., lactate dehydrogenase, other esterase and acid phosphatase isoenzymes). Differentiation of nonmonocytoid cells appears, at the isoenzyme level, to be quite different from that of the monocytoid cell lines.
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PMID:Changes in isoenzyme profiles during induction of differentiation in human myelomonocytic leukemia cell lines. 294

We describe the isolation of human fibronectin receptors (integrins) from two nonadherent promonocytic cell lines and from peripheral blood monocytes. Integrins purified from U-937 and THP-1 cells exhibited identical electrophoretic migrations on sodium dodecyl sulfate gels run under reducing (approximately Mr 150,000) and nonreducing (alpha, Mr 160,000; beta, Mr 130,000) conditions. Treatment of U-937 or THP-1 cells with phorbol esters induced these cells to express different integrins with electrophoretic mobilities (alpha, Mr 140,000; beta, Mr 115,000, nonreduced) identical to those from normal human peripheral blood monocytes. Receptors isolated from uninduced, nonadherent promonocytic leukemia cells (U-937 and THP-1) were distinct from glycoproteins IIb and IIIa and from leukocyte adhesion molecules (p150/95). However, receptors isolated here did react with an antibody known to block cell adhesion to fibronectin. The differences observed in apparent molecular masses of fibronectin receptors from uninduced and induced U-937 or THP-1 cells are removed by treatment of purified integrins with endoglycosidase F or N-glycanase. In summary, the data presented here demonstrate the purification of integrins by fibronectin affinity chromatography from human leukemia cells and normal peripheral blood monocytes. Our results suggest that these receptors differ in immature and mature monocytic cells, and are altered by glycosylation in the course of cellular maturation.
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PMID:Alteration of fibronectin receptors (integrins) in phorbol ester-treated human promonocytic leukemia cells. 297 31

The regulation of IgG Fc receptor (Fc gamma R) expression by retinoic acid (RA) in human myelomonocytic cells at different stages of maturation was studied. RA suppressed IgG-coated erythrocyte (EA) rosette formation of myelomonocytic cells blocked at relatively late stages of differentiation such as ML-1, U-937, THP-1-T, normal monocytes, and fresh cells of patients with acute myelomonocytic leukemia. However, RA increased the percentage of EA rosetting promyelocytes of HL-60 and of patients with acute promyelocytic leukemia and a part of myeloblasts isolated from acute myelogenous leukemia patients. Other myeloblasts including KG-1a, KG-1, and fresh cells from patients with acute myelogenous leukemia were not affected. A kinetic study using HL-60 and THP-1-T demonstrated that an increase required at least a 48-h exposure and that the maximum decrease required approximately 6 h. The RA effect on both cell lines was dose-dependent. The number of Fc gamma R of HL-60 and THP-1-T treated with RA became very close, although untreated THP-1 had almost 10 times as many as HL-60. Kd for IgG in both THP-1-T and HL-60, either untreated or treated with RA, remained unchanged. These observations indicate that one of the important roles of RA is regulation of Fc gamma R expression in myeloid cells.
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PMID:Retinoic acid regulates IgG Fc receptor expression in human myelomonocytic leukemia cells and normal peripheral monocytes. 297 58

A monoclonal antibody, TM316, IgM kappa, was raised against the human monocytoid leukaemia cell line THP-1, and was shown to inhibit polymorphonuclear leucocyte (PMN) chemotaxis. The molecular weight (MW) of the protein on the PMN membrane with which TM316 bound was about 78,000. TM316 inhibited the chemotactic response of human PMN induced by at least three kinds of chemotactic factors (activated serum, N-formyl-L-methionyl-L-leucyl-L-phenylalanine (FMLP), and a lymphocyte-derived chemotactic factor (LDCF)) to the same extent. The extent of inhibition of chemotaxis by TM316 was strongly correlated with the quantity of cellular surface antigen recognized by TM316, when a cell sorter was used for analysis. TM316 did not alter the number of Fc or complement receptors of PMN, nor did it affect luminol-enhanced chemiluminescence (CL), lysosomal enzyme release, adherence, or superoxide anion generation by PMN. TM316 seemed to recognize a common surface antigen which was necessary only for the process of chemotaxis.
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PMID:Inhibition of neutrophil chemotaxis by a monoclonal antibody (TM316). 306 89

