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1. Nikolaievs'kyĭ VV: [Distribution of Mycobacterium tuberculosis strains in the south of Ukraine based on genotyping data]. Mikrobiol Z; 2006 Sep-Oct;68(5):52-61
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  • Prevalence of Beijing family strains, which have been previously demonstrated to be associated with high levels of drug resistance, was different in Odessa and Nikolaev Regions (51.9% and 17.0%, respectively), and turned to be lower than in a majority of regions in Russia.
  • Other epidemiological groups were represented by the family strains T1, LAM1, LAM4, LAM5, S and Haarlem.
  • An urgent need in the large-scale investigations in the field of molecular epidemiology of TB agent under the spread of epidemic was demonstrated.
  • [MeSH-minor] Antitubercular Agents / pharmacology. Genotype. Humans. Ukraine / epidemiology

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  • (PMID = 17388120.001).
  • [ISSN] 1028-0987
  • [Journal-full-title] Mikrobiolohichnyĭ zhurnal (Kiev, Ukraine : 1993)
  • [ISO-abbreviation] Mikrobiol. Z.
  • [Language] ukr
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Ukraine
  • [Chemical-registry-number] 0 / Antitubercular Agents; 0 / DNA, Bacterial
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2. Hubeek I, Stam RW, Peters GJ, Broekhuizen R, Meijerink JP, van Wering ER, Gibson BE, Creutzig U, Zwaan CM, Cloos J, Kuik DJ, Pieters R, Kaspers GJ: The human equilibrative nucleoside transporter 1 mediates in vitro cytarabine sensitivity in childhood acute myeloid leukaemia. Br J Cancer; 2005 Dec 12;93(12):1388-94
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  • [Title] The human equilibrative nucleoside transporter 1 mediates in vitro cytarabine sensitivity in childhood acute myeloid leukaemia.
  • Cytarabine (ara-C) is the most effective agent for the treatment of acute myeloid leukaemia (AML).
  • Aberrant expression of enzymes involved in the transport/metabolism of ara-C could explain drug resistance.
  • We determined mRNA expression of these factors using quantitative-real-time-PCR in leukemic blasts from children diagnosed with de novo AML.
  • Expression of the inactivating enzyme pyrimidine nucleotidase-I (PN-I) was 1.8-fold lower in FAB-M5 as compared to FAB-M1/2 (P=0.007).
  • In conclusion, decreased expression of hENT1, which transports ara-C across the cell membrane, appears to be a major factor in ara-C resistance in childhood AML.
  • [MeSH-major] Antimetabolites, Antineoplastic / pharmacology. Cytarabine / pharmacology. Equilibrative Nucleoside Transporter 1 / physiology. Leukemia, Myeloid / drug therapy. Leukemia, Myeloid / genetics
  • [MeSH-minor] Acute Disease. Cell Membrane. Child. Drug Resistance, Neoplasm. Gene Expression Profiling. Humans. RNA, Messenger / biosynthesis. Reverse Transcriptase Polymerase Chain Reaction. Tumor Cells, Cultured

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  • [Cites] Br J Haematol. 1999 Mar;104(3):630-9 [10086807.001]
