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1. Eljaafari A, Van Snick J, Voisin A, Cormont F, Farre A, Bienvenu J, Bernaud J, Rigal D, Thomas X: Alloreaction increases or restores CD40, CD54, and/or HLA molecule expression in acute myelogenous leukemia blasts, through secretion of inflammatory cytokines: Dominant role for TNFbeta, in concert with IFNgamma. Leukemia; 2006 Nov;20(11):1992-2001
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  • [Title] Alloreaction increases or restores CD40, CD54, and/or HLA molecule expression in acute myelogenous leukemia blasts, through secretion of inflammatory cytokines: Dominant role for TNFbeta, in concert with IFNgamma.
  • Here, we addressed whether alloreaction-derived cytokines may also lead to acute myelogenous leukemia (AML) blast differentiation.
  • With this aim, supernatant (sn) harvested from major or minor histocompatibility antigen-mismatched mixed lymphocyte reaction (MLR) were used to culture French American Bristish (FAB) type M4 or M5 AML blasts.
  • Our results showed that the secreted factors induced upregulation of CD40, CD54, and/or HLA molecules in AML blasts.
  • But, in line of its much higher levels of secretion, TNFbeta, rather than TNFalpha, was likely to play a preponderant role in AML blast differentiation.
  • Moreover TNFbeta and IFNgamma were also likely to be involved in the AML blast differentiation-mediated by HLA-identical donor T-cell alloresponse against recipient AML blasts.
  • In conclusion, we show herein that upon allogeneic reaction, TNFbeta secretion contributes, in concert with IFNgamma, to increase or restore surface molecules involved in AML blast interaction with T cells.
  • [MeSH-major] Antigens, CD40 / metabolism. Histocompatibility Antigens Class II / metabolism. Intercellular Adhesion Molecule-1 / metabolism. Interferon-gamma / metabolism. Leukemia, Myeloid, Acute / metabolism. Lymphotoxin-alpha / metabolism
  • [MeSH-minor] Adult. Aged. Antibodies / pharmacology. Blood Proteins / chemistry. Blood Proteins / pharmacology. Cell Differentiation / drug effects. Cell Differentiation / physiology. Cells, Cultured. Culture Media, Serum-Free. Female. Humans. Immunophenotyping. Interleukin-1 / immunology. Interleukin-1 / metabolism. Interleukin-2 / metabolism. Interleukin-6 / immunology. Interleukin-6 / metabolism. Lymphocyte Culture Test, Mixed. Male. Middle Aged. Molecular Weight. Tumor Necrosis Factor-alpha / immunology. Tumor Necrosis Factor-alpha / metabolism. Up-Regulation

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  • (PMID = 16990783.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies; 0 / Antigens, CD40; 0 / Blood Proteins; 0 / Culture Media, Serum-Free; 0 / Histocompatibility Antigens Class II; 0 / Interleukin-1; 0 / Interleukin-2; 0 / Interleukin-6; 0 / Lymphotoxin-alpha; 0 / Tumor Necrosis Factor-alpha; 126547-89-5 / Intercellular Adhesion Molecule-1; 82115-62-6 / Interferon-gamma
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2. Takeyama H, Kajiguchi T, Miyata Y, Saito M: [In vitro growth and clinical response of leukemia cells to macrophage colony-stimulating factor (M-CSF) and granulocyte colony-stimulating factor (G-CSF) in acute leukemia]. Gan To Kagaku Ryoho; 2000 Jun;27(6):873-8
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  • [Title] [In vitro growth and clinical response of leukemia cells to macrophage colony-stimulating factor (M-CSF) and granulocyte colony-stimulating factor (G-CSF) in acute leukemia].
  • The in vitro growth and clinical response of leukemia cells to macrophage colony-stimulating factor (M-CSF) and granulocyte colony-stimulating factor (G-CSF) were studied in 24 patients with acute leukemia.
  • Among cases of acute myelogenous leukemia, a positive response to M-CSF (stimulation index > or = 2.5) was seen in 27.3% of the cases, and a significantly higher response rate (81.8%) was seen following G-CSF treatment of leukemia cells in vitro.
  • In cases of acute monocytic leukemia, M-CSF showed a higher stimulating index than that observed for non-monocytic leukemia.
  • G-CSF was administered in 19 cases and M-CSF in 5 cases after chemotherapy, and none of the patients showed leukemia cell proliferation in vivo.
  • There was no correlation between in vitro test results and clinical response of leukemia cells to the CSFs administered.
  • [MeSH-major] Granulocyte Colony-Stimulating Factor / pharmacology. Leukemia, Myeloid, Acute / pathology. Macrophage Colony-Stimulating Factor / pharmacology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cell Division / drug effects. Cytarabine / administration & dosage. Female. Humans. Idarubicin / administration & dosage. Male. Middle Aged. Myelodysplastic Syndromes / drug therapy. Myelodysplastic Syndromes / pathology. Tumor Cells, Cultured

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  • (PMID = 10897214.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] JAPAN
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; 143011-72-7 / Granulocyte Colony-Stimulating Factor; 81627-83-0 / Macrophage Colony-Stimulating Factor; ZRP63D75JW / Idarubicin
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3. Watanabe M, Ohata M, Hayakawa S, Isemura M, Kumazawa S, Nakayama T, Furugori M, Kinae N: Identification of 6-methylsulfinylhexyl isothiocyanate as an apoptosis-inducing component in wasabi. Phytochemistry; 2003 Mar;62(5):733-9
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  • The ethanol extract from Japanese horseradish wasabi was found to inhibit cell proliferation in human monoblastic leukemia U937 cells by inducing apoptotic cell death.
  • Thus, 6-HITC is potentially useful as a natural anti-cancer agent.
  • [MeSH-major] Apoptosis / drug effects. Isothiocyanates / pharmacology. Wasabia / chemistry
  • [MeSH-minor] Chromatin / ultrastructure. Chromatography, Gel. Chromatography, High Pressure Liquid / methods. DNA Fragmentation / drug effects. Dose-Response Relationship, Drug. Humans. Leukemia, Monocytic, Acute / metabolism. Microscopy, Fluorescence. Plants, Medicinal / chemistry. Stomach Neoplasms / metabolism. Tumor Cells, Cultured / cytology. Tumor Cells, Cultured / drug effects. Tumor Cells, Cultured / ultrastructure. U937 Cells

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  • (PMID = 12620325.001).
  • [ISSN] 0031-9422
  • [Journal-full-title] Phytochemistry
  • [ISO-abbreviation] Phytochemistry
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 6-methylsulfinylhexyl isothiocyanate; 0 / Chromatin; 0 / Isothiocyanates
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4. Tasaka T, Nagai M, Matsuhashi Y, Uehara E, Tamura T, Ishida T, Kakazu N, Abe T: Secondary acute monocytic leukemia with a translocation t(8;22)(p11;q13). Haematologica; 2002 May;87(5):ECR19
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  • [Title] Secondary acute monocytic leukemia with a translocation t(8;22)(p11;q13).
  • [MeSH-major] Chromosomes, Human, Pair 22. Chromosomes, Human, Pair 8. Leukemia, Monocytic, Acute / genetics. Neoplasms, Second Primary / genetics. Translocation, Genetic
  • [MeSH-minor] Acetyltransferases / genetics. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / adverse effects. Histone Acetyltransferases. Humans. Male. Middle Aged. Nuclear Proteins / genetics. Trans-Activators / genetics. Waldenstrom Macroglobulinemia / drug therapy

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  • (PMID = 12010682.001).
  • [ISSN] 0390-6078
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Nuclear Proteins; 0 / Trans-Activators; EC 2.3.1.- / Acetyltransferases; EC 2.3.1.48 / Histone Acetyltransferases; EC 2.3.1.48 / KAT6A protein, human
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5. Tanaka T, Fukunaga Y, Itoh H, Doi K, Yamashita J, Chun TH, Inoue M, Masatsugu K, Saito T, Sawada N, Sakaguchi S, Arai H, Nakao K: Therapeutic potential of thiazolidinediones in activation of peroxisome proliferator-activated receptor gamma for monocyte recruitment and endothelial regeneration. Eur J Pharmacol; 2005 Jan 31;508(1-3):255-65
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  • Thiazolidinediones, a new class of antidiabetic drugs that increase insulin sensitivity, have been shown to be ligands for peroxisome proliferator-activated receptor gamma (PPARgamma).
  • Troglitazone and pioglitazone, the two thiazolidinediones, as well as 15-deoxy-delta12,14-prostaglandin J2 inhibited in a dose-dependent manner the serum-induced proliferation of THP-1 (human monocytic leukemia cells) and of U937 (human monoblastic leukemia cells), which permanently express PPARgamma.
  • Oral administration of troglitazone to Watanabe heritable hyperlipidemic (WHHL) rabbits after balloon injury suppressed acute recruitment of monocytes/macrophages and accelerated re-endothelialization.
  • [MeSH-major] Endothelium, Vascular / drug effects. Monocytes / drug effects. PPAR gamma / genetics. Prostaglandin D2 / analogs & derivatives. Thiazolidinediones / pharmacology
  • [MeSH-minor] Angioplasty, Balloon / adverse effects. Animals. Aorta / drug effects. Aorta / injuries. Aorta / pathology. Arteriosclerosis / prevention & control. Binding, Competitive / drug effects. Cell Line. Cell Line, Tumor. Cell Movement / drug effects. Cell Proliferation / drug effects. Chemokine CCL2 / metabolism. Chemokine CCL2 / pharmacology. Chromans / pharmacology. Chromans / therapeutic use. Dose-Response Relationship, Drug. Gene Expression Regulation / drug effects. Humans. Macrophages / drug effects. Macrophages / metabolism. Macrophages / pathology. Male. RNA, Messenger / genetics. RNA, Messenger / metabolism. Rabbits. Receptors, CCR2. Receptors, Chemokine / genetics. Reverse Transcriptase Polymerase Chain Reaction. Time Factors. Tretinoin / pharmacology. Vascular Endothelial Growth Factor A / genetics. Wound Healing / drug effects

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  • (PMID = 15680279.001).
  • [ISSN] 0014-2999
  • [Journal-full-title] European journal of pharmacology
  • [ISO-abbreviation] Eur. J. Pharmacol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / 15-deoxy-delta(12,14)-prostaglandin J2; 0 / CCR2 protein, human; 0 / Chemokine CCL2; 0 / Chromans; 0 / PPAR gamma; 0 / RNA, Messenger; 0 / Receptors, CCR2; 0 / Receptors, Chemokine; 0 / Thiazolidinediones; 0 / Vascular Endothelial Growth Factor A; 5300-03-8 / alitretinoin; 5688UTC01R / Tretinoin; I66ZZ0ZN0E / troglitazone; RXY07S6CZ2 / Prostaglandin D2; X4OV71U42S / pioglitazone
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6. Yamada R, Horikawa K, Ishihara S, Hoshino K, Kawaguchi T, Iyama K, Mitsuya H, Asou N: Successful treatment of Aspergillus liver abscesses in a patient with acute monoblastic leukemia using combination antifungal therapy including micafungin as a key drug. Int J Hematol; 2010 May;91(4):711-5
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  • [Title] Successful treatment of Aspergillus liver abscesses in a patient with acute monoblastic leukemia using combination antifungal therapy including micafungin as a key drug.
  • In intensive chemotherapy for leukemia, invasive aspergillosis resulting in death is infrequently observed.
  • In such cases, aggressive diagnostic and therapeutic intervention is required.
  • Herein, we report a case of Aspergillus liver abscesses in a patient with acute monoblastic leukemia.
  • Therefore, our clinical experience suggests that the serum test is useful for the rapid diagnosis of invasive aspergillosis, especially in deep tissues, and that combination antifungal therapy with micafungin should be considered when initial monotherapy for fungal infection shows an insufficient effect.
  • [MeSH-major] Antifungal Agents / administration & dosage. Aspergillosis / drug therapy. Echinocandins / administration & dosage. Hepatitis / drug therapy. Leukemia, Monocytic, Acute / complications. Lipopeptides / administration & dosage. Liver Abscess / drug therapy
  • [MeSH-minor] Drug Therapy, Combination. Humans. Male. Middle Aged

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  • (PMID = 20352380.001).
  • [ISSN] 1865-3774
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antifungal Agents; 0 / Echinocandins; 0 / Lipopeptides; R10H71BSWG / micafungin
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7. Dimberg A, Nilsson K, Oberg F: Phosphorylation-deficient Stat1 inhibits retinoic acid-induced differentiation and cell cycle arrest in U-937 monoblasts. Blood; 2000 Oct 15;96(8):2870-8
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  • All-trans retinoic acid (ATRA) is a potent inducer of terminal differentiation of immature leukemic cell lines in vitro and of acute promyelocytic leukemia (APL) cells in vivo.
  • To investigate the role of Stat1 activation in ATRA signaling, sublines were established for the human monoblastic cell line U-937 constitutively expressing wild-type or phosphorylation-defective Stat1, mutated in the conserved tyrosine 701 required for dimerization and nuclear translocation.
  • Consistent with a functional importance of this activation, ectopic expression of Stat1(Y701F) suppressed ATRA-induced morphologic differentiation and expression of the monocytic surface markers CD11c and the granulocyte colony-stimulating factor receptor.
  • [MeSH-major] DNA-Binding Proteins / physiology. Protein Processing, Post-Translational. Trans-Activators / physiology. Transcription, Genetic / drug effects. Tretinoin / antagonists & inhibitors. U937 Cells / drug effects
  • [MeSH-minor] Amino Acid Substitution. Biological Transport / genetics. Cell Cycle / drug effects. Cell Differentiation / drug effects. Cell Nucleus / metabolism. Cholecalciferol / pharmacology. G0 Phase. G1 Phase. Gene Expression Regulation, Neoplastic / drug effects. Genes, Dominant. Genes, Reporter. Humans. Interferon Regulatory Factor-1. Mutagenesis, Site-Directed. Neoplasm Proteins / biosynthesis. Neoplasm Proteins / genetics. Phosphoproteins / biosynthesis. Phosphoproteins / genetics. Phosphorylation. Phosphotyrosine / physiology. Recombinant Fusion Proteins / physiology. STAT1 Transcription Factor. Transcription Factors / biosynthesis. Transcription Factors / genetics. Transfection

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  • (PMID = 11023524.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / IRF1 protein, human; 0 / Interferon Regulatory Factor-1; 0 / Neoplasm Proteins; 0 / Phosphoproteins; 0 / Recombinant Fusion Proteins; 0 / STAT1 Transcription Factor; 0 / STAT1 protein, human; 0 / Trans-Activators; 0 / Transcription Factors; 1C6V77QF41 / Cholecalciferol; 21820-51-9 / Phosphotyrosine; 5688UTC01R / Tretinoin
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8. Sagawa M, Shimizu T, Shimizu T, Awaya N, Mitsuhashi T, Ikeda Y, Okamoto S, Kizaki M: Establishment of a new human acute monocytic leukemia cell line TZ-1 with t(1;11)(p32;q23) and fusion gene MLL-EPS15. Leukemia; 2006 Sep;20(9):1566-71
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  • [Title] Establishment of a new human acute monocytic leukemia cell line TZ-1 with t(1;11)(p32;q23) and fusion gene MLL-EPS15.
  • Human leukemia cell lines are of great value in investigating basic and applied aspects of cell biology and clinical medicine.
  • There have been 37 leukemia cell lines carrying 11q23 translocation and MLL rearrangements; however, cell lines harboring with t(1;11)(p32;q23) have not been established.
  • We report here for the first time a new acute monocytic leukemia (AMoL) cell line with t(1;11)(p32;q23), designated TZ-1, and herein describe its biological characteristics.
  • Mononuclear cells isolated from the ascites from a patient with AMoL (French-American-British classification; acute myeloid leukemia M5a) were isolated and passaged by liquid culture medium for a year.
  • TZ-1 cells revealed typical monocytic features in morphology and had a t(1;11)(p32;q23) translocation.
  • The immunoprofiling as determined by flow cytometry showed that TZ-1 cells are positive for myeloid and monocytic markers with lymphoid-associated markers.
  • Taken together, these results suggest that TZ-1 is a new monocytic leukemia cell line with t(1;11) translocation and fusion gene MLL-EPS15.
  • The established cell line, TZ-1, could provide a valuable model in the analysis of the pathogenesis of MLL-EPS15-positive leukemia and in the development of new agents for this type of leukemia.
  • [MeSH-major] Chromosomes, Human, Pair 1. Chromosomes, Human, Pair 11. Leukemia, Monocytic, Acute / pathology. Translocation, Genetic

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  • (PMID = 16826222.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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9. Wu CY, Chi PL, Hsieh HL, Luo SF, Yang CM: TLR4-dependent induction of vascular adhesion molecule-1 in rheumatoid arthritis synovial fibroblasts: Roles of cytosolic phospholipase A(2)alpha/cyclooxygenase-2. J Cell Physiol; 2010 May;223(2):480-91
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  • In this study, we identified that cPLA(2)alpha acted as a modulator of LPS-induced VCAM-1 expression and THP-1 (human acute monocytic leukemia cell line) adherence.
  • [MeSH-major] Amine Oxidase (Copper-Containing) / metabolism. Cell Adhesion Molecules / metabolism. Cyclooxygenase 2 / metabolism. Fibroblasts / metabolism. Group IV Phospholipases A2 / metabolism. Synovial Membrane / metabolism. Toll-Like Receptor 4 / metabolism
  • [MeSH-minor] Arachidonic Acids / pharmacology. Arthritis, Rheumatoid / metabolism. Arthritis, Rheumatoid / physiopathology. Cell Adhesion / physiology. Cell Line. Cells, Cultured. Cyclooxygenase 2 Inhibitors / pharmacology. Dinoprostone / biosynthesis. Eicosapentaenoic Acid / pharmacology. Enzyme Inhibitors / pharmacology. Extracellular Signal-Regulated MAP Kinases / metabolism. Humans. Inflammation Mediators / pharmacology. Lipopolysaccharides / pharmacology. RNA Interference. RNA, Messenger / drug effects. Receptors, Prostaglandin E / antagonists & inhibitors. Receptors, Prostaglandin E / metabolism. Signal Transduction / physiology

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  • (PMID = 20112284.001).
  • [ISSN] 1097-4652
  • [Journal-full-title] Journal of cellular physiology
  • [ISO-abbreviation] J. Cell. Physiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Arachidonic Acids; 0 / Cell Adhesion Molecules; 0 / Cyclooxygenase 2 Inhibitors; 0 / Enzyme Inhibitors; 0 / Inflammation Mediators; 0 / Lipopolysaccharides; 0 / RNA, Messenger; 0 / Receptors, Prostaglandin E; 0 / TLR4 protein, human; 0 / Toll-Like Receptor 4; 149301-79-1 / arachidonyltrifluoromethane; AAN7QOV9EA / Eicosapentaenoic Acid; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS2 protein, human; EC 1.4.3.21 / AOC3 protein, human; EC 1.4.3.21 / Amine Oxidase (Copper-Containing); EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 3.1.1.4 / Group IV Phospholipases A2; K7Q1JQR04M / Dinoprostone
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10. de Jesus Marques-Salles T, Liehr T, Mkrtchyan H, Raimondi SC, Tavares de Souza M, de Figueiredo AF, Rouxinol S, Jordy Macedo FC, Abdelhay E, Santos N, Macedo Silva ML: A new chromosomal three-way rearrangement involving MLL masked by a t(9;19)(p11;p13) in an infant with acute myeloid leukemia. Cancer Genet Cytogenet; 2009 Feb;189(1):59-62
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  • [Title] A new chromosomal three-way rearrangement involving MLL masked by a t(9;19)(p11;p13) in an infant with acute myeloid leukemia.
  • Infants diagnosed with acute myelogenous leukemia (AML) are likely to have subtypes M4 or M5 characterized by 11q23 abnormalities like a t(9;11)(p22;q23).
  • Detection of all possible types of chromosomal abnormalities, including mixed lineage leukemia (MLL) gene rearrangements at 11q23, is of importance for the identification of biological subgroups, which might differ in drug resistance and/or clinical outcome.
  • Here, we report the clinical, conventional banding and molecular cytogenetics data of a 6-month-old boy with an AML-M5 presenting with a unique cryptic rearrangement involving the MLL gene: a three-way t(9;19;11)(p11.2;p13.1;q23).
  • [MeSH-major] Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 19 / genetics. Chromosomes, Human, Pair 9 / genetics. Leukemia, Myeloid, Acute / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Translocation, Genetic / genetics