Mouse monocytic Mm-A cell line is a highly leukemogenic variant cell line of the monocytic and non-leukemogenic Mm-1 cell line, which developed spontaneously from mouse myeloid leukemia M1 cells. Growth-inhibitory factor (GI factor) for Mm-A cells was found in conditioned medium (CM) of differentiation inducer-resistant myeloblastic M1 cells (clone R-1). The R-1 cells were cultured with or without 2% calf serum for 2 days, and the CM was fractionated with 50% ammonium sulfate and used as the GI factor preparation (termed R1CM). When Mm-A cells were cultured with 5% (v/v) R1CM for 3 days, their growth was inhibited about 80%. This inhibition of Mm-A cell growth by R1CM was irreversible. This GI factor also inhibited the growth of M1 cells that had been pretreated with inducer and had expressed some differentiation-associated properties but still retained a proliferative capacity. In contrast, it scarcely inhibited the growth of untreated M1 cells. The GI factor inhibited the growth of other mouse monomyeloblastic leukemic WEHI-3B D+ cells pretreated with a differentiation inducer, retinoic acid, and mouse monocytic leukemia J774.1 cells. However, it did not affect the growth of human monocytic (U937 and THP-1) or myeloid (KG-1, ML-1, and HL-60) cell lines. These results suggest that GI factor produced by parent myeloblastic and inducer-resistant M1 cells preferentially inhibits the growth of mouse monocytic leukemia cells in intermediate stages of differentiation from myeloblastic leukemia cells to mature macrophages.
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PMID:Production by undifferentiated myeloid leukemia cells of a novel growth-inhibitory factor(s) for partially differentiated myeloid leukemic cells. 311 48

THP-1 is an acute monocytic leukemia cell line which acquires phenotypic and functional monocytoid-like features following incubation with mezerein. The current study concerned the modulation of these features by rIFN gamma. rIFN gamma induces the time-dependent enhancement of HLA-DR expression in the presence or absence of mezerein but has no effect on the expression of Leu-M1, Leu-M2, or Leu-M3 antigens. CSF-1 production following mezerein activation was reduced by incubation in the presence of 10(3) and 10(4) units/ml rIFN gamma. This was confirmed through both biological assays with mouse bone marrow cells and an indirect ELISA. In contrast, the concentration of growth inhibitory activity in conditioned medium was increased by rIFN gamma. A small but significant increase in IL-1 beta concentration in conditioned medium was detected using a sensitive double-antibody ELISA and a radioimmunoassay. The results infer that the functional characteristics of this leukemia cell line are modulated by rIFN gamma in a manner qualitatively similar to that reported for IFN gamma treated normal monocytes.
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PMID:Regulation by interferon gamma of function in the acute monocytic leukemia cell line, THP-1. 312 95

A previously established human leukemia cell line, designated THP-6, was further characterized with respect to cell surface antigen expression and immunoglobulin(Ig) and T-cell receptor(TCR) gene status. THP-6 cells were positive for CD7 and CD5 antigens and terminal deoxynucleotidyl transferase, but negative for CD2, CD1, CD4, CD8, CD10, cytoplasmic and surface CD3 and HLA-DR antigens, suggesting a precursor T-cell line. Analysis of Ig and TCR beta chain genes revealed that THP-6 had a rearranged TCR beta chain gene and a germline Ig gene. These results, in agreement with its phenotype, confirmed that THP-6 was of the T-cell lineage.
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PMID:Characterization of a precursor T-cell line (THP-6) with rearranged T-cell receptor beta chain gene. 313 May 28

A monocytic cell line, termed Mono Mac, was established from peripheral blood of a patient with monoblastic leukemia. Two clones, designated Mono Mac I and Mono Mac 6, were isolated and both were assigned to the monocyte lineage on the basis of morphological, cytochemical and immunological criteria. Most importantly, the clones express NaF-sensitive non-specific-esterase, produce reactive oxygen and stain with MAb My4. Mono Mac 6, in addition, constitutively exhibits phagocytosis of antibody-coated erythrocytes in 80% of the cells and reacts with a panel of MAbs that are specific for mature monocytes, i.e., M42, LeuM3, 63D3, Mo2 and UCHMI. By contrast, the monoblastic cell lines U937 and THP-I are negative for all these markers. Only expression of My4 could be detected after differentiation induced by interferon-gamma (IFN-gamma). Similar treatment of Mono Mac I, however, resulted in staining with all the monocyte-specific MAbs mentioned above, while IFN-gamma treatment of Mono Mac 6 enhanced antigen expression. In addition, the cells showed an increased frequency of multinucleated cells with a rise from 4.8% to 21.9%. Mono Mac 6 appears to be the only one of the cell lines studied to constitutively express phenotypic and functional features of mature monocytes.
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PMID:Establishment of a human cell line (Mono Mac 6) with characteristics of mature monocytes. 316 33


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