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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Rabbit and monoclonal antibodies to human myeloid leukemia cells, monocytic leukemia cells and human thymocytes have shown the existence of common T-cell/myeloid/monocyte antigens. For this reason, the specificity of a series of monoclonal antibodies to human T-cells (OKT 1, 3, 4, 5, 6, 8, 9, 10; and NA1/34) was tested by immunofluorescence (cytofluorograph) and complement-mediated cytotoxicity against human myeloid leukemia and normal blood cells and leukemic cell lines. In addition, an immunohistological analysis of the specificity of OKT4, 9.3, Leu 3a, OKT3 and NA1/34 antibodies was performed using normal lymphoid tissues and a sensitive immunoperoxidase technique. Normal human peripheral blood mononuclear cells reacted with OKT3 ("pan T-cell", mean 54%), OKT4 ("helper T-cell", mean 35%) and OKT 5/8 ("suppressor T-cell", mean 18%) as previously reported. However, OKT3 reacted with the cell lines K562 (myeloid), RC2a and THP-1 (monocytoid) and U937 (macrophage) as well as with cells from 9/65 myeloid leukemia patients. OKT4 reacted with the cell lines HL60 (promyelocyte), RC2a and U937 and also with cells from 6/60 myeloid leukemia patients. OKT5 reacted with the cell lines K562 and THP-1. OKT1 ("pan T-cell") reacted with THP-1 and with myeloid and monocytic leukemia samples (5/32) as did OKT6 ("cortical thymocyte") (3/32). OKT10 ("common thymocyte") reacted with a range of leukemia cell lines (B-cell, pre- B-cell and macrophage) as well as 7/21 myeloid leukemia samples. In tissue sections Leu 3a, (9.3 and OKT4 to a lesser extent), stained paracortical lymphocytes, plus subcapsular and medullary macrophages, and dendritic cells present within the paracortex.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Monoclonal anti-T-cell antibodies react with circulating myeloid leukemia cells and normal tissue macrophages. 639 75

Medium conditioned by mezerein-treated human acute monocytic leukemia cells (THP-1) stimulated human fibroblast replication. Maximum mitogenic activity was elaborated by THP-1 cells with a 24-hr incubation in 10(-7) M mezerein (activator phase) followed by a 36-hr incubation in insulin-supplemented serum-free Roswell Park Memorial Institute (RPMI)-1640 medium (effector phase). Growth stimulation was not due to the presence of residual mezerein. We previously reported that leukemia cells also produced a growth inhibitor. Fibroblast stimulation was resolved by isoelectrofocusing into several active fractions separate from the growth inhibitory activity for malignant mammary cells. Conditioned medium was mitogenic for fibroblasts in the presence of high concentrations of fetal bovine and human whole blood sera. Growth stimulation was observed in plasma-derived serum only when supplemented with exogenous platelet-derived growth factor. Thus, this THP-1 cell product does not fulfill the role of a competence factor.
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PMID:Stimulation of diploid fibroblast growth with serum-free medium conditioned by mezerein-treated monocytic leukemia cells. 658 49

Two leukemia cell lines of different phenotypic expression were established from a single patient with non-T/non-B acute lymphocytic leukemia (ALL); one (THP-3-1) was derived from the peripheral blood taken on admission before chemotherapy and the other THP-3-2) during the terminal stage. Both THP-3-1 and THP-3-2 cells were positive for terminal deoxynucleotidyl transferase (TdT) and Ia-like antigen but negative for surface immunoglobulins (Ig), nuclear antigen of Epstein-Barr virus (EBNA) and receptors for sheep erythrocytes. However, there was a difference in the expression of common ALL antigen (J5) between the two cell lines. J5+ cells were found in only 5% of THP-3-1 and in 96% of THP-3-2.
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PMID:Two non-T/non-B leukemia cell lines (THP-3-1 and THP-3-2) established from a patient at different stages of the disease. 660 98

A novel cultured cell line, P31/Fujioka, of monocytoid nature was established from leukemic cells in the peripheral blood of a seven-year-old boy with acute monoblastic leukemia. The P31/Fujioka cells have abundant cytoplasm, an indented nucleus of monocytoid appearance, pseudopods detectable by electron microscopy and alpha-naphthyl butyrate esterase activity which is completely inhibited by NaF, but they have no peroxidase activity. Immunologically, the P31/Fujioka cells possess Fc gamma-receptor and phagocytic activity towards sensitized erythrocytes (oxEAIgG), and are reactive with various monoclonal antibodies such as OKM1, anti-Mol, FMC10, FMC12 and OKI1. Chromosome analysis revealed the presence of marker chromosome 11q--due to Nos. 7; 11 translocation and No. 9 pericentric inversion. These findings indicate that the P31/Fujioka cells are derived from the patient's monoblastic leukemia cells and show a more distinct monocyte antigen than other known monocytoid cultured cell lines, U-937 and THP-1. The absence of Epstein-Barr virus nuclear antigen of this line was confirmed.
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PMID:A novel monocytoid cultured cell line, P31/Fujioka, derived from acute monoblastic leukemia. 696 83

A human leukemic cell line (THP-1) cultured from the blood of a boy with acute monocytic leukemia is described. This cell line had Fc and C3b receptors, but no surface or cytoplasmic immunoglobulins. HLA haplotypes of THP-1 were HLA-A2, -A9, -B5, -DRW1 and -DRW2. The monocytic nature of the cell line was characterized by: (1) the presence of alpha-naphthyl butyrate esterase activities which could be inhibited by NaF; (2) lysozyme production; (3) the phagocytosis of latex particles and sensitized sheep erythrocytes; and (4) the ability to restore T-lymphocyte response to Con A. The cells did not possess Epstein-Barr virus-associated nuclear antigen. These results indicate that THP-1 is a leukemia cell line with distinct monocytic markers. During culture, THP-1 maintained these monocytic characteristics for over 14 months.
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PMID:Establishment and characterization of a human acute monocytic leukemia cell line (THP-1). 697 Jul 27