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  • (PMID = 19167614.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
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11. Kusari S, Zühlke S, Kosuth J, Cellárová E, Spiteller M: Light-independent metabolomics of endophytic Thielavia subthermophila provides insight into microbial hypericin biosynthesis. J Nat Prod; 2009 Oct;72(10):1825-35
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  • The endophytic metabolites exhibited photodynamic cytotoxicity against the human acute monocytic leukemia cell line (THP-1), at 92.7 vs 4.9%, and 91.1 vs 1.0% viability by resazurin and ATPlite assays, in light and in the dark, respectively.
  • [MeSH-major] Antineoplastic Agents / isolation & purification. Hypericum / microbiology. Perylene / analogs & derivatives. Sordariales / chemistry
  • [MeSH-minor] Base Sequence. Drug Screening Assays, Antitumor. Emodin / metabolism. Humans. Light. Metabolomics. Molecular Structure

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  • (PMID = 19746917.001).
  • [ISSN] 1520-6025
  • [Journal-full-title] Journal of natural products
  • [ISO-abbreviation] J. Nat. Prod.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 5QD5427UN7 / Perylene; 7V2F1075HD / hypericin; KA46RNI6HN / Emodin
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12. Song G, Liao X, Zhou L, Wu L, Feng Y, Han ZC: HI44a, an anti-CD44 monoclonal antibody, induces differentiation and apoptosis of human acute myeloid leukemia cells. Leuk Res; 2004 Oct;28(10):1089-96
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  • [Title] HI44a, an anti-CD44 monoclonal antibody, induces differentiation and apoptosis of human acute myeloid leukemia cells.
  • CD44 is a cell surface antigen that expresses on leukemia blasts from most acute myeloid leukemia (AML) patients.
  • It has been reported that ligation of CD44 with some specific anti-CD44 monoclonal antibodies can reverse the differentiation blockage of leukemia cell lines.
  • In this study, the differentiation and apoptosis-inducing effects of HI44a, another anti-CD44 monoclonal antibody (IgG2a), were investigated on leukemia cells obtained from 31 patients with AML-M2, AML-M3, AML-M4 or AML-M5.
  • When the AML cells were treated with HI44a, the percentage of nitroblue tetrazolium (NBT)+ cells was significantly increased.
  • The expression of CD11b, CD14 and CD15 on treated AML cells was also increased compared to control AML cells.
  • In addition, HI44a was found to induce apoptosis of leukemia cells, as evidenced by an annexin-V assay.
  • The mean percentage of apoptotic cells in HI44a-treated AML cells was significantly increased compared to that in control AML cells.
  • Moreover, the level of c-myc transcript expression on AML cells was found to be obviously decreased in all detected patients.
  • These results indicate that HI44a effectively induces both differentiation and apoptosis of AML cells and suggest that this activity of the anti-CD44 antibody may be associated with its inhibitory effect on c-myc transcript expression.
  • [MeSH-major] Antibodies, Monoclonal / pharmacology. Antigens, CD44 / drug effects. Apoptosis / drug effects. Cell Differentiation / drug effects. Leukemia, Myeloid / drug therapy
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Female. Genes, myc. Humans. Male. Middle Aged. Proto-Oncogene Proteins c-myc / drug effects. Reverse Transcriptase Polymerase Chain Reaction. Structure-Activity Relationship. Tumor Cells, Cultured

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  • (PMID = 15289023.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD44; 0 / HI44a monoclonal antibody; 0 / Proto-Oncogene Proteins c-myc
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13. Bunworasate U, Arnouk H, Minderman H, O'Loughlin KL, Sait SN, Barcos M, Stewart CC, Baer MR: Erythropoietin-dependent transformation of myelodysplastic syndrome to acute monoblastic leukemia. Blood; 2001 Dec 1;98(12):3492-4
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  • [Title] Erythropoietin-dependent transformation of myelodysplastic syndrome to acute monoblastic leukemia.
  • Acute monoblastic leukemia (acute myeloid leukemia [AML], French-American-British type M5a) with leukemia cutis developed in a patient 6 weeks after the initiation of erythropoietin (EPO) therapy for refractory anemia with ringed sideroblasts.
  • AML disappeared from both marrow and skin after the discontinuation of EPO.
  • Clinical and laboratory findings were consistent with the EPO-dependent transformation of myelodysplastic syndrome (MDS) to AML.
  • [MeSH-major] Erythropoietin / adverse effects. Leukemia, Monocytic, Acute / chemically induced. Myelodysplastic Syndromes / pathology
  • [MeSH-minor] Aged. Anemia, Sideroblastic / drug therapy. Anemia, Sideroblastic / pathology. Antigens, CD13 / analysis. Antigens, CD45 / analysis. Bone Marrow / pathology. Flow Cytometry. Humans. Male. Receptors, Erythropoietin / analysis. Skin / pathology


14. Evans MA, Smith DC, Holub JM, Argenti A, Hoff M, Dalglish GA, Wilson DL, Taylor BM, Berkowitz JD, Burnham BS, Krumpe K, Gupton JT, Scarlett TC, Durham Jr RW, Hall IH: Synthesis and cytotoxicity of substituted ethyl 2-phenacyl-3-phenylpyrrole-4-carboxylates. Arch Pharm (Weinheim); 2003 Jun;336(3):181-90
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  • They proved to be potent cytotoxic agents against the growth of murine L1210 and P388 leukemias and human HL-60 promyelocytic leukemia, HuT-78 lymphoma, and HeLa-S(3) uterine carcinoma.
  • Selective compounds were active against the growth of Tmolt(3) and Tmolt(4) leukemias and THP-1 acute monocytic leukemia, liver Hepe-2, ovary 1-A9, ileum HCT-8 adenocarcinoma, and osteosarcoma HSO.
  • DNA and RNA polymerases, PRPP-amido transferase, dihydrofolate reductase, thymidylate synthase, and TMP kinase activities were interfered with by the agent with reduction of d[NTP] pools.
  • [MeSH-major] Antineoplastic Agents / chemical synthesis. Pyrroles / chemical synthesis
  • [MeSH-minor] Animals. DNA Fragmentation. Drug Screening Assays, Antitumor. Enzyme Inhibitors / chemical synthesis. Enzyme Inhibitors / chemistry. Enzyme Inhibitors / pharmacology. Humans. Mice. Structure-Activity Relationship. Tumor Cells, Cultured

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  • (PMID = 12822184.001).
  • [ISSN] 0365-6233
  • [Journal-full-title] Archiv der Pharmazie
  • [ISO-abbreviation] Arch. Pharm. (Weinheim)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Enzyme Inhibitors; 0 / Pyrroles
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15. Yada-Hashimoto N, Nishio Y, Ohmichi M, Hayakawa J, Mabuchi S, Hisamoto K, Nakatsuji Y, Sasaki H, Seino-Noda H, Sakata M, Tasaka K, Murata Y: Estrogen and raloxifene inhibit the monocytic chemoattractant protein-1-induced migration of human monocytic cells via nongenomic estrogen receptor alpha. Menopause; 2006 Nov-Dec;13(6):935-41
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  • [Title] Estrogen and raloxifene inhibit the monocytic chemoattractant protein-1-induced migration of human monocytic cells via nongenomic estrogen receptor alpha.
  • OBJECTIVE: To investigate the effects of estradiol (E2) and raloxifene on the migration of human monocytic THP-1 cells to endothelium.
  • THP-1 cells, a human acute monocytic leukemia cell line, were used for the study.
  • THP-1 cells were exposed to E2 or raloxifene in the presence of monocytic chemoattractant protein-1 (MCP-1), a major chemoattractant for monocytes.
  • [MeSH-major] Chemokine CCL2 / pharmacology. Estradiol / analogs & derivatives. Estradiol / pharmacology. Estrogen Antagonists / pharmacology. Estrogen Receptor Modulators / pharmacology. Monocytes / drug effects. Raloxifene Hydrochloride / pharmacology
  • [MeSH-minor] Atherosclerosis / prevention & control. Cell Line, Tumor. Cell Movement / drug effects. Dactinomycin / pharmacology. Estrogen Receptor alpha / genetics. Estrogen Receptor beta / genetics. Gene Silencing. Humans. Nucleic Acid Synthesis Inhibitors / pharmacology. RNA, Small Interfering. Transfection

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  • (PMID = 17006379.001).
  • [ISSN] 1072-3714
  • [Journal-full-title] Menopause (New York, N.Y.)
  • [ISO-abbreviation] Menopause
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Chemokine CCL2; 0 / Estrogen Antagonists; 0 / Estrogen Receptor Modulators; 0 / Estrogen Receptor alpha; 0 / Estrogen Receptor beta; 0 / Nucleic Acid Synthesis Inhibitors; 0 / RNA, Small Interfering; 1CC1JFE158 / Dactinomycin; 22X328QOC4 / fulvestrant; 4F86W47BR6 / Raloxifene Hydrochloride; 4TI98Z838E / Estradiol
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16. Kobayashi H, Yazlovitskaya EM, Lin PC: Interleukin-32 positively regulates radiation-induced vascular inflammation. Int J Radiat Oncol Biol Phys; 2009 Aug 1;74(5):1573-9
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  • METHODS AND MATERIALS: Irradiated (0-6 Gy) human umbilical vein endothelial cells treated with or without various agents--a cytosolic phospholipase A2 (cPLA2) inhibitor, a cyclooxygenase-2 (Cox-2) inhibitor, or lysophosphatidylcholines (LPCs)--were used to assess IL-32 expression by Northern blot analysis and quantitative reverse transcriptase-polymerase chain reaction.
  • Expression of cell adhesion molecules and leukocyte adhesion to endothelial cells using human acute monocytic leukemia cell line (THP-1) cells was also analyzed.

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  • (PMID = 19616744.001).
  • [ISSN] 1879-355X
  • [Journal-full-title] International journal of radiation oncology, biology, physics
  • [ISO-abbreviation] Int. J. Radiat. Oncol. Biol. Phys.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA108856; United States / NIAMS NIH HHS / AR / R01 AR053718; United States / NINDS NIH HHS / NS / NS45888; United States / NIAMS NIH HHS / AR / R01 AR053718-03; United States / NCI NIH HHS / CA / R01 CA108856-05; United States / NINDS NIH HHS / NS / R01 NS045888-04; United States / NCI NIH HHS / CA / CA108856-05; United States / NINDS NIH HHS / NS / R01 NS045888; United States / NCI NIH HHS / CA / 5T32CA093240; United States / NIAMS NIH HHS / AR / AR053718-03; United States / NINDS NIH HHS / NS / NS045888-04; United States / NIAMS NIH HHS / AR / AR053718; United States / NCI NIH HHS / CA / CA108856; United States / NCI NIH HHS / CA / T32 CA093240
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cell Adhesion Molecules; 0 / Cyclooxygenase 2 Inhibitors; 0 / IL32 protein, human; 0 / Interleukins; 0 / NF-kappa B; 0 / Vascular Cell Adhesion Molecule-1; 0 / Vascular Endothelial Growth Factor A; EC 1.14.99.1 / Cyclooxygenase 2; EC 3.1.1.4 / Group IV Phospholipases A2; EC 3.4.21.- / PCSK7 protein, human; EC 3.4.21.- / Subtilisins
  • [Other-IDs] NLM/ NIHMS114038; NLM/ PMC2713876
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17. Di Giorgio C, Nikoyan A, Decome L, Botta C, Robin M, Reboul JP, Sabatier AS, Matta A, De Méo M: DNA-damaging activity and mutagenicity of 16 newly synthesized thiazolo[5,4-a]acridine derivatives with high photo-inducible cytotoxicity. Mutat Res; 2008 Feb 29;650(2):104-14
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  • In the dark, four molecules possessed cytotoxic activities against a THP1 acute monocytic leukemia cell line while 15 derivatives displayed photo-inducible cytotoxic activity against this cell line.
  • [MeSH-minor] Cell Survival / drug effects. Cells, Cultured. Humans. Intercalating Agents / toxicity. Mutagenicity Tests. Quantitative Structure-Activity Relationship

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  • (PMID = 18160333.001).
  • [ISSN] 0027-5107
  • [Journal-full-title] Mutation research
  • [ISO-abbreviation] Mutat. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Acridines; 0 / Intercalating Agents; 0 / Mutagens; 0 / Thiazoles
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18. Nishioka C, Ikezoe T, Yang J, Takeshita A, Taniguchi A, Komatsu N, Togitani K, Koeffler HP, Yokoyama A: Blockade of MEK/ERK signaling enhances sunitinib-induced growth inhibition and apoptosis of leukemia cells possessing activating mutations of the FLT3 gene. Leuk Res; 2008 Jun;32(6):865-72
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  • [Title] Blockade of MEK/ERK signaling enhances sunitinib-induced growth inhibition and apoptosis of leukemia cells possessing activating mutations of the FLT3 gene.
  • Activating mutations of this gene occur in nearly 30% of acute myelogenous leukemia (AML) patients.
  • In this study, we found that AZD6244 (ARRY-142886), a novel inhibitor of MEK1/2 kinases, effectively inhibited the proliferation of acute biphenotypic leukemia MV4-11 and acute monocytic leukemia MOLM13 cells.
  • Interestingly, when AZD6244 was combined with sunitinib, a FLT3 kinase inhibitor, growth inhibition and apoptosis of both MV4-11 and MOLM13 cells were synergistically enhanced in association with further down-regulation of phospho-ERK1/2 and p-p70S6K in these cells.
  • Taken together, concomitant blockade of FLT3 and MEK signaling represents a promising treatment strategy for individuals with leukemia who possess activating mutations of FLT3.
  • [MeSH-major] Apoptosis / drug effects. Indoles / therapeutic use. Leukemia / pathology. MAP Kinase Kinase 1 / antagonists & inhibitors. Mitogen-Activated Protein Kinase 1 / antagonists & inhibitors. Mitogen-Activated Protein Kinase 3 / antagonists & inhibitors. Mutation / genetics. Pyrroles / therapeutic use. fms-Like Tyrosine Kinase 3 / genetics
  • [MeSH-minor] Aged. Aged, 80 and over. Antineoplastic Combined Chemotherapy Protocols. Benzimidazoles / therapeutic use. Cell Proliferation / drug effects. Female. Humans. Leukemia, Megakaryoblastic, Acute / drug therapy. Leukemia, Megakaryoblastic, Acute / genetics. Leukemia, Megakaryoblastic, Acute / pathology. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / pathology. Male. Middle Aged. Ribosomal Protein S6 Kinases, 70-kDa / antagonists & inhibitors. Ribosomal Protein S6 Kinases, 70-kDa / metabolism. Signal Transduction / drug effects. Tumor Cells, Cultured

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  • (PMID = 17983653.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / AZD 6244; 0 / Benzimidazoles; 0 / Indoles; 0 / Pyrroles; 0 / sunitinib; EC 2.7.1.- / MAP2K1 protein, human; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 2.7.11.1 / Ribosomal Protein S6 Kinases, 70-kDa; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3; EC 2.7.12.2 / MAP Kinase Kinase 1
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19. Pogrebniak A, Hasmann M, Schemainda I, Pelka-Fleischer R, Nuessler V: Cytoprotective features of selenazofurin in hematopoietic cells. Int J Clin Pharmacol Ther; 2002 Aug;40(8):368-75
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  • The therapeutic potential of modulating intracellular NAD levels and activity of NAD-dependent enzymes by concomitant administration of conventional anticancer agents merits further research.
  • Our aim was to investigate the cytotoxic effects of Tz and Se in hematopoietic cells and to test their ability to potentiate the effects of DNA strand-disrupting agents.
  • MATERIAL: THP-1, a cell line, derived from human acute monoblastic leukemia, was used.
  • RESULTS: THP-1 cells were sensitive to cytotoxic effects of Tz and Se, with IC50 values of 2.5 x 10(-5) M for Tz and 2 x 10(-6) M for Se, as determined with the WST-1 test; 10 microM Se induced cell membrane disruption in more than 20% of THP-1 cells 48 hours after commencement of treatment, whereas the same concentration of Tz failed to increase membrane permeability.
  • Pretreatment of THP-1 cells with 0.5 - 1.5 microM Se had no effect on the time course of cell death, induced by treatment with the DNA-damaging agent 1-methyl-3-nitro-1 - nitrosoguanidinium (MNNG) for 36 hours.
  • CONCLUSIONS: Contrary to other investigations, we here demonstrate that preincubation with Se may partially protect cells from cell death induced by the alkylating agents MNNG and chlorambucil in the THP-1 cell line and in CLL lymphocytes presumably by affecting spontaneous cell death.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Antineoplastic Agents / therapeutic use. Organoselenium Compounds / pharmacology. Organoselenium Compounds / therapeutic use. Ribavirin / analogs & derivatives. Ribonucleosides / pharmacology. Ribonucleosides / therapeutic use
  • [MeSH-minor] Cell Death / drug effects. Cell Line. Cell Survival / drug effects. Chlorambucil / pharmacology. Dose-Response Relationship, Drug. Humans. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Leukemia, Monocytic, Acute / drug therapy. Methylnitronitrosoguanidine / pharmacology

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  • (PMID = 12467305.001).
  • [ISSN] 0946-1965
  • [Journal-full-title] International journal of clinical pharmacology and therapeutics
  • [ISO-abbreviation] Int J Clin Pharmacol Ther
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Organoselenium Compounds; 0 / Ribonucleosides; 12H3O2UGSF / Methylnitronitrosoguanidine; 18D0SL7309 / Chlorambucil; 49717AWG6K / Ribavirin; 83705-13-9 / selenazofurin; ULJ82834RE / tiazofurin
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20. Miyazawa M, Ito Y, Yoshida Y, Sakaguchi H, Suzuki H: Phenotypic alterations and cytokine production in THP-1 cells in response to allergens. Toxicol In Vitro; 2007 Apr;21(3):428-37
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  • We have previously shown that THP-1 cells, human acute monocytic leukemia cell line, can discriminate between allergens and irritants by measuring expression of surface markers, CD86 and CD54, following chemical exposure.
  • [MeSH-major] Allergens / toxicity. Cytokines / metabolism. Dinitrochlorobenzene / toxicity. Irritants / toxicity. Monocytes / drug effects. Nickel / toxicity. Sodium Dodecyl Sulfate / toxicity
  • [MeSH-minor] Antigens, CD / metabolism. Antigens, CD40 / metabolism. Biomarkers / metabolism. Cell Line, Tumor. Dose-Response Relationship, Drug. Flow Cytometry. Humans. Immunoglobulins / metabolism. Langerhans Cells / drug effects. Langerhans Cells / metabolism. Membrane Glycoproteins / metabolism. Phenotype

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  • (PMID = 17118622.001).
  • [ISSN] 0887-2333
  • [Journal-full-title] Toxicology in vitro : an international journal published in association with BIBRA
  • [ISO-abbreviation] Toxicol In Vitro
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Allergens; 0 / Antigens, CD; 0 / Antigens, CD40; 0 / Biomarkers; 0 / CD83 antigen; 0 / Cytokines; 0 / Immunoglobulins; 0 / Irritants; 0 / Membrane Glycoproteins; 368GB5141J / Sodium Dodecyl Sulfate; 4FLT4T3WUN / nickel sulfate; 7OV03QG267 / Nickel; GE3IBT7BMN / Dinitrochlorobenzene
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21. Hu XR, He JS, Ye XJ, Zheng WY, Wu WJ, Lin MF: Candida tropicalis arthritis in a patient with acute leukemia. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2008 Oct;16(5):1215-8
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  • [Title] Candida tropicalis arthritis in a patient with acute leukemia.
  • A case of Candida tropicalis arthritis of knee occurred in a patient with acute monocytic leukemia was reported during the recovery phase of post chemotherapy myelosuppression and agranulocytosis.
  • But the arthritis relapsed at 4 - 6 weeks after the drug withdrawal.
  • The treatment emphasis showed be placed on the full dosage and full treatment course of antifungal agent.

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  • (PMID = 18928631.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] ENG
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antifungal Agents
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22. Liang YH, Li P, Zhao JX, Liu X, Huang QF: [Acetyl-11-keto-beta-boswellic acid and arsenic trioxide regulate the productions and activities of matrix metalloproteinases in human skin fibroblasts and human leukemia cell line THP-1]. Zhong Xi Yi Jie He Xue Bao; 2010 Nov;8(11):1060-9
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  • [Title] [Acetyl-11-keto-beta-boswellic acid and arsenic trioxide regulate the productions and activities of matrix metalloproteinases in human skin fibroblasts and human leukemia cell line THP-1].
  • OBJECTIVE: In order to reveal the treatment mechanism of Chinese medicine with the effect of activating blood and resolving putridity, we selected acetyl-11-keto-beta-boswellic acid (AKBA) and arsenic trioxide (ATO), the main monomeric components of frankincense and arsenolite which are two most commonly used Chinese medicine with effect of activating blood and resolving putridity.
  • We combined AKBA and ATO as a compound, and explored its regulatory role in productions and activities of matrix metalloproteinase (MMP)-1, MMP-2 and MMP-9 in human skin fibroblasts (HSFbs) and human acute monocytic leukemia cell line THP-1 in inflammatory state.
  • [MeSH-major] Arsenicals / pharmacology. Fibroblasts / drug effects. Matrix Metalloproteinases / metabolism. Monocytes / drug effects. Oxides / pharmacology. Triterpenes / pharmacology

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  • (PMID = 21078271.001).
  • [ISSN] 1672-1977
  • [Journal-full-title] Zhong xi yi jie he xue bao = Journal of Chinese integrative medicine
  • [ISO-abbreviation] Zhong Xi Yi Jie He Xue Bao
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Arsenicals; 0 / Oxides; 0 / Triterpenes; 0 / acetyl-11-ketoboswellic acid; EC 3.4.24.- / Matrix Metalloproteinases; S7V92P67HO / arsenic trioxide
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23. Li W, Xi S, Zhang M: [The cytotoxic effect of a low density lipoprotein delivered aclarubicin on leukemia cells]. Zhonghua Xue Ye Xue Za Zhi; 2001 Dec;22(12):636-8
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  • [Title] [The cytotoxic effect of a low density lipoprotein delivered aclarubicin on leukemia cells].
  • OBJECTIVE: To investigate the feasibility and effectiveness of low density lipoprotein (LDL) particles as a carrier of a lipophilic anthracycline drug aclarubicin (ACR) for targeting delivery to an acute monocytic leukemia cell line THP-1.
  • The 3H-TdR incorporation test showed that the complex was more effective in the inhibition of DNA synthesis than that of the free drug.
  • [MeSH-major] Aclarubicin / administration & dosage. Antibiotics, Antineoplastic / administration & dosage. Leukemia / drug therapy. Lipoproteins, LDL / administration & dosage
  • [MeSH-minor] Cell Line, Tumor. Cell Proliferation / drug effects. DNA / biosynthesis. Humans

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  • (PMID = 16200711.001).
  • [ISSN] 0253-2727
  • [Journal-full-title] Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi
  • [ISO-abbreviation] Zhonghua Xue Ye Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Lipoproteins, LDL; 74KXF8I502 / Aclarubicin; 9007-49-2 / DNA
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24. Lewis NR, Pallis M, Russell NH: Fas receptor-Fas ligand system is independent of both CD34 status and chemosensitivity in acute myeloid leukemia. Exp Hematol; 2000 May;28(5):535-42
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  • [Title] Fas receptor-Fas ligand system is independent of both CD34 status and chemosensitivity in acute myeloid leukemia.
  • OBJECTIVE: To determine whether the Fas receptor-Fas ligand (FasR-FasL) system, which triggers apoptosis in sensitive cells, is an important mechanism of cytotoxicity in acute myeloblastic leukemia (AML).
  • MATERIALS AND METHODS: We investigated FasR expression in primary AML cells and its upregulation by tumor necrosis factor (TNF), as well as the apoptosis induced by anti-Fas antibody and the potential interaction between the FasR-FasL system and the cytotoxic drug daunorubicin (DNR).
  • RESULTS: FasR was expressed on all 25 AML samples and three normal bone marrow harvests.
  • 6-2.1 in normal bone marrow CD34(+) cells and 1.5-5.1 in AML cells, median 2.4) and was related to the morphologic FAB classification, with the highest expression in FAB types M4 and M5 (range 1.6-5.1, median 3.2).
  • FasR was heterogeneously upregulated in all AML cells on treatment with TNF-alpha.
  • Apoptosis could be induced in all AML samples, but not in normal bone marrow CD34(+)ve cells, by the CH11 anti-FasR antibody, although the response was variable (range 4.1-37.6%, median 16.5%).
  • The monocytic differentiated M4 and M5 AML cells exhibited the greatest sensitivity to Fas-mediated apoptosis (range 4.4-37.6, median 20.65%); however, no relationship was found between sensitivity to Fas-mediated apoptosis and FasR expression or CD34 positivity.
  • Apoptosis in response to DNR was observed in all AML cases; however, sensitivity was heterogeneous and found to be unrelated to FasR expression or sensitivity to Fas-mediated apoptosis.
  • The blocking anti-FasR antibody ZB4 blocked anti-FasR-mediated apoptosis but had no inhibitory effect on DNR-induced apoptosis in AML blasts.
  • CONCLUSION: In AML, DNR induces apoptosis through an Fas-independent pathway.
  • However, the induction of apoptosis through the Fas pathway might be a novel and effective approach for leukemia immunotherapy, particularly because Fas-mediated apoptosis was noted in CD34(+) and CD34(-) cases.
  • [MeSH-major] Antigens, CD34 / immunology. Antigens, CD95 / immunology. Hematopoietic Stem Cells / immunology. Leukemia, Myeloid, Acute / immunology. Membrane Glycoproteins / immunology
  • [MeSH-minor] Apoptosis. Blast Crisis / immunology. Blast Crisis / pathology. Bone Marrow Cells / cytology. Bone Marrow Cells / immunology. Bone Marrow Cells / pathology. Fas Ligand Protein. HL-60 Cells. Humans. Leukemia, Erythroblastic, Acute / immunology. Leukemia, Monocytic, Acute / immunology. Leukemia, Myelomonocytic, Acute / immunology. Tumor Cells, Cultured

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  • (PMID = 10812243.001).
  • [ISSN] 0301-472X
  • [Journal-full-title] Experimental hematology
  • [ISO-abbreviation] Exp. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] NETHERLANDS
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Antigens, CD95; 0 / FASLG protein, human; 0 / Fas Ligand Protein; 0 / Membrane Glycoproteins
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25. Choi W, Eum SY, Lee YW, Hennig B, Robertson LW, Toborek M: PCB 104-induced proinflammatory reactions in human vascular endothelial cells: relationship to cancer metastasis and atherogenesis. Toxicol Sci; 2003 Sep;75(1):47-56
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  • Recent evidence suggests that selected PCBs may be potent developmental agents of vascular inflammatory responses by inducing cellular oxidative stress and activating redox-responsive transcription factors.
  • In addition, PCB 104 elevated the adhesion of THP-1 cells (a human acute monocytic leukemia cell line) to endothelial cell monolayers.

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  • (PMID = 12805654.001).
  • [ISSN] 1096-6080
  • [Journal-full-title] Toxicological sciences : an official journal of the Society of Toxicology
  • [ISO-abbreviation] Toxicol. Sci.
  • [Language] ENG
  • [Grant] United States / NIEHS NIH HHS / ES / P42 ES007380; United States / NIEHS NIH HHS / ES / P42 ES 07380
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 2,2',4,6,6'-pentachlorobiphenyl; 0 / Chemokine CCL2; 0 / E-Selectin; 0 / Environmental Pollutants; 0 / Reactive Oxygen Species; 126547-89-5 / Intercellular Adhesion Molecule-1; DFC2HB4I0K / Polychlorinated Biphenyls
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26. Niitsu N, Umeda M, Honma Y: Myeloid and monocytoid leukemia cells have different sensitivity to differentiation-inducing activity of deoxyadenosine analogs. Leuk Res; 2000 Jan;24(1):1-9
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  • [Title] Myeloid and monocytoid leukemia cells have different sensitivity to differentiation-inducing activity of deoxyadenosine analogs.
  • The differentiation-inducing effect of clinically applicable analogs of deoxyadenosine on myelomonocytic leukemia cells was examined.
  • Monocytoid leukemia cells were more sensitive to the analogs than were erythroid or myeloid leukemia cells based on the inhibition of cell growth and induction of cell differentiation.
  • Monocytoid leukemia cells were highly sensitive to combined treatment with 2'-deoxycoformycin (dCF) and 9-beta-D-arabinofuranosyladenine (Ara A) for inducing cell differentiation.
  • Ara A induced the differentiation of monocytoid leukemia U937 and THP-1 cells at concentrations which were 1/1000-10000 of that at which it induced the differentiation of other cell lines in the presence of dCF.
  • In combination with a low concentration of 1alpha,25-dihydroxyvitamin D3 (VD3), the induction of the monocytic differentiation was greater in monoblastic U937 cells.
  • Adenosine deaminase-resistant analogs such as fludarabine (FLU) and cladribine (CdA) also induced the differentiation of human myelomonocytic leukemia cells, and these analogs synergistically enhanced the differentiation induced by all-trans retinoic acid (ATRA) or VD3.
  • CdA was the most potent analog for inducing the differentiation of myeloid leukemia NB4 and HL-60 cells in the presence or absence of ATRA.
  • These findings indicate that dCF + Ara A and CdA may be effective for the therapy of acute monocytoid and myeloid leukemia, respectively.
  • [MeSH-major] Antimetabolites, Antineoplastic / pharmacology. Cladribine / pharmacology. Leukemia, Myeloid / pathology. Monocytes / drug effects. Neoplastic Stem Cells / drug effects. Vidarabine / analogs & derivatives. Vidarabine / pharmacology
  • [MeSH-minor] Acute Disease. Adenosine Deaminase Inhibitors. Calcitriol / pharmacology. Cell Differentiation / drug effects. Deoxyadenosines / pharmacology. Dose-Response Relationship, Drug. Drug Synergism. Enzyme Inhibitors / pharmacology. HL-60 Cells / drug effects. Humans. K562 Cells / drug effects. Neoplasm Proteins / antagonists & inhibitors. Pentostatin / pharmacology. Tretinoin / pharmacology. Tumor Cells, Cultured / drug effects. U937 Cells / drug effects

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  • (PMID = 10634639.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] ENGLAND
  • [Chemical-registry-number] 0 / Adenosine Deaminase Inhibitors; 0 / Antimetabolites, Antineoplastic; 0 / Deoxyadenosines; 0 / Enzyme Inhibitors; 0 / Neoplasm Proteins; 14365-44-7 / 5'-amino-5'-deoxyadenosine; 395575MZO7 / Pentostatin; 47M74X9YT5 / Cladribine; 5688UTC01R / Tretinoin; FA2DM6879K / Vidarabine; FXC9231JVH / Calcitriol; P2K93U8740 / fludarabine
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27. Sunnaram BL, Gandemer V, Sebillot M, Grandgirard N, Amiot L, Leray E, Goasguen JE: LRP overexpression in monocytic lineage. Leuk Res; 2003 Aug;27(8):755-9
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  • [Title] LRP overexpression in monocytic lineage.
  • The failure to chemotherapy is a multi factorial phenomenon and lung resistance protein (LRP) overexpression has already been discussed as implicated in drug resistance.
  • In 1996, we studied the expression of LRP and P170 (MDR) in a series of leukemias, at the time of diagnosis, by immunocytochemical (ICC) method.
  • The observation of a strong and unusual expression of LRP in acute myeloid leukemia (AML) with monocytic component led us to test (for P170 and LRP) a new series of 47 AML with different FAB subtypes.
  • We demonstrate that LRP is not correlated with clinical outcome but is statistically related to monoblastic leukemias.
  • Code 5 reaction was found in 10/13 M5 versus the other FAB subtypes (P<10(-3)).
  • The strongest LRP overexpression was also found in chronic myelomonocytic leukemia (four cases), reactive monocytosis (three cases) and in a dendritic cell line.
  • In conclusion, we report that LRP is rather a marker of monocytic lineage than a prognostic index for MDR and we suggest that detection of LRP by ICC could be an argument for the diagnosis of monoblastic and monocytic leukemias.
  • [MeSH-major] Leukemia, Myeloid / pathology. Monocytes / chemistry. Neoplasm Proteins / analysis
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Aged, 80 and over. Antibodies, Monoclonal. Cell Lineage. Child. Child, Preschool. Female. Glycoproteins / analysis. Humans. Immunohistochemistry. Infant. Infant, Newborn. Male. Middle Aged. Survival Rate. Vault Ribonucleoprotein Particles

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  • (PMID = 12801535.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Glycoproteins; 0 / Neoplasm Proteins; 0 / Vault Ribonucleoprotein Particles; 0 / major vault protein; 0 / p-170 glycoprotein, human
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28. Zhang GS, Peng HL, Dai CW, Gong FJ, Xu YX, Xiao L, Pei MF, Shen JK, Yang JJ: [Acute monocytic leukemia after orthotopic liver transplantation: clinical features, molecular genetics, and significance thereof]. Zhonghua Yi Xue Za Zhi; 2005 Dec 28;85(49):3504-8
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  • [Title] [Acute monocytic leukemia after orthotopic liver transplantation: clinical features, molecular genetics, and significance thereof].
  • OBJECTIVE: To study the clinical features and molecular genetics of acute monocytic leukemia (AML) after orthotopic liver transplantation and significance thereof.
  • METHODS: The clinical manifestations, laboratory findings, development, diagnosis, treatment, and prognosis of the first case of AML after orthotopic liver transplantation in the world, a Chinese, male, aged 46, were observed.
  • The diagnosis of chronic myelomonocytic leukemia was made.
  • Five months after the liver transplantation the disease developed to AML.
  • The patient underwent combined chemotherapy (HA or DA regimens) for 5 courses and showed a partial remission both hematologically and in bone marrow examination at first, however, became resistant to all chemotherapeutic agents.
  • RT-PCR showed absence of wild type FLT3 allele.
  • At last the patient died of infection. (2) A FLT3-ITD mutation of "insertion" type was identified in the BMMCs.
  • CONCLUSION: Orthotopic liver transplantation may be complicated with acute leukemia heterogeneous in clinical features and hematology.
  • [MeSH-major] Leukemia, Monocytic, Acute / etiology. Leukemia, Monocytic, Acute / genetics. Liver Transplantation / adverse effects. Postoperative Complications
  • [MeSH-minor] HSP70 Heat-Shock Proteins / genetics. Humans. Male. Middle Aged. Mutation. Prognosis. Proto-Oncogene Proteins c-pim-1 / genetics. Reverse Transcriptase Polymerase Chain Reaction. fms-Like Tyrosine Kinase 3 / genetics

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  • (PMID = 16686070.001).
  • [ISSN] 0376-2491
  • [Journal-full-title] Zhonghua yi xue za zhi
  • [ISO-abbreviation] Zhonghua Yi Xue Za Zhi
  • [Language] chi
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / HSP70 Heat-Shock Proteins; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 2.7.11.1 / PIM1 protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins c-pim-1
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29. Guo H, Ma Y, Zhang B, Sun B, Niu R, Ying G, Zhang N: Pivotal Advance: PKCzeta is required for migration of macrophages. J Leukoc Biol; 2009 Jun;85(6):911-8
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  • Knockdown of PKCzeta by small interference RNA impaired CSF-1-induced chemotaxis of human acute monocytic leukemia cell line THP-1, which was probably a result of a decrease in CSF-1-induced phosphorylation of LIN-11, Is11, and MEC-3 protein domain kinase (LIMK)/cofilin and actin polymerization.
  • [MeSH-minor] Actins / metabolism. Animals. Cell Line, Tumor. Chemokine CCL2 / pharmacology. Chemotaxis / drug effects. Down-Regulation / drug effects. Gene Knockdown Techniques. Humans. Macrophage Colony-Stimulating Factor / pharmacology. Macrophages, Peritoneal / cytology. Macrophages, Peritoneal / drug effects. Macrophages, Peritoneal / enzymology. Mice. RNA, Small Interfering / metabolism

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  • (PMID = 19201988.001).
  • [ISSN] 1938-3673
  • [Journal-full-title] Journal of leukocyte biology
  • [ISO-abbreviation] J. Leukoc. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Actins; 0 / Chemokine CCL2; 0 / RNA, Small Interfering; 81627-83-0 / Macrophage Colony-Stimulating Factor; EC 2.7.11.1 / protein kinase C zeta; EC 2.7.11.13 / Protein Kinase C
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30. Scarlett TC, Durham RW, Hall IH, Crosswicks RJ, Berkowitz JD, Burnham BS: Synthesis and cytotoxicity of cyanoborane adducts of n6-benzoyladenine and 6-triphenylphosphonylpurine. Met Based Drugs; 2002;9(1-2):19-32
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  • N6-Benzoyladenine-cyanoborane (2), and 6-triphenylphosphonylpurine-cyanoborane (3) were selected for investigation of cytotoxicity in murine and human tumor cell lines, effects on human HL-60 leukemic metabolism and DNA strand scission to determine the feasibility of these compounds as clinical antineoplastic agents.
  • Neither compound was active against the growth of lung 549, breast MCF-7, osteosarcoma HSO, melanoma SK2, KB nasopharynx, and THP-1 acute monocytic leukemia.
  • In mode of action studies in human leukemia HL-60 cells, both compounds demonstrated inhibition of DNA and protein syntheses after 60 min at 100 muM.
  • Overall, these antineoplastic agents caused reduction of DNA and protein replication, which would lead to killing of cancer cells.