Some monoepoxides of linoleic acid (LA) were converted to monochlorohydrins in low-pH solutions containing chloride ions (Cl-). Conversely, monochlorohydrins of LA were converted to monoepoxides in high-pH solutions. We attempted to determine whether these monochlorohydrins and monoepoxides were produced from LA by the cytochrome-c-H2O2-and/or myeloperoxidase-H2O2-system. The existence of monoepoxides and monochlorohydrins of LA in leukocytes was confirmed by high-performance liquid chromatography (HPLC). Furthermore, leukotoxin in human leukemia cells (THP-1) was stained immunohistochemically by a monoclonal anti-leukotoxin antibody.
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PMID:pH dependent alterations of monoepoxides and monochlorohydrins of linoleic acid, and their existence in vivo. 748 65

Several 6-chloro-2,3-disubstituted imidazo[1,2-b]pyridazines, selected from a number of synthetic imidazo[1,2-b]pyridazines which lacked significant binding activity at central benzodiazepine receptors, potently inhibit [3H]diazepam, [3H]Ro5-4864 and [3H]PK11195 binding to rat kidney mitochondrial membranes. In membrane preparations from cultures of THP-1 cells, a human monocytic leukaemia cell line, the isoquinoline carboxamide PK11195 is strongly bound but the benzodiazepine ligands, diazepam and Ro5-4864, are much more weakly bound. The imidazopyridazine compounds which bind strongly to mitochondrial benzodiazepine receptors are very potent displacers of [3H]PK11195 bound to the THP-1 membranes. It appears that the binding properties of these new imidazopyridazine ligands at 'peripheral-type' benzodiazepine receptors resemble those of the isoquinoline carboxamides more than those of the benzodiazepines.
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PMID:New imidazo[1,2-b]pyridazine ligands for peripheral-type benzodiazepine receptors on mitochondria and monocytes. 749 Oct 86

Binding of circulating cells to endothelium is mediated by recognition between endothelial adhesion molecules and their counter-receptors. The beta 2 integrins are a group of adhesion molecules, mainly expressed on leukocytes, that mediate intercellular binding by recognizing their counterparts on endothelial cells, among others ICAM-1. In this study we have studied the regulation of this interaction in myelomonocytic cells treated with genistein, a tyrosine kinase inhibitor with several other biological functions. We show that genistein upregulates the surface expression of the beta 2-integrins in the monoblastic THP-1 and to a lesser extent in the promyelocytic HL-60 leukemia cell lines. This upregulation leads to an increase in the adherence of THP-1 cells to ICAM-1. Genistein also modulates the expression of ICAM-1 on endothelial cells by potentiating the upregulating effect of TNF and IFN-gamma. Genistein may thus enhance intercellular binding by affecting both the endothelium and the circulating cells.
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PMID:Genistein enhances the ICAM-mediated adhesion by inducing the expression of ICAM-1 and its counter-receptors. 752 Nov 64

Impaired polyglutamylation of methotrexate (MTX) and thus poor retention is believed to be the basis of intrinsic resistance in blasts from patients with acute myeloid leukemia (AML) to MTX. We studied additional samples from patients with this disease, and confirmed that polyglutamylation of MTX was poor in ANLL blast cells. However, in one subset of ANLL, acute monocytic leukemia, (M5) leukemia blasts were found to be capable of accumulating and forming long-chain MTX polyglutamates. An acute monocytic leukemia cell line, THP-1 also was found to accumulate high levels of MTX polyglutamates and was relatively sensitive to MTX, strengthening the concept that M5 blasts may be sensitive to this drug. MTX may be an overlooked drug for the treatment of acute monocytic leukemia.
Leukemia 1995 Feb
PMID:Acute monocytic leukemia: a myeloid leukemia subset that may be sensitive to methotrexate. 753 68

Inflammatory genes are regulated in cells of monocyte (Mo) lineage by a variety of cellular encounters, including adhesion mediated by integrins. The role of the beta 1 family of integrins in the direct induction of immediate early gene expression was analyzed by using the tissue factor (TF) gene. Engagement of alpha 4 or beta 1 on Mo, but not members of the beta 2 integrin family, with specific mAbs as surrogate ligands immediately and directly induced high level surface expression of TF, and accumulation of TF mRNA, as well as production of TNF-alpha and HIV-1 virus. The mechanism responsible for induction of TF gene transcription mediated by the engagement of alpha 4 or beta 1 was elucidated by using THP-1 monoblastic leukemia cells. Functional analysis of plasmids containing the TF promoter expressing the luciferase reporter gene identified a cis-acting integrin-responsive element (InRE), which contained two AP-1 sites as well as a single kappa B-like site. Mutation of either the AP-1 sites or kappa B-like site greatly diminished responsiveness to integrin engagement. This InRE also conferred responsiveness to a heterologous promoter in the same reporter plasmid. Binding of mAbs to either alpha 4 or beta 1 led to nuclear translocation of the c-Rel/p65 heterodimer that preferentially bound to the TF kappa B-like site. In contrast, constitutive binding of AP-1 proteins to the two AP-1 sites was not increased by alpha 4 or beta 1 integrin engagement. These studies expand knowledge of integrin regulation of immediate early gene expression in Mo and molecular encounters that are inferred to play an active role in Mo effector functions.
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PMID:Integrin regulation of an inflammatory effector gene. Direct induction of the tissue factor promoter by engagement of beta 1 or alpha 4 integrin chains. 753 94


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