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  • (PMID = 18475422.001).
  • [ISSN] 0793-0291
  • [Journal-full-title] Metal-based drugs
  • [ISO-abbreviation] Met Based Drugs
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2365297
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31. Gerber A, Heimburg A, Reisenauer A, Wille A, Welte T, Bühling F: Proteasome inhibitors modulate chemokine production in lung epithelial and monocytic cells. Eur Respir J; 2004 Jul;24(1):40-8
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  • [Title] Proteasome inhibitors modulate chemokine production in lung epithelial and monocytic cells.
  • The present study investigated the influence of cysteine proteinase and proteasome inhibitors on chemokine production in lung epithelial cells and monocytic cells.
  • The lung carcinoma cell lines A549, SK-MES, NCI-H727, virus-transformed bronchial epithelial cell line BEAS-2B, primary lung epithelial cells, and the acute monocytic leukaemia cell lines Mono-Mac-6 and THP-1 were incubated with proteasome (N-acetyl-L-leucyl-L-leucyl-L-norleucinal (ALLN), beta-lactone) or cysteine proteinase inhibitor (L-trans-Epoxysuccinyl-Leu-3-methylbutylamide-ethyl ester) and the influence on chemokine production (interleukin-8: IL-8, monocyte chemoattractant protein-1, RANTES) was quantified at protein and mRNA levels.
  • The significant increase in IL-8 production after proteasome inhibition was also observed in primary lung epithelial cells and in monocytic cells.
  • In conclusion, it was shown that proteasome inhibitors stimulate interleukin-8 secretion in lung epithelial cells and monocytic cells, thus recruiting neutrophils.
  • [MeSH-major] Chemokines / metabolism. Epithelial Cells / metabolism. Lung / cytology. Monocytes / drug effects. Protease Inhibitors / pharmacology
  • [MeSH-minor] Analysis of Variance. Base Sequence. Cell Line, Tumor. Cell Proliferation / drug effects. Cell Survival. Humans. Interleukin-8 / metabolism. Lung Neoplasms. Molecular Sequence Data. Probability. RNA, Neoplasm / analysis. RNA, Neoplasm / drug effects. Reverse Transcriptase Polymerase Chain Reaction. Sensitivity and Specificity


32. Minami J, Takada K, Aoki K, Shimada Y, Okawa Y, Usui N, Ohkawa K: Purification and characterization of C-terminal truncated forms of histone H2A in monocytic THP-1 cells. Int J Biochem Cell Biol; 2007;39(1):171-80
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  • [Title] Purification and characterization of C-terminal truncated forms of histone H2A in monocytic THP-1 cells.
  • We investigated histone H2A-immunoreactive proteins in acute monocytic leukemia THP-1 cells using three polyclonal antibodies raised against peptides corresponding to distinct regions of H2A.
  • Two unknown immunoreactive proteins (9- and 12-kDa proteins), H2A (14kDa) and ubiquitinated H2A (23kDa) were found in the cell lysates prepared by immediate direct addition of SDS-PAGE sample buffer to the cells as well as in the nuclear and chromatin fractions.
  • The unknown proteins were successfully purified by immunoaffinity chromatography from the cell nucleus extract and identified as 9-kDa H2A(1-87) and 12-kDa H2A(1-114), suggesting that both were produced by limited proteolysis of intact H2A(1-129).
  • Truncated H2A proteins in THP-1 cells were transiently increased in amount by short-term treatment with phorbol 12-myristate 13-acetate or all-trans-retinoic acid, both of which induce macrophage-like differentiation.
  • [MeSH-minor] Antineoplastic Agents / pharmacology. Carcinogens / pharmacology. Cell Differentiation / drug effects. Cell Line, Tumor. Humans. Leupeptins. Protein Processing, Post-Translational / drug effects. Tetradecanoylphorbol Acetate / pharmacology. Tretinoin / pharmacology

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  • (PMID = 16979371.001).
  • [ISSN] 1357-2725
  • [Journal-full-title] The international journal of biochemistry & cell biology
  • [ISO-abbreviation] Int. J. Biochem. Cell Biol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies; 0 / Antineoplastic Agents; 0 / Carcinogens; 0 / Chromatin; 0 / Histones; 0 / Leupeptins; 0 / Ubiquitins; 0 / chromatin conjugate protein A24; 133407-82-6 / benzyloxycarbonylleucyl-leucyl-leucine aldehyde; 5688UTC01R / Tretinoin; NI40JAQ945 / Tetradecanoylphorbol Acetate
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33. Sano K, Hayakawa A, Piao JH, Kosaka Y, Nakamura H: Novel SH3 protein encoded by the AF3p21 gene is fused to the mixed lineage leukemia protein in a therapy-related leukemia with t(3;11) (p21;q23). Blood; 2000 Feb 1;95(3):1066-8
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  • [Title] Novel SH3 protein encoded by the AF3p21 gene is fused to the mixed lineage leukemia protein in a therapy-related leukemia with t(3;11) (p21;q23).
  • The mixed lineage leukemia (MLL) gene located at chromosome band 11q23 is frequently rearranged in patients with therapy-related acute monocytic leukemia who received topoisomerase II inhibitors.
  • We have identified a novel fusion partner of MLL (FAB M5b) in a patient who developed t-AML 9 years after treatment for acute lymphoblastic leukemia (ALL).
  • The leukemic cells had a sole karyotypic abnormality of t(3;11) (p21;q23).
  • Screening of a genomic DNA library, prepared from leukemic cell DNA, identified rearranged clones composed of MLL and a novel gene on chromosome 3p21 (AF3p21).
  • The AF3p21 gene encodes a protein of 722 amino acids, which contains an Src homology 3 (SH3) domain, a proline-rich domain, and a bipartite nuclear localizing signal (NLS).
  • [MeSH-major] Adaptor Proteins, Signal Transducing. Leukemia, Monocytic, Acute / genetics. Muscle Proteins. Neoplasms, Second Primary / genetics. Nuclear Proteins / genetics. Oncogene Proteins, Fusion / genetics. src Homology Domains / genetics
  • [MeSH-minor] Adolescent. Amino Acid Sequence. Antineoplastic Combined Chemotherapy Protocols / adverse effects. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Base Sequence. Bone Marrow Transplantation. Combined Modality Therapy. Cyclophosphamide / administration & dosage. Cyclophosphamide / adverse effects. DNA, Complementary / genetics. Daunorubicin / administration & dosage. Daunorubicin / adverse effects. Etoposide / administration & dosage. Etoposide / adverse effects. Female. Humans. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Molecular Sequence Data. Myeloid-Lymphoid Leukemia Protein. Nitrosourea Compounds / administration & dosage. Nitrosourea Compounds / adverse effects. Sequence Alignment. Sequence Homology, Nucleic Acid

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  • (PMID = 10648423.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / AF3p21-MLL fusion protein, human; 0 / Adaptor Proteins, Signal Transducing; 0 / DNA, Complementary; 0 / Muscle Proteins; 0 / NCKIPSD protein, human; 0 / Nitrosourea Compounds; 0 / Nuclear Proteins; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; 6PLQ3CP4P3 / Etoposide; 8N3DW7272P / Cyclophosphamide; RYH2T97J77 / ranimustine; ZS7284E0ZP / Daunorubicin
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34. Lee WJ, Ou HC, Hsu WC, Chou MM, Tseng JJ, Hsu SL, Tsai KL, Sheu WH: Ellagic acid inhibits oxidized LDL-mediated LOX-1 expression, ROS generation, and inflammation in human endothelial cells. J Vasc Surg; 2010 Nov;52(5):1290-300
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  • Furthermore, oxLDL induced the phosphorylation of p38 mitogen-activated protein kinase, activated the NF-κB-mediated inflammatory signaling molecules interleukin-(IL) 6 and IL-8 and the adhesion molecules intercellular adhesion molecule-1, vascular cell adhesion molecule-1, and E-selectin, and stimulated the adherence of THP-1 (a human acute monocytic leukemia cell line) to HUVECs.
  • [MeSH-major] Anti-Inflammatory Agents / pharmacology. Antioxidants / pharmacology. Ellagic Acid / pharmacology. Endothelial Cells / drug effects. Inflammation / prevention & control. Lipoproteins, LDL / metabolism. Reactive Oxygen Species / metabolism. Scavenger Receptors, Class E / metabolism
  • [MeSH-minor] Cell Adhesion Molecules / metabolism. Cells, Cultured. Dose-Response Relationship, Drug. Down-Regulation. Enzyme Inhibitors / pharmacology. Humans. Inflammation Mediators / metabolism. Interleukin-6 / metabolism. Interleukin-8 / metabolism. NADPH Oxidase / antagonists & inhibitors. NADPH Oxidase / metabolism. NF-kappa B / metabolism. Nitric Oxide / metabolism. Nitric Oxide Synthase Type II / metabolism. Nitric Oxide Synthase Type III / metabolism. Onium Compounds / pharmacology. Phosphorylation. Signal Transduction / drug effects. Superoxides / metabolism. p38 Mitogen-Activated Protein Kinases / metabolism

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  • [Copyright] Copyright © 2010 Society for Vascular Surgery. Published by Mosby, Inc. All rights reserved.
  • [CommentIn] J Vasc Surg. 2010 Nov;52(5):1300 [21050989.001]
  • (PMID = 20692795.001).
  • [ISSN] 1097-6809
  • [Journal-full-title] Journal of vascular surgery
  • [ISO-abbreviation] J. Vasc. Surg.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents; 0 / Antioxidants; 0 / Cell Adhesion Molecules; 0 / Enzyme Inhibitors; 0 / IL6 protein, human; 0 / IL8 protein, human; 0 / Inflammation Mediators; 0 / Interleukin-6; 0 / Interleukin-8; 0 / Lipoproteins, LDL; 0 / NF-kappa B; 0 / OLR1 protein, human; 0 / Onium Compounds; 0 / Reactive Oxygen Species; 0 / Scavenger Receptors, Class E; 0 / oxidized low density lipoprotein; 11062-77-4 / Superoxides; 19YRN3ZS9P / Ellagic Acid; 31C4KY9ESH / Nitric Oxide; 6HJ411TU98 / diphenyleneiodonium; EC 1.14.13.39 / NOS2 protein, human; EC 1.14.13.39 / NOS3 protein, human; EC 1.14.13.39 / Nitric Oxide Synthase Type II; EC 1.14.13.39 / Nitric Oxide Synthase Type III; EC 1.6.3.1 / NADPH Oxidase; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases
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35. Osmond RI, Das S, Crouch MF: Development of cell-based assays for cytokine receptor signaling, using an AlphaScreen SureFire assay format. Anal Biochem; 2010 Aug;403(1-2):94-101
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  • The signal transducers and activators of transcription (STAT) proteins are a small family of signaling proteins that are crucial for cytokine and growth factor receptor-mediated signaling in various blood cell types.
  • Indeed, traditional methods such as the Western blot or ELISA remain a standard method for determining the phosphorylation status of endogenous STAT proteins.
  • Here we present data for the rapid detection of endogenous receptor-mediated phosphorylation of multiple STAT proteins using the bead-based AlphaScreen SureFire technology.
  • With three different cell lines (human acute monocytic leukemia THP-1 cells, human erythroleukemic TF-1 cells, and human T lymphocytic Jurkat cells), we have optimized a rapid and homogeneous methodology for monitoring endogenous, receptor-mediated signaling via STAT 1, STAT 3, or STAT 5 phosphorylation, in response to several agonists.
  • These assays, which can be tailored for both standard research applications or high-throughput drug screening applications, afford quantitative data for receptor-mediated signaling mechanisms in an endogenous, cellular environment.

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  • [Copyright] Copyright 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20382104.001).
  • [ISSN] 1096-0309
  • [Journal-full-title] Analytical biochemistry
  • [ISO-abbreviation] Anal. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptors, Cytokine; 0 / STAT Transcription Factors; 0 / STAT1 Transcription Factor; 0 / STAT3 Transcription Factor; 0 / STAT5 Transcription Factor
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36. Wang YF, Song QS, Zhang YM, Ma DL, Wang Y, Ke XY: [Sensitizing effect of recombinant human PDCD5 protein on chemotherapy of acute monocytic leukemia cell line U937 and its mechanism]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2010 Apr;18(2):277-81
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  • [Title] [Sensitizing effect of recombinant human PDCD5 protein on chemotherapy of acute monocytic leukemia cell line U937 and its mechanism].
  • RT-PCR was performed to observe the expression level of drug-resistant genes.
  • The results showed that the percentage of apoptotic cells and the activity of caspase-3 remarkably increased in U937 cells treated with rhPDCD5 combined with chemotherapeutic drug; the cell cycle arrest induced by anti-tumor drug was also enhanced when combined with rhPDCD5; meanwhile, the expression levels of drug-resistant genes were down-regulated in jointly treated U937 cells.
  • It is concluded that the chemosensitizing mechanisms of rhPDCD5 are complex. rhPDCD5 may increase the cytotoxicity of anti-tumor drugs by promoting the caspase-3-related apoptosis, influencing cell cycle, decreasing the expression of drug-resistant genes and reversing drug-resistance.

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  • (PMID = 20416151.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Apoptosis Regulatory Proteins; 0 / Neoplasm Proteins; 0 / PDCD5 protein, human; 0 / Recombinant Proteins; EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / Caspase 3
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37. Lynn EG, Siow YL, Frohlich J, Cheung GT, O K: Lipoprotein-X stimulates monocyte chemoattractant protein-1 expression in mesangial cells via nuclear factor-kappa B. Kidney Int; 2001 Aug;60(2):520-32
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  • The majority of patients with this disorder develop progressive glomerulosclerosis.
  • Conditioned media collected from Lp-X-treated mesangial cells stimulated human acute monocytic leukemia (THP-1) monocyte chemotaxis (165 to 200%).
  • [MeSH-minor] Amino Acid Sequence. Animals. Calcium Channel Blockers / pharmacology. Cells, Cultured. Chemotaxis, Leukocyte / drug effects. Chemotaxis, Leukocyte / immunology. Cholesterol / metabolism. Diglycerides / metabolism. Diltiazem / pharmacology. Enzyme Inhibitors / pharmacology. Foam Cells / metabolism. Gene Expression / drug effects. Gene Expression / immunology. Genes, Recessive. Glomerulosclerosis, Focal Segmental / immunology. Glomerulosclerosis, Focal Segmental / metabolism. Humans. Indoles / pharmacology. Male. Molecular Sequence Data. Monocytes / cytology. Phosphatidylcholines / metabolism. Protein Kinase C / antagonists & inhibitors. Protein Kinase C / metabolism. Pyrroles / pharmacology. RNA, Messenger / analysis. Rats. Rats, Sprague-Dawley. Staurosporine / pharmacology. Type C Phospholipases / metabolism

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  • (PMID = 11473635.001).
  • [ISSN] 0085-2538
  • [Journal-full-title] Kidney international
  • [ISO-abbreviation] Kidney Int.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Calcium Channel Blockers; 0 / Chemokine CCL2; 0 / Diglycerides; 0 / Enzyme Inhibitors; 0 / Indoles; 0 / Lipoprotein-X; 0 / NF-kappa B; 0 / Phosphatidylcholines; 0 / Pyrroles; 0 / RNA, Messenger; 151342-35-7 / Ro 32-0432; 97C5T2UQ7J / Cholesterol; EC 2.7.11.13 / Protein Kinase C; EC 3.1.4.- / Type C Phospholipases; EE92BBP03H / Diltiazem; H88EPA0A3N / Staurosporine
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38. Prayongratana K, Kulpraneet M, Panichchob P, Tantisiriwat W: Acute monoblastic leukemia with t(10;11)(p12;q23) presenting with pulmonary involvement: a case report and literature review. J Med Assoc Thai; 2008 Apr;91(4):559-63
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  • [Title] Acute monoblastic leukemia with t(10;11)(p12;q23) presenting with pulmonary involvement: a case report and literature review.
  • A forty-three-year-old Thai man presented with acute fever and dyspnea for one week with bilateral patchy infiltration, pancytopenia with monoblast.
  • Bone marrow study was consistent with acute monoblastic leukemia.
  • Lung lesions rapidly progressed to acute respiratory failure, which required intubation.
  • Invasive pulmonary aspergillosis was suspected and successfully treated with antifungal agent.
  • This may be due to the low incidence of leukemic infiltration of acute leukemia patients, which is 0.48% and 3.06% in acute myeloid leukemia and acute monoblastic leukemia, respectively.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Leukemia, Monocytic, Acute / pathology. Lung Neoplasms / secondary
  • [MeSH-minor] Adult. Antibiotics, Antineoplastic / therapeutic use. Antifungal Agents / therapeutic use. Antimetabolites, Antineoplastic / therapeutic use. Aspergillosis, Allergic Bronchopulmonary / pathology. Bronchoalveolar Lavage. Cytarabine / therapeutic use. Echinocandins / therapeutic use. Humans. Idarubicin / therapeutic use. Male. Pyrimidines / therapeutic use. Thailand. Triazoles / therapeutic use. Voriconazole

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  • (PMID = 18556867.001).
  • [ISSN] 0125-2208
  • [Journal-full-title] Journal of the Medical Association of Thailand = Chotmaihet thangphaet
  • [ISO-abbreviation] J Med Assoc Thai
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Thailand
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Antifungal Agents; 0 / Antimetabolites, Antineoplastic; 0 / Echinocandins; 0 / Pyrimidines; 0 / Triazoles; 04079A1RDZ / Cytarabine; F0XDI6ZL63 / caspofungin; JFU09I87TR / Voriconazole; ZRP63D75JW / Idarubicin
  • [Number-of-references] 22
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39. Niitsu N, Yamamoto-Yamaguchi Y, Kasukabe T, Okabe-Kado J, Umeda M, Honma Y: Antileukemic efficacy of 2-deoxycoformycin in monocytic leukemia cells. Blood; 2000 Aug 15;96(4):1512-6
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  • [Title] Antileukemic efficacy of 2-deoxycoformycin in monocytic leukemia cells.
  • 2'-Deoxycoformycin (dCF) as a single agent has been reported to be less effective against myeloid than against lymphoid malignancies in clinical trials.
  • However, previous studies have shown that in the presence of 2'-deoxyadenosine (dAd), human monocytoid leukemia cell lines are much more sensitive to dCF with regard to the inhibition of cell proliferation.
  • Thus, dCF might be useful for treating monocytoid leukemia with the aid of dAd analogs.
  • In the presence of 10 micromol/L dAd, the concentration of dCF required to inhibit the viability of primary monocytoid leukemia cells was much lower than that required to inhibit normal or non-monocytoid leukemic cells.
  • Athymic nude mice were inoculated with human monocytoid leukemia U937 cells and treated with dCF or a dAd analog or both.
  • These data suggest that the combination of dCF and AraA may be useful for the clinical treatment of acute monocytic leukemia. (Blood.
  • [MeSH-major] Antibiotics, Antineoplastic / pharmacology. Leukemia, Monocytic, Acute / drug therapy. Pentostatin / pharmacology
  • [MeSH-minor] Animals. Antimetabolites / pharmacology. Antimetabolites / therapeutic use. Cell Survival / drug effects. Humans. Mice. Mice, Nude. U937 Cells. Vidarabine / pharmacology. Vidarabine / therapeutic use

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  • (PMID = 10942399.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Antimetabolites; 395575MZO7 / Pentostatin; FA2DM6879K / Vidarabine
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40. Nakayama M, Takahashi K, Kitamuro T, Murakami O, Shirato K, Shibahara S: Transcriptional control of adrenomedullin induction by phorbol ester in human monocytic leukemia cells. Eur J Biochem; 2000 Jun;267(12):3559-66
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  • [Title] Transcriptional control of adrenomedullin induction by phorbol ester in human monocytic leukemia cells.
  • In this study, we investigated the induction of adrenomedullin gene expression in THP-1 acute monocytic leukemia cells during differentiation into macrophage-like cells by 12-O-tetradecanoylphorbol-13-acetate (TPA), and identified a cis-regulatory region of the human adrenomedullin gene responsible for TPA-induced adrenomedullin expression.

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  • (PMID = 10848972.001).
  • [ISSN] 0014-2956
  • [Journal-full-title] European journal of biochemistry
  • [ISO-abbreviation] Eur. J. Biochem.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / Peptides; 0 / Transcription Factor AP-2; 0 / Transcription Factors; 148498-78-6 / Adrenomedullin; 1CC1JFE158 / Dactinomycin; NI40JAQ945 / Tetradecanoylphorbol Acetate
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41. Krance RA, Hurwitz CA, Head DR, Raimondi SC, Behm FG, Crews KR, Srivastava DK, Mahmoud H, Roberts WM, Tong X, Blakley RL, Ribeiro RC: Experience with 2-chlorodeoxyadenosine in previously untreated children with newly diagnosed acute myeloid leukemia and myelodysplastic diseases. J Clin Oncol; 2001 Jun 01;19(11):2804-11
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  • [Title] Experience with 2-chlorodeoxyadenosine in previously untreated children with newly diagnosed acute myeloid leukemia and myelodysplastic diseases.
  • PURPOSE: To develop more effective chemotherapy regimens for childhood acute myelogenous leukemia (AML).
  • PATIENTS AND METHODS: Between June 1991 and December 1996, we administered the nucleoside analog 2-chlorodeoxyadenosine (2-CDA) to 73 children with primary AML and 20 children with secondary AML or myelodysplastic syndrome (MDS).
  • RESULTS: Seventy-two patients with primary AML were assessable for response.
  • Patients with French-American-British (FAB) M5 AML had a higher rate of CR after treatment with 2-CDA (45% after one course and 70.6% after two courses) than did others (P =.002).
  • In contrast, no patient with FAB M7 AML (n = 10) entered CR after treatment with 2-CDA.
  • Seven patients with secondary AML or MDS (n = 14) had a partial response to one course of 2-CDA.
  • CONCLUSION: This agent was well tolerated, and its toxicity was acceptable.
  • Future trials should examine the effectiveness of 2-CDA given in combination with other agents effective against AML.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Cladribine / pharmacology. Leukemia, Myeloid, Acute / drug therapy. Myelodysplastic Syndromes / drug therapy

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  • (PMID = 11387351.001).
  • [ISSN] 0732-183X
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P01-CA-20180; United States / NCI NIH HHS / CA / P30-CA-21765
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 47M74X9YT5 / Cladribine
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42. Humeniuk-Polaczek R, Marcinkowska E: Impaired nuclear localization of vitamin D receptor in leukemia cells resistant to calcitriol-induced differentiation. J Steroid Biochem Mol Biol; 2004 Apr;88(4-5):361-6
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  • [Title] Impaired nuclear localization of vitamin D receptor in leukemia cells resistant to calcitriol-induced differentiation.
  • Calcitriol, the hormonal form of vitamin D(3), induces differentiation of monocytic leukemia cell lines in vitro, without inducing cytotoxicity of the cells.
  • Besides this broad in vitro activity, a clinical implementation of calcitriol, or its analogs, as agents for differentiation therapy has been unsuccessful until now.
  • A better understanding of cellular activities of calcitriol necessary for completion of cell differentiation program could help find better solutions for differentiation therapy of myeloid leukemias.
  • In this paper we describe work carried on subline of acute monocytic leukemia, THP-1 resistant to calcitriol induced differentiation.
  • [MeSH-major] Active Transport, Cell Nucleus. Calcitriol / pharmacology. Drug Resistance, Neoplasm. Leukemia / pathology. Receptors, Calcitriol / metabolism
  • [MeSH-minor] Cell Differentiation / drug effects. Cell Division / drug effects. Cell Line, Tumor. Humans. Leukemia, Monocytic, Acute / drug therapy. Leukemia, Monocytic, Acute / pathology. Monocytes / drug effects. Tetradecanoylphorbol Acetate / pharmacology

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  • (PMID = 15145445.001).
  • [ISSN] 0960-0760
  • [Journal-full-title] The Journal of steroid biochemistry and molecular biology
  • [ISO-abbreviation] J. Steroid Biochem. Mol. Biol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Receptors, Calcitriol; FXC9231JVH / Calcitriol; NI40JAQ945 / Tetradecanoylphorbol Acetate
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43. Luca DC, Almanaseer IY: Simultaneous presentation of multiple myeloma and acute monocytic leukemia. Arch Pathol Lab Med; 2003 Nov;127(11):1506-8
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  • [Title] Simultaneous presentation of multiple myeloma and acute monocytic leukemia.
  • Acute leukemia frequently has been described as a late complication of chemotherapy with alkylating agents in patients treated for multiple myeloma.
  • However, the simultaneous occurrence of multiple myeloma and acute leukemia in the same patient, without previous exposure to chemotherapy, is a rare association.
  • We describe a case of concomitant involvement by multiple myeloma and acute monocytic leukemia.
  • [MeSH-major] Leukemia, Monocytic, Acute / diagnosis. Multiple Myeloma / diagnosis

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  • (PMID = 14567751.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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44. Kintscher U, Goetze S, Wakino S, Kim S, Nagpal S, Chandraratna RA, Graf K, Fleck E, Hsueh WA, Law RE: Peroxisome proliferator-activated receptor and retinoid X receptor ligands inhibit monocyte chemotactic protein-1-directed migration of monocytes. Eur J Pharmacol; 2000 Aug 11;401(3):259-70
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  • We studied the effects of peroxisome proliferator-activated receptor (PPAR) gamma, alpha, and retinoid X receptor alpha (RXRalpha) ligands on MCP-1-directed migration and matrix metalloproteinase expression of a human acute monocytic leukemia cell line (THP-1).
  • [MeSH-major] Cell Movement / drug effects. Chemokine CCL2 / pharmacology. Monocytes / drug effects. Receptors, Cytoplasmic and Nuclear / agonists. Receptors, Retinoic Acid / agonists. Thiazolidinediones. Transcription Factors / agonists
  • [MeSH-minor] 5,8,11,14-Eicosatetraynoic Acid / pharmacology. Chemotaxis / drug effects. Chromans / pharmacology. Dose-Response Relationship, Drug. Enzyme Activation / drug effects. Enzyme Inhibitors / pharmacology. Flavonoids / pharmacology. Humans. Matrix Metalloproteinase 9 / drug effects. Matrix Metalloproteinase 9 / metabolism. Mitogen-Activated Protein Kinases / antagonists & inhibitors. Mitogen-Activated Protein Kinases / metabolism. Pyrimidines / pharmacology. Tetradecanoylphorbol Acetate / pharmacology. Thiazoles / pharmacology. Tissue Inhibitor of Metalloproteinase-1 / drug effects. Tissue Inhibitor of Metalloproteinase-1 / metabolism. Tumor Cells, Cultured

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  • (PMID = 10936484.001).
  • [ISSN] 0014-2999
  • [Journal-full-title] European journal of pharmacology
  • [ISO-abbreviation] Eur. J. Pharmacol.
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / HL-58328-03
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] NETHERLANDS
  • [Chemical-registry-number] 0 / 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one; 0 / Chemokine CCL2; 0 / Chromans; 0 / Enzyme Inhibitors; 0 / Flavonoids; 0 / Pyrimidines; 0 / Receptors, Cytoplasmic and Nuclear; 0 / Receptors, Retinoic Acid; 0 / Thiazoles; 0 / Thiazolidinediones; 0 / Tissue Inhibitor of Metalloproteinase-1; 0 / Transcription Factors; 0 / retinoic acid receptor alpha; 05V02F2KDG / rosiglitazone; 1191-85-1 / 5,8,11,14-Eicosatetraynoic Acid; 86C4MRT55A / pirinixic acid; EC 2.7.11.24 / Mitogen-Activated Protein Kinases; EC 3.4.24.35 / Matrix Metalloproteinase 9; I66ZZ0ZN0E / troglitazone; NI40JAQ945 / Tetradecanoylphorbol Acetate
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45. Mun GI, Boo YC: Identification of CD44 as a senescence-induced cell adhesion gene responsible for the enhanced monocyte recruitment to senescent endothelial cells. Am J Physiol Heart Circ Physiol; 2010 Jun;298(6):H2102-11
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  • Senescent human umbilical vein endothelial cells (HUVECs) prepared by continuous subculturing in vitro showed higher binding affinity for monocytes (THP-1 cells, human acute monocytic leukemia cell line) compared with young cells.
  • [MeSH-minor] Aging / genetics. Aging / physiology. Antibodies / pharmacology. Atherosclerosis / physiopathology. Cell Adhesion / drug effects. Cell Adhesion / genetics. Cell Adhesion / physiology. Cell Line, Tumor. Cells, Cultured. Humans. Phenotype. RNA, Small Interfering / pharmacology. Umbilical Veins / cytology

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  • (PMID = 20382854.001).
  • [ISSN] 1522-1539
  • [Journal-full-title] American journal of physiology. Heart and circulatory physiology
  • [ISO-abbreviation] Am. J. Physiol. Heart Circ. Physiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies; 0 / Antigens, CD44; 0 / CD44 protein, human; 0 / RNA, Small Interfering
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46. Nishio S, Sugiyama T, Shouji T, Yoshizaki A, Kitagawa R, Ushijima K, Kamura T: Pilot study evaluating the efficacy and toxicity of irinotecan plus oral etoposide for platinum- and taxane-resistant epithelial ovarian cancer. Gynecol Oncol; 2007 Aug;106(2):342-7
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  • Acute myeloid leukemia (M5) developed as a secondary malignancy in 1 patient.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Ovarian Neoplasms / drug therapy
  • [MeSH-minor] Administration, Oral. Adult. Aged. Bridged Compounds / pharmacology. Camptothecin / administration & dosage. Camptothecin / adverse effects. Camptothecin / analogs & derivatives. Drug Resistance, Neoplasm. Etoposide / administration & dosage. Etoposide / adverse effects. Female. Humans. Middle Aged. Organoplatinum Compounds / pharmacology. Pilot Projects. Taxoids / pharmacology

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  • (PMID = 17499346.001).
  • [ISSN] 0090-8258
  • [Journal-full-title] Gynecologic oncology
  • [ISO-abbreviation] Gynecol. Oncol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Bridged Compounds; 0 / Organoplatinum Compounds; 0 / Taxoids; 1605-68-1 / taxane; 6PLQ3CP4P3 / Etoposide; 7673326042 / irinotecan; XT3Z54Z28A / Camptothecin
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47. Charrad RS, Gadhoum Z, Qi J, Glachant A, Allouche M, Jasmin C, Chomienne C, Smadja-Joffe F: Effects of anti-CD44 monoclonal antibodies on differentiation and apoptosis of human myeloid leukemia cell lines. Blood; 2002 Jan 1;99(1):290-9
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  • [Title] Effects of anti-CD44 monoclonal antibodies on differentiation and apoptosis of human myeloid leukemia cell lines.
  • Acute myeloid leukemia (AML) is a heterogeneous leukemia characterized by the blockage of myeloid differentiation at different stages, which define distinct AML subtypes.
  • We have recently reported that the ligation of CD44 with 2 activating monoclonal antibodies (mAbs), A3D8 and H90, triggers terminal differentiation of leukemic blasts in AML-M1/2 to AML-M5 subtypes, which are the most frequent ones.
  • However, fresh AML blasts have short in vitro lifespans.
  • Therefore, to find relevant in vitro cellular models for further studying the mechanisms involved in CD44-induced differentiation, we investigated whether CD44 ligation with A3D8 and H90 mAbs can induce terminal differentiation of THP-1, NB4, and HL60 cells, each interesting models of AML-M5 (monoblastic subtype), AML-M3 (promyelocytic subtype), and AML-M2 (myeloblastic subtype), respectively.
  • We also study whether CD44 ligation induces a loss of proliferative capacity, an important feature of late-stage myeloid differentiation.
  • In the second part of our study, we investigated whether A3D8 and H90 anti-CD44 mAbs can induce the differentiation and inhibit the proliferation of KG1a cells, which are very immature AML-M0 blasts.
  • This result may provide a new experimental basis for a differentiative therapy in AML-M0 patients.
  • [MeSH-major] Antibodies, Monoclonal / pharmacology. Antigens, CD44 / physiology. Apoptosis. Cell Differentiation. Leukemia, Myeloid, Acute / pathology
  • [MeSH-minor] Cell Division / drug effects. Granulocytes / pathology. HL-60 Cells / pathology. Humans. Tretinoin / pharmacology. Tumor Cells, Cultured


48. Sung TJ, Lee DH, Kim SK, Jun YH: Congenital acute myeloid leukemia with t(8;16) and t(17;19) double translocation: case presentation and literature review. J Korean Med Sci; 2010 Jun;25(6):945-9
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  • [Title] Congenital acute myeloid leukemia with t(8;16) and t(17;19) double translocation: case presentation and literature review.
  • Congenital leukemia is uncommon and excluding transient myeloproliferation associated with Down syndrome, makes up approximately 1% of childhood leukemias.
  • Bone marrow morphology was consistent with acute myeloid leukemia (M5) and cytogenetic studies revealed t(8;16) and t(17;19) double translocation.
  • Although prognosis of congenital leukemia is known to be dismal, recent reports showed spontaneous remissions.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Translocation, Genetic

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  • (PMID = 20514319.001).
  • [ISSN] 1598-6357
  • [Journal-full-title] Journal of Korean medical science
  • [ISO-abbreviation] J. Korean Med. Sci.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Korea (South)
  • [Number-of-references] 30
  • [Other-IDs] NLM/ PMC2877231
  • [Keywords] NOTNLM ; Drug Therapy / Leukemia / Leukemic Infiltration / Translocation, Genetic
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49. Arabi Y, Kumar A, Wood K, Flaten A: The feasibility of nitric oxide delivery with high frequency jet ventilation. Respirology; 2005 Nov;10(5):673-7
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  • A 27-year-old female with acute monocytic leukaemia (M5) developed acute respiratory distress syndrome (ARDS).
  • Approval of the Institutional Review Board and the Food and Drug Administration was obtained to use nitric oxide (NO) with HFJV on a compassionate basis considering the grave situation.
  • [MeSH-minor] Adult. Fatal Outcome. Female. Humans. Leukemia, Monocytic, Acute / complications

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  • (PMID = 16268924.001).
  • [ISSN] 1323-7799
  • [Journal-full-title] Respirology (Carlton, Vic.)
  • [ISO-abbreviation] Respirology
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Australia
  • [Chemical-registry-number] 31C4KY9ESH / Nitric Oxide
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50. Saito B, Nakamaki T, Nakashima H, Usui T, Hattori N, Kawakami K, Tomoyasu S: Reversible posterior leukoencephalopathy syndrome after repeat intermediate-dose cytarabine chemotherapy in a patient with acute myeloid leukemia. Am J Hematol; 2007 Apr;82(4):304-6
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  • [Title] Reversible posterior leukoencephalopathy syndrome after repeat intermediate-dose cytarabine chemotherapy in a patient with acute myeloid leukemia.
  • Acute monoblastic leukemia was diagnosed.
  • No infiltration of leukemia cells was seen.
  • These details suggest not only that direct cerebral neurotoxicity of cytarabine but also that some type of allergic response may have been involved in the development of RPLS.
  • [MeSH-major] Antimetabolites, Antineoplastic / adverse effects. Brain Diseases / chemically induced. Cytarabine / adverse effects. Leukemia, Monocytic, Acute / drug therapy. Neurotoxicity Syndromes / etiology
  • [MeSH-minor] Drug Hypersensitivity. Humans. Male. Middle Aged. Syndrome

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  • (PMID = 16947320.001).
  • [ISSN] 0361-8609
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 04079A1RDZ / Cytarabine
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51. Mezzanotte L, Fazzina R, Michelini E, Tonelli R, Pession A, Branchini B, Roda A: In vivo bioluminescence imaging of murine xenograft cancer models with a red-shifted thermostable luciferase. Mol Imaging Biol; 2010 Aug;12(4):406-14
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  • PURPOSE: Conventional in vivo bioluminescence imaging using wild-type green-emitting luciferase is limited by absorption and scattering of the bioluminescent signal through tissues.
  • METHODS: Human hepatoblastoma cell line (HepG2) and human acute monocytic leukemia cell line (Thp1) cells were genetically engineered using retroviral vector technology to stably express the red-shifted or the wild-type green luciferase.
  • A xenograft model of liver cancer was established by subcutaneous injection of the HepG2-engineered cells in the flank regions of mice, and a leukemia model was generated by intravenous injection of the engineered Thp1 cells.
  • Imaging was performed with both intact and scarified live animals to quantify the absorption effects of the skin and deep tissue.
  • CONCLUSION: Two different bioluminescent mouse cancer models demonstrate the utility of a new red-shifted thermostable luciferase, Ppy RE-TS, that improved the in vivo imaging performance when compared with wild-type P.
  • While wild-type luciferase is currently a popular reporter for in vivo imaging methods, this study demonstrates the potential of red-emitting firefly luciferase mutants to enhance the performance of bioluminescence imaging experiments.
  • [MeSH-minor] Absorption / drug effects. Animals. Benzothiazoles / administration & dosage. Benzothiazoles / pharmacology. Cell Count. Cell Line, Tumor. Color. Disease Progression. Enzyme Stability / drug effects. Hep G2 Cells. Humans. Injections, Intraperitoneal. Kinetics. Mice. Photons. Substrate Specificity / drug effects. Transfection. Tumor Burden / drug effects

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  • (PMID = 19937390.001).
  • [ISSN] 1860-2002
  • [Journal-full-title] Molecular imaging and biology : MIB : the official publication of the Academy of Molecular Imaging
  • [ISO-abbreviation] Mol Imaging Biol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzothiazoles; 0 / D-luciferin; EC 1.13.12.- / Luciferases
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52. Adachi R, Honma Y, Masuno H, Kawana K, Shimomura I, Yamada S, Makishima M: Selective activation of vitamin D receptor by lithocholic acid acetate, a bile acid derivative. J Lipid Res; 2005 Jan;46(1):46-57
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  • The vitamin D receptor (VDR), a member of the nuclear receptor superfamily, mediates the biological actions of the active form of vitamin D, 1alpha,25-dihydroxyvitamin D(3).
  • Recently, VDR was found to respond to bile acids as well as other nuclear receptors, farnesoid X receptor (FXR) and pregnane X receptor (PXR).
  • To elucidate the structure-function relationship between VDR and bile acids, we examined the effect of several LCA derivatives on VDR activation and identified compounds with more potent activity than LCA.
  • Unlike LCA, LCA acetate inhibited the proliferation of human monoblastic leukemia cells and induced their monocytic differentiation.
  • The development of VDR agonists derived from bile acids should be useful to elucidate ligand-selective VDR functions.
  • [MeSH-minor] Animals. Bile Acids and Salts. Cell Differentiation / drug effects. Cell Line. Cell Line, Tumor. Cell Proliferation / drug effects. Humans. Leukemia, Monocytic, Acute / pathology. Mice. Mice, Inbred C57BL. Mutation. Protein Binding. Structure-Activity Relationship

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  • (PMID = 15489543.001).
  • [ISSN] 0022-2275
  • [Journal-full-title] Journal of lipid research
  • [ISO-abbreviation] J. Lipid Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Bile Acids and Salts; 0 / Receptors, Calcitriol; 0 / lithocholic acid acetate; 5QU0I8393U / Lithocholic Acid
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53. Witcher M, Shiu HY, Guo Q, Miller WH Jr: Combination of retinoic acid and tumor necrosis factor overcomes the maturation block in a variety of retinoic acid-resistant acute promyelocytic leukemia cells. Blood; 2004 Nov 15;104(10):3335-42
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  • [Title] Combination of retinoic acid and tumor necrosis factor overcomes the maturation block in a variety of retinoic acid-resistant acute promyelocytic leukemia cells.
  • Retinoic acid (RA) overcomes the maturation block in t(15:17) acute promyelocytic leukemia (APL), leading to granulocytic differentiation.
  • Previously, we showed that RA and tumor necrosis factor (TNF) promote monocytic differentiation of the APL cell line NB4 and U937 monoblastic cells.
  • Here, we report that combining TNF with RA leads to maturation of several RA-resistant APL cells along a monocytic pathway, whereas UF-1, a patient-derived RA-resistant cell line, showed characteristics of granulocytic differentiation.
  • We found distinct differences in gene regulation between UF-1 cells and cells showing monocytic differentiation.
  • Although IRF-7 was up-regulated by TNF and RA in all cells tested, expression of c-jun and PU.1 correlated with monocytic differentiation.
  • Using neutralizing antibodies against m-CSF-1R or its ligand, we found that inhibiting this pathway strongly reduced CD14 expression in response to RA and TNF, suggesting that this pathway is essential for their synergy in RA-resistant leukemia cells.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Drug Resistance, Neoplasm. Leukemia, Promyelocytic, Acute. Tretinoin / pharmacology. Tumor Necrosis Factor-alpha / pharmacology
  • [MeSH-minor] Antibodies / pharmacology. Cell Differentiation / drug effects. Cell Differentiation / immunology. Cell Line, Tumor. Cell Survival / drug effects. Cell Survival / immunology. Drug Synergism. Gene Expression Regulation, Leukemic / drug effects. Humans. Monocytes / cytology. Monocytes / metabolism. Neoplasm Proteins / genetics. Nuclear Proteins / genetics. Receptor, Macrophage Colony-Stimulating Factor / immunology. Receptor, Macrophage Colony-Stimulating Factor / metabolism. Receptors, Retinoic Acid / genetics. Transcription Factors / genetics. Transcription Factors / metabolism. Tumor Suppressor Proteins

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  • (PMID = 15256426.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies; 0 / Antineoplastic Agents; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / Receptors, Retinoic Acid; 0 / Transcription Factors; 0 / Tumor Necrosis Factor-alpha; 0 / Tumor Suppressor Proteins; 0 / retinoic acid receptor alpha; 143220-95-5 / PML protein, human; 5688UTC01R / Tretinoin; EC 2.7.10.1 / Receptor, Macrophage Colony-Stimulating Factor
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54. Demircioğlu F, Oren H, Yilmaz S, Arslansoyu S, Eren S, Irken G: Chemotherapy-induced acral erythema in a pediatric patient with acute monoblastic leukemia. Pediatr Hematol Oncol; 2008 Apr-May;25(3):211-5
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  • [Title] Chemotherapy-induced acral erythema in a pediatric patient with acute monoblastic leukemia.
  • Chemotherapy-induced acral erythema or palmoplantar erythrodysesthesia syndrome is a well-defined reaction to some of the chemotherapeutic agents such as methotrexate, cytarabine, doxorubicin, fluorouracil, and bleomycin.
  • The authors present a case of acral erythema in a young patient with acute monoblastic leukemia to emphasize this high-dose chemotherapy-induced side effect, which is rarely seen in children and is usually self-limited.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Erythema / chemically induced. Leukemia, Monocytic, Acute / complications

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  • (PMID = 18432504.001).
  • [ISSN] 1521-0669
  • [Journal-full-title] Pediatric hematology and oncology
  • [ISO-abbreviation] Pediatr Hematol Oncol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; 11056-06-7 / Bleomycin; 80168379AG / Doxorubicin; U3P01618RT / Fluorouracil; YL5FZ2Y5U1 / Methotrexate
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55. Laengle UW, Markstein R, Cazaubon C, Roman D: Antiglaucoma drug GLC756 and its effect on cellular cAMP and tumor necrosis factor alpha release in vitro of activated human monocytic leukemia cells. Jpn J Ophthalmol; 2009 Mar;53(2):159-63
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  • [Title] Antiglaucoma drug GLC756 and its effect on cellular cAMP and tumor necrosis factor alpha release in vitro of activated human monocytic leukemia cells.
  • PURPOSE: GLC756, a putative antiglaucoma drug with dopamine D(2) agonist and D(1) antagonist properties, significantly decreases tumor necrosis factor alpha (TNF-alpha) levels in lipopolysaccharide (LPS)-induced rats.
  • The present study describes the effects of GLC756 on cellular adenosine 3', 5'-cyclic monophosphate (cAMP) in relation to TNF-alpha production on LPS-stimulated human acute monocytic leukemia cells.
  • METHODS: A human peripheral blood acute monocytic leukemia cell line (THP-1) was activated via LPS.
  • [MeSH-major] Antihypertensive Agents / pharmacology. Cyclic AMP / metabolism. Leukemia, Monocytic, Acute / drug therapy. Quinolines / pharmacology. Tumor Necrosis Factor-alpha / metabolism
  • [MeSH-minor] Betamethasone / pharmacology. Cell Line, Tumor / drug effects. Enzyme-Linked Immunosorbent Assay. Glucocorticoids / pharmacology. Humans. Lipopolysaccharides / pharmacology. Ophthalmic Solutions / pharmacology. Receptors, Dopamine D1 / antagonists & inhibitors. Receptors, Dopamine D2 / agonists

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  • (PMID = 19333701.001).
  • [ISSN] 1613-2246
  • [Journal-full-title] Japanese journal of ophthalmology
  • [ISO-abbreviation] Jpn. J. Ophthalmol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antihypertensive Agents; 0 / Glucocorticoids; 0 / Lipopolysaccharides; 0 / Ophthalmic Solutions; 0 / Quinolines; 0 / Receptors, Dopamine D1; 0 / Receptors, Dopamine D2; 0 / SDZ GLC 756; 0 / Tumor Necrosis Factor-alpha; 9842X06Q6M / Betamethasone; E0399OZS9N / Cyclic AMP
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56. Ji YY, Zhang WG, Chen YX, Zhao XM, He AL, Liu J, Wang JL, Wang FX, Zhang PY, Zhang WJ: [Efficiency of GHA priming therapy on patients with acute monocytic leukemia and its mechanism]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2010 Feb;18(1):213-8
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  • [Title] [Efficiency of GHA priming therapy on patients with acute monocytic leukemia and its mechanism].
  • The aim of this study was to explore the clinical efficiency and side effects of GHA-priming therapy on patients with acute monocytic leukemia, and to analyze its mechanism.
  • 37 patients with refractory, relapse, hypocellular acute monocytic leukemia and elderly patients with AML-M(5) were treated with GHA-priming therapy (G-CSF, homoharringtonine and low dosage of cytarabine).
  • It is concluded that the GHA priming therapy can be used to treat patients with refractory, relapse, senile and hypocellular acute monocytic leukemia with satisfied response rate and low hematological and non-hematological toxicities.
  • G-CSF can enhance cytotoxicity of drugs such as Ara-C and HHT by promoting G(0) phase cells into the reproductive cycle.
  • MLAA-34 is a novel anti-apoptotic factor of acute monocytic leukemia.

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  • (PMID = 20137150.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] Clinical Trial; English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Harringtonines; 04079A1RDZ / Cytarabine; 143011-72-7 / Granulocyte Colony-Stimulating Factor; 6FG8041S5B / homoharringtonine
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57. Ansa-Addo EA, Lange S, Stratton D, Antwi-Baffour S, Cestari I, Ramirez MI, McCrossan MV, Inal JM: Human plasma membrane-derived vesicles halt proliferation and induce differentiation of THP-1 acute monocytic leukemia cells. J Immunol; 2010 Nov 1;185(9):5236-46
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  • [Title] Human plasma membrane-derived vesicles halt proliferation and induce differentiation of THP-1 acute monocytic leukemia cells.
  • The myeloid-differentiating agents all-trans retinoic acid/PMA and histamine, the inflammatory mediator that inhibits promonocyte proliferation, induced an intracellular Ca(2+)-mediated PMV (as opposed to exosome) release from THP-1 promonocytes.
  • In this study, to our knowledge we show for the first time that TGF-β1 is carried on the surface of PMVs, and we confirm the presence within PMVs of certain leaderless proteins, with reported roles in myeloid cell differentiation.
  • Our in vitro findings support a model in which TGF-β1-bearing PMVs, released from promonocytic leukemia cells (THP-1) or primary peripheral blood monocytes on exposure to sublytic complement or after treatment with a differentiation therapy agent, such as all-trans retinoic acid, significantly reduce proliferation of THP-1 cells.
  • [MeSH-minor] Apoptosis / physiology. Blotting, Western. Cell Line, Tumor. Cell Proliferation. Cell Separation. Electrophoresis, Polyacrylamide Gel. Enzyme-Linked Immunosorbent Assay. Exocytosis. Flow Cytometry. Fluorescent Antibody Technique. Humans. Leukemia, Monocytic, Acute / metabolism. Microscopy, Electron, Transmission

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  • (PMID = 20921526.001).
  • [ISSN] 1550-6606
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Transforming Growth Factor beta1
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58. Forrest AR, Kanamori-Katayama M, Tomaru Y, Lassmann T, Ninomiya N, Takahashi Y, de Hoon MJ, Kubosaki A, Kaiho A, Suzuki M, Yasuda J, Kawai J, Hayashizaki Y, Hume DA, Suzuki H: Induction of microRNAs, mir-155, mir-222, mir-424 and mir-503, promotes monocytic differentiation through combinatorial regulation. Leukemia; 2010 Feb;24(2):460-6
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  • [Title] Induction of microRNAs, mir-155, mir-222, mir-424 and mir-503, promotes monocytic differentiation through combinatorial regulation.
  • Acute myeloid leukemia (AML) involves a block in terminal differentiation of the myeloid lineage and uncontrolled proliferation of a progenitor state.
  • Using phorbol myristate acetate (PMA), it is possible to overcome this block in THP-1 cells (an M5-AML containing the MLL-MLLT3 fusion), resulting in differentiation to an adherent monocytic phenotype.
  • [MeSH-minor] Cell Cycle / drug effects. Cell Proliferation / drug effects. Cells, Cultured. Humans. Tetradecanoylphorbol Acetate / pharmacology

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  • (PMID = 19956200.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / MIRN155 microRNA, human; 0 / MIRN222 microRNA, human; 0 / MIRN503 microRNA, human; 0 / MicroRNAs; NI40JAQ945 / Tetradecanoylphorbol Acetate
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59. Fujigaki H, Saito K, Lin F, Fujigaki S, Takahashi K, Martin BM, Chen CY, Masuda J, Kowalak J, Takikawa O, Seishima M, Markey SP: Nitration and inactivation of IDO by peroxynitrite. J Immunol; 2006 Jan 1;176(1):372-9
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  • In this study we found that IDO activity was inhibited by the peroxynitrite generator, 3-(4-morpholinyl)sydnonimine, in PMA-differentiated cytokine-induced THP-1 (acute monocytic leukemia) cells and IFN-gamma-stimulated PBMCs, whereas IDO protein expression was unaffected compared with that in untreated cells.
  • [MeSH-major] Indoleamine-Pyrrole 2,3,-Dioxygenase / drug effects. Leukocytes, Mononuclear / drug effects. Peroxynitrous Acid / pharmacology
  • [MeSH-minor] Amino Acid Sequence. Blotting, Western. Cell Line, Tumor. Chromatography, High Pressure Liquid. Humans. Molecular Sequence Data. Mutagenesis, Site-Directed. Spectrometry, Mass, Electrospray Ionization. Tyrosine / analogs & derivatives. Tyrosine / biosynthesis. Tyrosine / chemistry. Tyrosine / drug effects

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  • (PMID = 16365430.001).
  • [ISSN] 0022-1767
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Indoleamine-Pyrrole 2,3,-Dioxygenase; 14691-52-2 / Peroxynitrous Acid; 3604-79-3 / 3-nitrotyrosine; 42HK56048U / Tyrosine
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60. Wu JY, Chung KT, Liu YW, Lu FJ, Tsai RS, Chen CH, Chen CH: Synthesis and biological evaluation of novel C(6) modified baicalein derivatives as antioxidative agents. J Agric Food Chem; 2008 Apr 23;56(8):2838-45
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  • [Title] Synthesis and biological evaluation of novel C(6) modified baicalein derivatives as antioxidative agents.
  • Baicalein, one of the major flavones, was found to be responsible for the antioxidative activity of the traditional Chinese medicinal herb Huang-Qin ( Scutellaria baicalensis Georgi), which is widely used as an antioxidative, anti-inflammatory, and antitumor agent.
  • Flow cytometrical method was employed to measure the intracellular antioxidative activity and GSH depletion capacity of these derivatives in human acute monocytic leukemia cell line (THP-1).
  • [MeSH-minor] Alkylation. Benzene Derivatives / pharmacology. Benzothiazoles. Cell Line, Tumor. Free Radical Scavengers / chemistry. Glutathione / metabolism. Humans. Leukemia, Monocytic, Acute. Sulfonic Acids. Terpenes / chemistry

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  • (PMID = 18348528.001).
  • [ISSN] 0021-8561
  • [Journal-full-title] Journal of agricultural and food chemistry
  • [ISO-abbreviation] J. Agric. Food Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antioxidants; 0 / Benzene Derivatives; 0 / Benzothiazoles; 0 / Flavanones; 0 / Free Radical Scavengers; 0 / Sulfonic Acids; 0 / Terpenes; 28752-68-3 / 2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid; 49QAH60606 / baicalein; GAN16C9B8O / Glutathione; PG7JD54X4I / cumene hydroperoxide
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61. Reddy PP, Rao RR, Shashidhar J, Sastry BS, Rao JM, Babu KS: Phytochemical investigation of labdane diterpenes from the rhizomes of Hedychium spicatum and their cytotoxic activity. Bioorg Med Chem Lett; 2009 Nov 1;19(21):6078-81
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  • A comprehensive reinvestigation of chemical constituents from the rhizomes of Hedychium spicatum led to the isolation of two new labdane-type diterpene (1, 2), together with six known compounds (3-8).
  • In addition, all the isolates were tested for their cytotoxicity against the THP-1 (human acute monocytic leukemia), HL-60 (human promyelocytic leukemia), A-375 (human malignant melanoma) and A-549 (human lung carcinoma) cancerous cell lines.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / chemistry. Diterpenes / chemistry. Zingiberaceae / chemistry
  • [MeSH-minor] Cell Line, Tumor. Drug Screening Assays, Antitumor. Humans. Magnetic Resonance Spectroscopy. Molecular Conformation. Plant Extracts / chemistry. Rhizome / chemistry

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  • (PMID = 19782567.001).
  • [ISSN] 1464-3405
  • [Journal-full-title] Bioorganic & medicinal chemistry letters
  • [ISO-abbreviation] Bioorg. Med. Chem. Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / 14,15,16-trinor-7,11-labdadien-13-oic acid; 0 / 7-hydroxy-15,16-epoxy-17-al-7,11,13(16),14-labdatetraene-6-one; 0 / Antineoplastic Agents, Phytogenic; 0 / Diterpenes; 0 / Plant Extracts
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62. Itoh M, Kuwahara J, Itoh K, Fukuda Yi, Kohya M, Shindo M, Shishido K: Apoptosis-inducing activity of synthetic intermediates of halichlorine. Bioorg Med Chem Lett; 2002 Aug 19;12(16):2069-72
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  • Synthetic intermediates of alkaloid halichlorine with the azaspiro core structure have been found to induce apoptosis of cultured human cells including an acute monocytic leukemia cell line (THP-1) at micromolar concentrations.
  • The novel biological activity of the intermediates was suggested to depend on the skeletal structure and silyloxymethyl functionality on the five-membered ring.
  • [MeSH-major] Alkaloids / chemical synthesis. Alkaloids / pharmacology. Apoptosis / drug effects. Spiro Compounds / chemical synthesis. Spiro Compounds / pharmacology
  • [MeSH-minor] Animals. Caspase 3. Caspase 7. Caspases / metabolism. Chromatin / drug effects. Chromatin / metabolism. Dose-Response Relationship, Drug. Enzyme Activation / drug effects. Humans. Molecular Structure. Time Factors. Tumor Cells, Cultured

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  • (PMID = 12127506.001).
  • [ISSN] 0960-894X
  • [Journal-full-title] Bioorganic & medicinal chemistry letters
  • [ISO-abbreviation] Bioorg. Med. Chem. Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Alkaloids; 0 / Chromatin; 0 / Spiro Compounds; 0 / halichlorine; EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / CASP7 protein, human; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspase 7; EC 3.4.22.- / Caspases
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63. Walter R, Schoedon G, Bächli E, Betts DR, Hossle JP, Calandra T, Joller-Jemelka HI, Fehr J, Schaffner A: Establishment and characterization of an arsenic-sensitive monoblastic leukaemia cell line (SigM5). Br J Haematol; 2000 May;109(2):396-404
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  • [Title] Establishment and characterization of an arsenic-sensitive monoblastic leukaemia cell line (SigM5).
  • Few human monoblastic cell lines have been characterized to date.
  • We have established the SigM5 cell line from a patient with acute monoblastic leukaemia (FAB M5a).
  • SigM5 monoblasts were sensitive to arsenic trioxide (As2O3) previously not described to induce apoptosis in monoblastic cells.
  • Differing considerably in morphology, immunophenotype and sensitivity to arsenics from the widely used cell lines U937, HL-60 and THP-1, SigM5 is a new monoblastic cell line useful for studying leukaemogenesis, monocyte differentiation and tumour cell susceptibility to arsenic compounds.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Arsenicals / pharmacology. Cell Culture Techniques / methods. Leukemia, Monocytic, Acute / pathology. Leukocytes, Mononuclear / pathology. Oxides / pharmacology
  • [MeSH-minor] Apoptosis / drug effects. Cell Differentiation. Cell Line / immunology. Cell Line / pathology. Chromosomes, Human, Pair 8. Humans. Karyotyping. Microscopy, Electron. Polyploidy


64. Li M, Liu ZH, Chen Q, Zhou WQ, Yu MW, Lü GX, Lü XL, Shen YN, Liu WD, Wu SX: Insoluble beta-glucan from the cell wall of Candida albicans induces immune responses of human THP-1 monocytes through Dectin-1. Chin Med J (Engl); 2009 Mar 5;122(5):496-501
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  • It has been demonstrated that Dectin-1 as the principal C-type lectin pattern-recognition receptor (PRR) can recognize fungal beta-glucan and induce immune responses.
  • In this study, we sought to clarify whether insoluble beta-glucan from the cell wall of C. albicans (CaIG) could induce immune responses in human THP-1 monocytes (a human acute monocytic leukemia cell line) and to determine the underlying mechanisms.
  • The secretion of TNF-a and IL-8 were measured by enzyme-linked immunosorbent assay (ELISA).
  • [MeSH-major] Candida albicans / metabolism. Cell Wall / metabolism. Membrane Proteins / metabolism. Monocytes / drug effects. Monocytes / immunology. Nerve Tissue Proteins / metabolism. beta-Glucans / pharmacology
  • [MeSH-minor] Blotting, Western. Cell Line, Tumor. Enzyme-Linked Immunosorbent Assay. Gene Expression / drug effects. Humans. Hydrogen Peroxide / metabolism. Interleukin-8 / genetics. Interleukin-8 / metabolism. Lectins, C-Type. Reverse Transcriptase Polymerase Chain Reaction. Toll-Like Receptor 2 / genetics. Tumor Necrosis Factor-alpha / genetics. Tumor Necrosis Factor-alpha / metabolism

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  • [CommentIn] Chin Med J (Engl). 2009 Mar 5;122(5):483-5 [19323895.001]
  • (PMID = 19323897.001).
  • [ISSN] 0366-6999
  • [Journal-full-title] Chinese medical journal
  • [ISO-abbreviation] Chin. Med. J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Interleukin-8; 0 / Lectins, C-Type; 0 / Membrane Proteins; 0 / Nerve Tissue Proteins; 0 / Toll-Like Receptor 2; 0 / Tumor Necrosis Factor-alpha; 0 / beta-Glucans; 0 / dectin 1; BBX060AN9V / Hydrogen Peroxide
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65. Lee SH, Kim EJ, Suk K, Kim IS, Lee WH: TL1A induces the expression of TGF-β-inducible gene h3 (βig-h3) through PKC, PI3K, and ERK in THP-1 cells. Cell Immunol; 2010;266(1):61-6
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  • βig-h3, an extracellular matrix protein involved in various biological processes including cellular growth, differentiation, adhesion, migration, and angiogenesis, has been shown to be elevated in various inflammatory processes.
  • In order to find out whether the TL1A-induced inflammatory activation of macrophages is associated with the up-regulation of βig-h3 expression, the human acute monocytic leukemia cell line (THP-1) was stimulated with either recombinant human TL1A- or DR3-specific monoclonal antibodies.
  • [MeSH-major] Extracellular Matrix Proteins / metabolism. Extracellular Signal-Regulated MAP Kinases / metabolism. Monocytes / metabolism. Phosphatidylinositol 3-Kinases / metabolism. Protein Kinase C / metabolism. Signal Transduction / drug effects. Transforming Growth Factor beta / metabolism. Tumor Necrosis Factor Ligand Superfamily Member 15 / pharmacology
  • [MeSH-minor] Antibodies, Monoclonal / immunology. Antibodies, Monoclonal / pharmacology. Cell Line, Tumor. Enzyme Inhibitors / pharmacology. Gene Expression / drug effects. Gene Expression / genetics. Humans. NF-kappa B / antagonists & inhibitors. NF-kappa B / metabolism. Phosphorylation / drug effects. Protein Kinase Inhibitors / pharmacology. Receptors, Tumor Necrosis Factor, Member 25 / immunology. Recombinant Proteins / pharmacology

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  • [Copyright] Copyright © 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20863486.001).
  • [ISSN] 1090-2163
  • [Journal-full-title] Cellular immunology
  • [ISO-abbreviation] Cell. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Enzyme Inhibitors; 0 / Extracellular Matrix Proteins; 0 / NF-kappa B; 0 / Protein Kinase Inhibitors; 0 / Receptors, Tumor Necrosis Factor, Member 25; 0 / Recombinant Proteins; 0 / TNFRSF25 protein, human; 0 / TNFSF15 protein, human; 0 / Transforming Growth Factor beta; 0 / Tumor Necrosis Factor Ligand Superfamily Member 15; 148710-76-3 / betaIG-H3 protein; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.13 / Protein Kinase C; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases
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66. Rots MG, Pieters R, Jansen G, Kaspers GJ, Van Zantwijk CH, Noordhuis P, Voorn DA, Van Wering ER, Creutzig U, Veerman AJ, Peters GJ: A possible role for methotrexate in the treatment of childhood acute myeloid leukaemia, in particular for acute monocytic leukaemia. Eur J Cancer; 2001 Mar;37(4):492-8
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  • [Title] A possible role for methotrexate in the treatment of childhood acute myeloid leukaemia, in particular for acute monocytic leukaemia.
  • Acute myeloid leukaemia (AML) is thought to be methotrexate (MTX)-resistant.
  • However, a small study suggested that acute monocytic leukemia (AML-M5) is sensitive to MTX.
  • We measured MTX accumulation/polyglutamylation in 20 AML-nonM5, 37 AML-M5 and 83 common/preB-acute lymphoblastic leukaemia (c/preB-ALL) samples.
  • Membrane transport was determined in 11 childhood AMLs (including 3 AML-M5) and in 25 c/preB-ALL samples.
  • MTX sensitivity was determined in 23 AML-nonM5, 15 AML-M5 and 63 common/preB-ALL samples using the thymidylate synthase (TS) inhibition assay.
  • MTX transport was higher in AML samples compared with c/preB-ALL precluding a transport defect in AML.
  • Accumulation of long-chain polyglutamates MTX-Glu(4-6) was 3-fold lower for AML-nonM5 compared with c/preB-ALL cells (median 268 versus 889 pmol MTX-Glu(4-6)/10(9) cells; P < or = 0.001); for AML-M5 samples, median accumulation of MTX-Glu(4-6) was 0 pmol/10(9) cells (P < or = 0.001).
  • After short-term MTX exposure, AML-nonM5 was 6-fold more resistant to MTX compared with c/preB-ALL cells (2.16 versus 0.39 microM; P < 0.001), while AML-M5 was 2-fold more resistant (P = 0.02).
  • In both AML-nonM5 and AML-M5 cells, MTX resistance was circumvented by continuous MTX exposure (median TSI(50) values: 0.052 and 0.041 microM, respectively) compared with a c/preB-ALL value of 0.066 microM.
  • In conclusion, AML-M5 is relatively sensitive to MTX compared with other AML-subtypes even though polyglutamylation of MTX is poor.
  • Using continuous exposure, AML-nonM5 and AML-M5 cells were at least as sensitive to MTX as c/preB-ALL cells.
  • This report suggests that MTX might be an overlooked drug in the treatment of childhood AML.
  • [MeSH-major] Antimetabolites, Antineoplastic / therapeutic use. Leukemia, Monocytic, Acute / drug therapy. Methotrexate / therapeutic use
  • [MeSH-minor] Biological Transport. Child. Drug Resistance, Neoplasm. Humans. Thymidylate Synthase / antagonists & inhibitors. Tumor Cells, Cultured

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  • (PMID = 11267859.001).
  • [ISSN] 0959-8049
  • [Journal-full-title] European journal of cancer (Oxford, England : 1990)
  • [ISO-abbreviation] Eur. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; EC 2.1.1.45 / Thymidylate Synthase; YL5FZ2Y5U1 / Methotrexate
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67. Wang X, Zheng Y, Xu Y, Ben J, Gao S, Zhu X, Zhuang Y, Yue S, Bai H, Chen Y, Jiang L, Ji Y, Xu Y, Fan L, Sha J, He Z, Chen Q: A novel peptide binding to the cytoplasmic domain of class A scavenger receptor reduces lipid uptake in THP-1 macrophages. Biochim Biophys Acta; 2009 Jan;1791(1):76-83
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  • In the present study we tried to reduce cellular uptake of acetylated low density lipoprotein (AcLDL) by inducing the interaction between the CSR-A and a novel peptide H11, which was screened from a phage-displayed peptide library.
  • The peptide H11 inhibited the binding and uptake of DiI-AcLDL and attenuated lipid accumulation in the differentiated human acute monocytic leukemia cell line (THP-1) macrophages.
  • [MeSH-major] Lipid Metabolism / drug effects. Macrophages / metabolism. Peptides / pharmacology. Scavenger Receptors, Class A / metabolism
  • [MeSH-minor] Cell Line. Humans. Mitogen-Activated Protein Kinase 9 / antagonists & inhibitors. Peptide Library. Recombinant Fusion Proteins / pharmacology. Signal Transduction / drug effects

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  • (PMID = 19049904.001).
  • [ISSN] 0006-3002
  • [Journal-full-title] Biochimica et biophysica acta
  • [ISO-abbreviation] Biochim. Biophys. Acta
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Peptide Library; 0 / Peptides; 0 / Recombinant Fusion Proteins; 0 / Scavenger Receptors, Class A; EC 2.7.1.24 / Mitogen-Activated Protein Kinase 9
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68. Tamayose K, Sugimoto K, Ando M, Oshimi K: Mononucleosis syndrome and acute monocytic leukemia. Eur J Haematol; 2002 Apr;68(4):236-8
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  • [Title] Mononucleosis syndrome and acute monocytic leukemia.
  • The association of infectious mononucleosis and an immunocompromised host such as occurs in acute leukemia is reported.
  • Patients with mononucleosis syndrome caused by other agents are rare.
  • We report a case of acute monocytic leukemia (AMoL) who developed varicella zoster virus (VZV) mononucleosis syndrome in the bone marrow recovery phase after myelosuppression due to high-dose cytarabine.
  • [MeSH-major] Cytarabine / adverse effects. Herpes Zoster / etiology. Herpesvirus 3, Human. Immunosuppressive Agents / adverse effects. Infectious Mononucleosis / etiology. Leukemia, Monocytic, Acute / complications. Leukemia, Monocytic, Acute / drug therapy

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  • (PMID = 12071940.001).
  • [ISSN] 0902-4441
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Immunosuppressive Agents; 04079A1RDZ / Cytarabine
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69. Wang C, Chen Z, Li Z, Cen J: The essential roles of matrix metalloproteinase-2, membrane type 1 metalloproteinase and tissue inhibitor of metalloproteinase-2 in the invasive capacity of acute monocytic leukemia SHI-1 cells. Leuk Res; 2010 Aug;34(8):1083-90
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  • [Title] The essential roles of matrix metalloproteinase-2, membrane type 1 metalloproteinase and tissue inhibitor of metalloproteinase-2 in the invasive capacity of acute monocytic leukemia SHI-1 cells.
  • The frequency of extramedullary infiltration (EMI) in acute myeloblastic leukemia (AML) is reported up to 40% and most prevalent in myelo-monoblastic and monoblastic subtypes of AML (M4 and M5 according to FAB classification).
  • To explore mechanism underlying EMI, we analyzed SHI-1 cells, a highly invasive human acute monocytic leukemia cell line, and found their strong expression of matrix metalloproteinase 2 (MMP-2), membrane type 1 MMP (MT1-MMP) and tissue inhibitor of metalloproteinase 2 (TIMP-2).
  • SHI-1 cells showed higher invasive ability to traverse reconstituted basement membranes (Matrigel) and stronger activation of proMMP-2 than other leukemia cell line such as NB4, K562, U937 and THP-1 cells.
  • Our study indicated that increasing TIMP-2 in AML patients with EMI may potentially cause adverse effects, particularly in patients containing high levels of MMP-2 and MT1-MMP.
  • [MeSH-major] Leukemia, Monocytic, Acute / metabolism. Leukemia, Monocytic, Acute / pathology. Matrix Metalloproteinase 14 / metabolism. Matrix Metalloproteinase 2 / metabolism. Tissue Inhibitor of Metalloproteinase-2 / metabolism
  • [MeSH-minor] Bone Marrow / metabolism. Bone Marrow / pathology. Collagen / metabolism. Drug Combinations. Humans. Immunoblotting. Laminin / metabolism. Matrix Metalloproteinase Inhibitors. Neoplasm Invasiveness. Proteoglycans / metabolism. RNA, Messenger / genetics. RNA, Messenger / metabolism. RNA, Small Interfering / pharmacology. Reverse Transcriptase Polymerase Chain Reaction. Stromal Cells / metabolism. Stromal Cells / pathology. Tumor Cells, Cultured

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  • [Copyright] Copyright (c) 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 20138666.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Drug Combinations; 0 / Laminin; 0 / Matrix Metalloproteinase Inhibitors; 0 / Proteoglycans; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 119978-18-6 / matrigel; 127497-59-0 / Tissue Inhibitor of Metalloproteinase-2; 9007-34-5 / Collagen; EC 3.4.24.24 / Matrix Metalloproteinase 2; EC 3.4.24.80 / MMP14 protein, human; EC 3.4.24.80 / Matrix Metalloproteinase 14
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70. Chen J, Gu LJ, Ying DM: [Low dose methotrexate combined with GM-CSF induced differentiation of U937 cells]. Zhonghua Xue Ye Xue Za Zhi; 2003 Aug;24(8):430-2
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  • OBJECTIVE: To explore the effect of methotrexate on acute monoblastic leukemia cells, and the potential role of low-dose methotrexate in the treatment of monoblastic leukemia.
  • CONCLUSION: Monoblastic leukemia might be treated with low-dose methotrexate plus GM-CSF as a differentiation induction regimen.
  • [MeSH-major] Cell Differentiation / drug effects. Granulocyte-Macrophage Colony-Stimulating Factor / pharmacology. Methotrexate / pharmacology
  • [MeSH-minor] Cell Line, Tumor. Drug Synergism. Humans. Leukemia, Monocytic, Acute / pathology. Telomerase / drug effects. Telomerase / metabolism. U937 Cells

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  • (PMID = 14642183.001).
  • [ISSN] 0253-2727
  • [Journal-full-title] Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi
  • [ISO-abbreviation] Zhonghua Xue Ye Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor; EC 2.7.7.49 / Telomerase; YL5FZ2Y5U1 / Methotrexate
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71. Schmutz C, Cartwright A, Williams H, Haworth O, Williams JH, Filer A, Salmon M, Buckley CD, Middleton J: Monocytes/macrophages express chemokine receptor CCR9 in rheumatoid arthritis and CCL25 stimulates their differentiation. Arthritis Res Ther; 2010;12(4):R161
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  • Tumour necrosis factor alpha (TNFα) increased CCR9 expression on human acute monocytic leukemia cell line THP-1 monocytic cells.
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Cell Differentiation / immunology. Cell Line. Female. Flow Cytometry. Humans. Male. Middle Aged. Reverse Transcriptase Polymerase Chain Reaction. Synovial Membrane / immunology. Synovial Membrane / metabolism. Synovial Membrane / pathology. Tumor Necrosis Factor-alpha / pharmacology. Up-Regulation / drug effects. Up-Regulation / immunology

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  • (PMID = 20738854.001).
  • [ISSN] 1478-6362
  • [Journal-full-title] Arthritis research & therapy
  • [ISO-abbreviation] Arthritis Res. Ther.
  • [Language] eng
  • [Grant] United Kingdom / Arthritis Research UK / / 16390; United Kingdom / Arthritis Research UK / / 18547; United Kingdom / Medical Research Council / / G9818340; United Kingdom / Arthritis Research UK / / 20088; United Kingdom / Wellcome Trust / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CC chemokine receptor 9; 0 / CCL25 protein, human; 0 / Chemokines, CC; 0 / Receptors, CCR; 0 / Tumor Necrosis Factor-alpha
  • [Other-IDs] NLM/ PMC2945064
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72. Hiçsönmez G, Cetin M, Tuncer AM, Yenicesu I, Aslan D, Ozyürek E, Unal S: Children with acute myeloblastic leukemia presenting with extramedullary infiltration: the effects of high-dose steroid treatment. Leuk Res; 2004 Jan;28(1):25-34
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  • [Title] Children with acute myeloblastic leukemia presenting with extramedullary infiltration: the effects of high-dose steroid treatment.
  • To evaluate whether children with acute myeloblastic leukemia (AML) presenting with extramedullary infiltration (EMI) have different clinical, morphologic features and prognosis from children without EMI, a 127 consecutive previously untreated children with AML were entered in this study.
  • Fifty-one children (40%) had EMI at diagnosis and 27% of these showed multiple site involvement.
  • Twenty-seven of 127 children (21%) presented myeloid tumors.
  • However, analysis of clinical and biological features at diagnosis showed that WBC count > or =50 x 10(9) l(-1), hepatosplenomegaly >5 cm, FAB AML-M4 and AML-M5 subtypes and CD13, CD14 expression of bone marrow (BM) leukemic cells (>20%) were more frequent in children with EMI.
  • In both protocols remission was achieved with combined high-dose methylprednisolone (HDMP) as a differentiating and apoptosis inducing agent with mild cytotoxic chemotherapy (low-dose cytosine arabinoside (LD Ara-C), weekly mitoxantrone and Ara-C or 6-thioguanine).
  • However, in patients who presented with myeloblastoma and treated with a more intensive post-remission therapy (AML-94), the 4-year disease-free survival (DFS) and event-free survival (EFS) rates were not found to be significantly different from children who had no EMI (P>0.05).
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid / diagnosis. Leukemic Infiltration / diagnosis
  • [MeSH-minor] Acute Disease. Antigens, CD13 / metabolism. Antigens, CD14 / metabolism. Blast Crisis. Bone Marrow Cells / metabolism. Bone Marrow Cells / pathology. Child. Child, Preschool. Cytarabine / administration & dosage. Female. Humans. Male. Methylprednisolone / administration & dosage. Mitoxantrone / administration & dosage. Prognosis. Remission Induction. Survival Rate. Thioguanine / administration & dosage. Treatment Outcome

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  • (PMID = 14630077.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD14; 04079A1RDZ / Cytarabine; BZ114NVM5P / Mitoxantrone; EC 3.4.11.2 / Antigens, CD13; FTK8U1GZNX / Thioguanine; X4W7ZR7023 / Methylprednisolone
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73. Nagashima N, Kano R, Hirai A, Yamazaki J, Inoue C, Hisasue M, Moore PF, Hasegawa A: Acute monocytic leukaemia in a cat. Vet Rec; 2005 Sep 17;157(12):347-9
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  • [Title] Acute monocytic leukaemia in a cat.
  • A three-year-old cat with lymphadenopathy, non-regenerative anaemia and marked leucocytosis (171.3 x 10(9) white blood cells/l) was diagnosed with monocytic leukaemia and treated with a combination of anticancer drugs.
  • A number of mature and immature monocyte-like cells were detected in the peripheral blood and bone marrow; they proved to be monocytic cells by cytochemical examination and an analysis of their cell surface phenotype, indicating that the cat suffered from acute myeloid leukaemia, subclassified as monocytic leukaemia (M5).
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cat Diseases / diagnosis. Leukemia, Monocytic, Acute / veterinary
  • [MeSH-minor] Animals. Cats. Fatal Outcome. Female. Prognosis. Remission Induction

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  • (PMID = 16170003.001).
  • [ISSN] 0042-4900
  • [Journal-full-title] The Veterinary record
  • [ISO-abbreviation] Vet. Rec.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
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74. Pae HO, Oh GS, Kim NY, Shin MK, Lee HS, Yun YG, Oh H, Kim YM, Chung HT: Roles of extracellular signal-regulated kinase and p38 mitogen-activated protein kinase in apoptosis of human monoblastic leukemia U937 cells by lectin-II isolated from Korean mistletoe. In Vitr Mol Toxicol; 2001;14(2):99-106
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  • [Title] Roles of extracellular signal-regulated kinase and p38 mitogen-activated protein kinase in apoptosis of human monoblastic leukemia U937 cells by lectin-II isolated from Korean mistletoe.
  • We have previously demonstrated that cytotoxic lectin-II isolated from Korean mistletoe induces apoptotic cell death in the human monoblastic leukemia cell line, U937, via the activation of the stress-activated protein kinases/c-Jun N-terminal kinase (SAPK/JNK).
  • [MeSH-major] Apoptosis / drug effects. Mistletoe. Mitogen-Activated Protein Kinase 1 / metabolism. Mitogen-Activated Protein Kinases / metabolism. Plant Preparations. Plant Proteins. Signal Transduction / physiology. Toxins, Biological / pharmacology
  • [MeSH-minor] DNA Fragmentation / drug effects. Flavonoids / pharmacology. Humans. Imidazoles / pharmacology. JNK Mitogen-Activated Protein Kinases. Leukemia, Monocytic, Acute / metabolism. Mitogen-Activated Protein Kinase 3. Pyridines / pharmacology. Ribosome Inactivating Proteins, Type 2. Tetradecanoylphorbol Acetate / pharmacology. U937 Cells / metabolism. p38 Mitogen-Activated Protein Kinases

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  • (PMID = 11690563.001).
  • [ISSN] 1097-9336
  • [Journal-full-title] In vitro & molecular toxicology
  • [ISO-abbreviation] In Vitr Mol Toxicol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one; 0 / Flavonoids; 0 / Imidazoles; 0 / Plant Preparations; 0 / Plant Proteins; 0 / Pyridines; 0 / Ribosome Inactivating Proteins, Type 2; 0 / SB 203580; 0 / Toxins, Biological; 0 / ribosome inactivating protein, Viscum; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3; EC 2.7.11.24 / Mitogen-Activated Protein Kinases; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases; NI40JAQ945 / Tetradecanoylphorbol Acetate
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75. Nakamaki T, Okabe-Kado J, Yamamoto-Yamaguchi Y, Hino Ki, Tomoyasu S, Honma Y, Kasukabe T: Role of MmTRA1b/phospholipid scramblase1 gene expression in the induction of differentiation of human myeloid leukemia cells into granulocytes. Exp Hematol; 2002 May;30(5):421-9
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  • [Title] Role of MmTRA1b/phospholipid scramblase1 gene expression in the induction of differentiation of human myeloid leukemia cells into granulocytes.
  • MmTRA1b gene expression was increased during differentiation of human monoblastic leukemia U937 cells using some differentiation inducers but not 1alpha,25-dihydroxyvitamin D(3) (a typical monocytic differentiation inducer).
  • To further elucidate the role of human MmTRA1b gene expression in the differentiation of myelogenous leukemia cells, we measured MmTRA1b gene expression in several myeloid leukemia cell lines and primary leukemia cells.
  • RESULTS: Expression of the MmTRA1b gene was markedly induced during granulocytic differentiation of promyelocytic leukemia NB4 and HT93 cells induced by all-trans retinoic acid (ATRA).
  • The level of MmTRA1b mRNA was significantly increased during differentiation toward granulocytes, but not monocytes/macrophages, in bipotential myeloid leukemia HL-60 cells.
  • The level of MmTRA1 mRNA was not increased during erythroid differentiation induced by hemin in erythroid leukemia K562 and HEL cells or during megakaryocytic differentiation induced by 12-O-tetradecanoylphorbol-13-acetate in K562 cells.
  • Expression of the MmTRA1b gene also was not induced when apoptosis of NB4 cells was induced by antileukemic drugs.
  • MmTRA1b mRNA also was clearly induced in ATRA-treated primary acute promyelocytic leukemia cells during granulocytic differentiation.
  • CONCLUSION: MmTRA1b mRNA was specifically induced during granulocytic differentiation of acute promyelocytic leukemia cells and was associated with induction of their differentiation.
  • [MeSH-major] Carrier Proteins / genetics. Cell Differentiation / genetics. Gene Expression Regulation, Neoplastic. Granulocytes / physiology. Leukemia, Myeloid / genetics. Membrane Proteins / genetics. Phospholipid Transfer Proteins

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  • (PMID = 12031648.001).
  • [ISSN] 0301-472X
  • [Journal-full-title] Experimental hematology
  • [ISO-abbreviation] Exp. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / Membrane Proteins; 0 / Phospholipid Transfer Proteins; 0 / RNA, Messenger; EC 3.6.1.- / Ca(2+) Mg(2+)-ATPase; FXC9231JVH / Calcitriol
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76. Tsan MF, White JE, Maheshwari JG, Bremner TA, Sacco J: Resveratrol induces Fas signalling-independent apoptosis in THP-1 human monocytic leukaemia cells. Br J Haematol; 2000 May;109(2):405-12
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  • [Title] Resveratrol induces Fas signalling-independent apoptosis in THP-1 human monocytic leukaemia cells.
  • Resveratrol, a natural product present in wine, has recently been shown to inhibit the growth of a number of cancer cell lines in vitro.
  • In the current study, we have demonstrated that resveratrol inhibits the growth of THP-1 human monocytic leukaemia cells in a dose-dependent manner with a median effective dose of 12 microM.
  • Thus, resveratrol may be a potential chemotherapeutic agent for the control of acute monocytic leukaemia.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / pharmacology. Apoptosis / drug effects. Leukemia, Monocytic, Acute / pathology. Stilbenes / pharmacology
  • [MeSH-minor] Analysis of Variance. Antigens, CD95 / analysis. Cell Line. Fas Ligand Protein. Flow Cytometry. Fluorescent Antibody Technique. Humans. Immunoblotting. Jurkat Cells / drug effects. Membrane Glycoproteins / analysis

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  • (PMID = 10848832.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] ENGLAND
  • [Chemical-registry-number] 0 / Antigens, CD95; 0 / Antineoplastic Agents, Phytogenic; 0 / FASLG protein, human; 0 / Fas Ligand Protein; 0 / Membrane Glycoproteins; 0 / Stilbenes; Q369O8926L / resveratrol
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77. Goemans BF, Zwaan CM, Harlow A, Loonen AH, Gibson BE, Hählen K, Reinhardt D, Creutzig U, Heinrich MC, Kaspers GJ: In vitro profiling of the sensitivity of pediatric leukemia cells to tipifarnib: identification of T-cell ALL and FAB M5 AML as the most sensitive subsets. Blood; 2005 Nov 15;106(10):3532-7
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  • [Title] In vitro profiling of the sensitivity of pediatric leukemia cells to tipifarnib: identification of T-cell ALL and FAB M5 AML as the most sensitive subsets.
  • Tipifarnib, a farnesyl transferase inhibitor (FTI), was developed to target malignancies with activated RAS, including leukemia.
  • We tested 52 pediatric acute myeloid leukemia (AML) and 36 pediatric acute lymphoblastic leukemia (ALL) samples for in vitro sensitivity to tipifarnib using a total cell-kill assay and compared these results to those obtained with normal bone marrow (N BM) samples (n = 25).
  • AML samples were significantly more sensitive to tipifarnib compared to B-cell precursor ALL (BCP ALL) or N BM samples.
  • Within AML, French-American-British (FAB) M5 samples were most sensitive to tipifarnib.
  • T-cell ALL samples were significantly more sensitive than BCP ALL and N BM samples.
  • In AML there was a marked correlation between tipifarnib resistance and daunorubicin or etoposide resistance, but not to cytarabine or 6-thioguanine.
  • RAS mutations were present in 32% of AML and 18% of ALL samples, but there was no correlation between RAS mutational status and sensitivity to tipifarnib.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Biomarkers, Tumor / metabolism. Drug Resistance, Neoplasm. Leukemia, Monocytic, Acute / enzymology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / enzymology. Quinolones / pharmacology
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Drug Screening Assays, Antitumor. Farnesyltranstransferase / antagonists & inhibitors. Farnesyltranstransferase / metabolism. Female. Humans. Male. Mutation. Oncogene Protein p21(ras) / genetics. Oncogene Protein p21(ras) / metabolism. Tumor Cells, Cultured

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  • (PMID = 16051737.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Biomarkers, Tumor; 0 / Quinolones; 192185-72-1 / tipifarnib; EC 2.5.1.29 / Farnesyltranstransferase; EC 3.6.5.2 / Oncogene Protein p21(ras)
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78. Rand JH, Wu XX, Quinn AS, Chen PP, Hathcock JJ, Taatjes DJ: Hydroxychloroquine directly reduces the binding of antiphospholipid antibody-beta2-glycoprotein I complexes to phospholipid bilayers. Blood; 2008 Sep 1;112(5):1687-95
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  • Treatment with the antimalarial drug hydroxychloroquine (HCQ) has been associated with reduced risk of thrombosis in the antiphospholipid (aPL) syndrome (APS) and, in an animal model of APS, with reduction of experimentally induced thrombosis.
  • HCQ, at concentrations of 1 mug/mL and greater, significantly reduced the binding of aPL-beta2GPI complexes to phospholipid surfaces and THP-1 (human acute monocytic leukemia cell line) monocytes.
  • The drug also reduced the binding of the individual proteins to bilayers.
  • This effect appears to be due to reversible interactions between HCQ and the proteins and may contribute to the observed reduction of thrombosis in human and experimental APS.

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  • (PMID = 18577708.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / R01 HL061331; United States / NHLBI NIH HHS / HL / HL-61331
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Antiphospholipid; 0 / Anticoagulants; 0 / Antigen-Antibody Complex; 0 / Antimalarials; 0 / Lipid Bilayers; 0 / Multiprotein Complexes; 0 / Phospholipids; 0 / beta 2-Glycoprotein I; 4QWG6N8QKH / Hydroxychloroquine
  • [Other-IDs] NLM/ PMC2518879
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79. Kanehara H, Tohda G, Oida K, Suzuki J, Ishii H, Miyamori I: Thrombomodulin expression by THP-1 but not by vascular endothelial cells is upregulated by pioglitazone. Thromb Res; 2002 Nov 25;108(4):227-34
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  • Since the expression of thrombomodulin (TM) by monocytes is upregulated during differentiation into macrophages, we investigated the effect of pioglitazone, a thiazolidinedione (TZD) that is a synthetic ligand of PPARgamma, on the expression of TM by a human monocyte/macrophage cell line; human acute monocytic leukemia (THP-1) cells.
  • PGF(2alpha) an agent known to inactivate PPARgamma, diminished the stimulatory effect of pioglitazone and PGJ2 on TM protein expression.
  • [MeSH-major] Endothelium, Vascular / drug effects. Prostaglandin D2 / analogs & derivatives. Thiazoles / pharmacology. Thiazolidinediones. Thrombomodulin / genetics
  • [MeSH-minor] Antibodies, Monoclonal / pharmacology. Antigens, CD14 / metabolism. Antigens, CD4 / metabolism. Blotting, Northern. Cell Differentiation / drug effects. Cell Line. Dose-Response Relationship, Drug. Flow Cytometry. Gene Expression Regulation / drug effects. HL-60 Cells. Humans. RNA, Messenger / drug effects. RNA, Messenger / genetics. RNA, Messenger / metabolism. Receptors, Cytoplasmic and Nuclear / genetics. Receptors, Cytoplasmic and Nuclear / metabolism. Thromboplastin / genetics. Thromboplastin / metabolism. Transcription Factors / genetics. Transcription Factors / metabolism. Tumor Cells, Cultured. Up-Regulation / drug effects

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  • (PMID = 12617986.001).
  • [ISSN] 0049-3848
  • [Journal-full-title] Thrombosis research
  • [ISO-abbreviation] Thromb. Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD14; 0 / Antigens, CD4; 0 / RNA, Messenger; 0 / Receptors, Cytoplasmic and Nuclear; 0 / Thiazoles; 0 / Thiazolidinediones; 0 / Thrombomodulin; 0 / Transcription Factors; 60203-57-8 / 9-deoxy-delta-9-prostaglandin D2; 9035-58-9 / Thromboplastin; RXY07S6CZ2 / Prostaglandin D2; X4OV71U42S / pioglitazone
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80. Honma Y, Niitsu N: Vidarabine and 2-deoxycoformycin as antileukemic agents against monocytic leukemia. Leuk Lymphoma; 2000 Sep;39(1-2):57-66
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  • [Title] Vidarabine and 2-deoxycoformycin as antileukemic agents against monocytic leukemia.
  • Although 2'-deoxycoformycin (dCF) has been reported in clinical trials to be less effective against myeloid than lymphoid malignancies, it may be useful for treating monocytic leukemia with the aid of 2'-deoxyadenosine (dAd) analogs.
  • In the presence of 10 microM dAd, the concentration of dCF required to inhibit the viability of monocytoid leukemia cells was much lower than that required on normal or non-monocytoid malignant cells in primary culture.
  • Although dCF alone slightly but significantly prolonged the survival of mice inoculated with U937 monocytic leukemia cells, combined treatment with dCF and AraA markedly prolonged the survival.
  • These results suggest that the combination of dCF and AraA may be useful for the clinical treatment of acute monocytic leukemia.
  • [MeSH-major] Leukemia, Monocytic, Acute / drug therapy. Pentostatin / therapeutic use. Vidarabine / therapeutic use
  • [MeSH-minor] Animals. Antibiotics, Antineoplastic / therapeutic use. Antimetabolites / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Apoptosis / drug effects. Dose-Response Relationship, Drug. Humans

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  • (PMID = 10975384.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] SWITZERLAND
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Antimetabolites; 395575MZO7 / Pentostatin; FA2DM6879K / Vidarabine
  • [Number-of-references] 47
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81. Roberts JD Jr, Chiche JD, Kolpa EM, Bloch DB, Bloch KD: cGMP-dependent protein kinase I interacts with TRIM39R, a novel Rpp21 domain-containing TRIM protein. Am J Physiol Lung Cell Mol Physiol; 2007 Oct;293(4):L903-12
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  • To identify molecular targets of PKGI, an interaction trap screen in yeast was performed using a cDNA encoding the catalytic region of PKGI and a human lung cDNA library.
  • We identified a cDNA that encodes a putative PKGI-interactor that is a novel variant of TRIM39, a member of the really interesting new gene (RING) finger family of proteins.
  • Indirect immunofluorescence using an antibody generated against the conserved domains of TRIM39 and TRIM39R revealed the proteins in speckled intranuclear structures in human acute monocytic leukemia (THP-1) and human epidermal carcinoma line (HEp-2) cells.
  • Although PKGI has been observed to interact with proteins that regulate cytoskeletal function and gene expression, this investigation shows for the first time that PKGI interacts with tripartite motif (TRIM) proteins, which, through diverse molecular pathways, are often observed to regulate important aspects of cellular homeostasis.

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  • (PMID = 17601797.001).
  • [ISSN] 1040-0605
  • [Journal-full-title] American journal of physiology. Lung cellular and molecular physiology
  • [ISO-abbreviation] Am. J. Physiol. Lung Cell Mol. Physiol.
  • [Language] ENG
  • [Databank-accession-numbers] GENBANK/ EU012025
  • [Grant] United States / NHLBI NIH HHS / HL / HL080316-02; United States / NIDDK NIH HHS / DK / DK-051179; United States / NHLBI NIH HHS / HL / HL-74352; United States / NHLBI NIH HHS / HL / HL-04237; United States / NHLBI NIH HHS / HL / HL-080316; United States / NHLBI NIH HHS / HL / R01 HL080316-02; United States / NHLBI NIH HHS / HL / R01 HL080316; United States / NHLBI NIH HHS / HL / HL-57172
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / RNA, Messenger; 0 / TRIM39 protein, human; EC 2.7.- / Phosphotransferases; EC 2.7.11.12 / Cyclic GMP-Dependent Protein Kinase Type I; EC 2.7.11.12 / Cyclic GMP-Dependent Protein Kinases; EC 2.7.11.12 / PRKG1 protein, human
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82. Tasaka T, Matsuhashi Y, Uehara E, Tamura T, Kakazu N, Abe T, Nagai M: Secondary acute monocytic leukemia with a translocation t(8;16)(p11;p13): case report and review of the literature. Leuk Lymphoma; 2004 Mar;45(3):621-5
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  • [Title] Secondary acute monocytic leukemia with a translocation t(8;16)(p11;p13): case report and review of the literature.
  • Acute myeloblastic leukemia cases carrying the translocation t(8;16) (p11;p13) are characterized by the M4 and M5 subtypes, erythrophagocytosis by the blast cells and a poor prognosis, suggesting a new clinical entity.
  • She was diagnosed as having breast cancer and acute monocytic leukemia (M5b).
  • Eleven cases of therapy-related t(8;16) leukemia including the present case have been reported, but prior treatment with paclitaxel and carboplatin-based chemotherapy has never been reported.
  • The relation of histone acetylase and therapy-related leukemia is discussed.
  • [MeSH-major] Chromosomes, Human, Pair 16. Chromosomes, Human, Pair 8. Leukemia, Monocytic, Acute / genetics. Neoplasms, Second Primary / genetics. Translocation, Genetic
  • [MeSH-minor] Aged. Antineoplastic Combined Chemotherapy Protocols / adverse effects. Carboplatin / adverse effects. Cell Transformation, Neoplastic / genetics. Female. Humans. Ovarian Neoplasms / complications. Ovarian Neoplasms / drug therapy. Paclitaxel / adverse effects

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  • The Weizmann Institute of Science GeneCards and MalaCards databases. gene/protein/disease-specific - MalaCards for monocytic leukemia .
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  • (PMID = 15160929.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] BG3F62OND5 / Carboplatin; P88XT4IS4D / Paclitaxel
  • [Number-of-references] 26
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83. Agarwal SK, Marshall GD Jr: Role of CD28/B7 costimulation in the dexamethasone-induced suppression of IFN-gamma. J Interferon Cytokine Res; 2000 Nov;20(11):927-34
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  • In vitro exposure of peripheral blood mononuclear cells (PBMC) to glucocorticoids (GC), at concentrations observed during psychologic stress, induces a shift in the human type 1/type 2 cytokine balance toward a type 2 cytokine response.
  • The CD28/B7 costimulation pathway has been reported to modulate the type 1/type 2 cytokine balance and may contribute to the GC-associated cytokine alterations.
  • Therefore, we sought to determine the effect of dexamethasone (Dex) on the expression and function of the human CD28/B7 costimulatory pathway and whether these alterations contribute to the Dex-induced type 1/type 2 cytokine alterations.
  • Dex inhibited the expression of both CD80 and CD86 on THP-1 cells, a human acute monocytic leukemia cell line, as determined by flow cytometry.
  • These data suggest that Dex induces a modulation of the CD28/B7 costimulatory pathway that contributes to the shift in the type 1/type 2 cytokine balance toward a predominant type 2 cytokine response.
  • [MeSH-minor] Abatacept. Antibodies, Monoclonal / immunology. Antigens, CD86. Antigens, Differentiation / metabolism. CTLA-4 Antigen. Cell Line. Humans. Interleukin-12 / pharmacology. Lymphocyte Activation. Monocytes / drug effects. Monocytes / immunology. Monocytes / metabolism. Th1 Cells / drug effects. Th1 Cells / immunology. Th1 Cells / metabolism. Th2 Cells / drug effects. Th2 Cells / immunology. Th2 Cells / metabolism

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  • (PMID = 11096449.001).
  • [ISSN] 1079-9907
  • [Journal-full-title] Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research
  • [ISO-abbreviation] J. Interferon Cytokine Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD; 0 / Antigens, CD28; 0 / Antigens, CD80; 0 / Antigens, CD86; 0 / Antigens, Differentiation; 0 / CD86 protein, human; 0 / CTLA-4 Antigen; 0 / CTLA4 protein, human; 0 / Glucocorticoids; 0 / Immunoconjugates; 0 / Membrane Glycoproteins; 187348-17-0 / Interleukin-12; 7D0YB67S97 / Abatacept; 7S5I7G3JQL / Dexamethasone; 82115-62-6 / Interferon-gamma
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84. Crews KR, Wimmer PS, Hudson JQ, Howard SC, Ribeiro RC, Razzouk BI: Pharmacokinetics of 2-chlorodeoxyadenosine in a child undergoing hemofiltration and hemodialysis for acute renal failure. J Pediatr Hematol Oncol; 2002 Nov;24(8):677-80
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pharmacokinetics of 2-chlorodeoxyadenosine in a child undergoing hemofiltration and hemodialysis for acute renal failure.
  • The authors describe the clinical course and the pharmacokinetics of 2-CdA in a child with acute monoblastic leukemia who experienced acute renal failure during treatment with cytarabine and 2-CdA.
  • The average clearance rate, reflecting systemic clearance and clearance by continuous venovenous hemofiltration and hemodialysis, was 12.4 L/hour per m for the first 3 days of 2-CdA therapy.
  • Because high 2-CdA plasma concentrations were observed in this patient, clinicians are advised to exercise caution when using this drug in patients with renal dysfunction.
  • [MeSH-major] Acute Kidney Injury / metabolism. Antimetabolites, Antineoplastic / pharmacokinetics. Cladribine / pharmacokinetics. Hemofiltration. Leukemia, Monocytic, Acute / drug therapy. Renal Dialysis
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / adverse effects. Antineoplastic Combined Chemotherapy Protocols / pharmacokinetics. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Aspergillosis / complications. Child. Combined Modality Therapy. Cytarabine / administration & dosage. Cytarabine / adverse effects. Daunorubicin / administration & dosage. Etoposide / administration & dosage. Fatal Outcome. Humans. Leukapheresis. Male. Metabolic Clearance Rate. Recombinant Proteins / therapeutic use. Remission Induction. Urate Oxidase / therapeutic use

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  • (PMID = 12439044.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 21765
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Recombinant Proteins; 04079A1RDZ / Cytarabine; 47M74X9YT5 / Cladribine; 6PLQ3CP4P3 / Etoposide; EC 1.7.3.3 / Urate Oxidase; ZS7284E0ZP / Daunorubicin; DAV regimen
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85. Masurier C, Boutin S, Veron P, Bernard J, Danos O, Davoust J: Enhanced lentiviral transduction of monocyte-derived dendritic cells in the presence of conditioned medium from dying monocytes. Hum Gene Ther; 2007 Feb;18(2):161-70
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  • Importantly, we found that MCM derived from a human acute monocytic leukemia cell line, THP-1, was equally effective.
  • Altogether our results show that a soluble factor present in dying monocyte cultures can replace advantageously facilitating agents such as Polybrene, to achieve high LV transductions levels.
  • [MeSH-major] Culture Media, Conditioned / pharmacology. Dendritic Cells / cytology. Dendritic Cells / drug effects. Lentivirus / genetics. Monocytes / cytology. Monocytes / secretion. Transduction, Genetic / methods

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  • (PMID = 17326725.001).
  • [ISSN] 1043-0342
  • [Journal-full-title] Human gene therapy
  • [ISO-abbreviation] Hum. Gene Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Culture Media, Conditioned
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86. Rosner M, Siegel N, Fuchs C, Slabina N, Dolznig H, Hengstschläger M: Efficient siRNA-mediated prolonged gene silencing in human amniotic fluid stem cells. Nat Protoc; 2010 Jun;5(6):1081-95
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Human amniotic fluid stem cells (hAFSCs) are a very promising new type of fetal stem cells with numerous applications for basic science and cell-based therapies.
  • They harbor a high differentiation potential and a low risk for tumor development, can be grown in large quantities and do not raise the ethical concerns associated with embryonic stem cells.
  • We also show the successful use of this protocol in primary nontransformed nonimmortalized fibroblasts, cervical adenocarcinoma cells, transformed embryonic kidney cells, immortalized endometrial stromal cells and acute monocytic leukemia cells, suggesting a wide spectrum of applications in various cell types.

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  • (PMID = 20539284.001).
  • [ISSN] 1750-2799
  • [Journal-full-title] Nature protocols
  • [ISO-abbreviation] Nat Protoc
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / RNA, Small Interfering
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