  • [Cites] Blood. 2003 Feb 15;101(4):1270-6 [12406912.001]
  • [Cites] Br J Haematol. 1999 Jul;106(1):78-85 [10444166.001]
  • [Cites] Klin Padiatr. 1999 Jul-Aug;211(4):239-44 [10472557.001]
  • [Cites] Leukemia. 2005 Apr;19(4):537-44 [15690069.001]
  • [Cites] Blood. 2000 Oct 15;96(8):2879-86 [11023525.001]
  • [Cites] J Mol Diagn. 2001 May;3(2):55-61 [11333300.001]
  • [Cites] J Biol Chem. 2001 Jan 26;276(4):2914-27 [11032837.001]
  • [Cites] Cancer Res. 2001 Oct 1;61(19):7217-24 [11585758.001]
  • [Cites] Eur J Cancer. 2003 Mar;39(5):691-7 [12628850.001]
  • [Cites] Leuk Res. 2003 Dec;27(12):1075-6 [12921942.001]
  • [Cites] Oncogene. 2003 Oct 20;22(47):7524-36 [14576856.001]
  • [Cites] Curr Opin Investig Drugs. 2003 Dec;4(12):1442-50 [14763130.001]
  • [Cites] Ann Hematol. 2004;83 Suppl 1:S108-12 [15124698.001]
  • [Cites] Cancer Res. 1978 Mar;38(3):579-85 [203385.001]
  • [Cites] J Clin Invest. 1982 Feb;69(2):479-89 [6948829.001]
  • [Cites] Mol Pharmacol. 1983 Jan;23(1):159-64 [6306421.001]
  • [Cites] Science. 1983 Aug 5;221(4610):514-9 [6306767.001]
  • [Cites] Semin Oncol. 1985 Jun;12(2 Suppl 3):65-74 [3892704.001]
  • [Cites] Ann Intern Med. 1985 Oct;103(4):620-5 [3862359.001]
  • [Cites] Cancer Res. 1985 Nov;45(11 Pt 2):5952-7 [4053067.001]
  • [Cites] Cancer Res. 1986 Mar;46(3):1079-83 [3484676.001]
  • [Cites] Pharmacol Ther. 1985;30(3):287-99 [2433703.001]
  • [Cites] Semin Oncol. 1987 Jun;14(2 Suppl 1):159-66 [3589690.001]
  • [Cites] Leukemia. 1988 May;2(5):253-60 [3287015.001]
  • [Cites] Blood. 1990 Dec 1;76(11):2327-36 [2257305.001]
  • [Cites] Cancer Res. 1991 May 15;51(10):2559-65 [2021937.001]
  • [Cites] Br J Cancer. 1991 Sep;64(3):469-74 [1911186.001]
  • [Cites] Cancer Res. 1992 May 1;52(9):2389-93 [1568208.001]
  • [Cites] Leukemia. 1993 Jul;7(7):1005-11 [7686601.001]
  • [Cites] Cancer Surv. 1993;17:123-56 [8137339.001]
  • [Cites] Leukemia. 1994 Jul;8(7):1224-9 [8035616.001]
  • [Cites] Cancer Res. 1994 Oct 15;54(20):5401-7 [7923172.001]
  • [Cites] Br J Cancer. 1994 Dec;70(6):1047-52 [7981053.001]
  • [Cites] Blood. 1995 Oct 15;86(8):3097-108 [7579404.001]
  • [Cites] Leukemia. 1995 Nov;9(11):1864-9 [7475276.001]
  • [Cites] Leuk Res. 1996 Aug;20(8):677-82 [8913321.001]
  • [Cites] Adv Cancer Res. 1998;72:197-233 [9338077.001]
  • [Cites] FEBS Lett. 1997 Dec 15;419(2-3):263-7 [9428647.001]
  • [Cites] Adv Exp Med Biol. 1998;431:667-71 [9598149.001]
  • [Cites] Cancer Res. 1998 Sep 15;58(18):4173-9 [9751631.001]
  • [Cites] Trends Pharmacol Sci. 1998 Oct;19(10):424-30 [9803833.001]
  • [Cites] Leuk Lymphoma. 1998 Oct;31(3-4):405-9 [9869205.001]
  • [Cites] J Biol Chem. 2001 Nov 30;276(48):45270-5 [11584005.001]
  • [Cites] Hematol Oncol. 2001 Dec;19(4):151-7 [11754391.001]
  • [Cites] Curr Opin Oncol. 2002 Jan;14(1):3-9 [11790973.001]
  • [Cites] Leuk Res. 2002 Jul;26(7):621-9 [12008078.001]
  • [Cites] Br J Haematol. 2002 Jun;117(4):860-8 [12060121.001]
  • [Cites] Lancet Oncol. 2002 Jul;3(7):415-24 [12142171.001]
  • [Cites] Mol Cancer Ther. 2002 Apr;1(6):371-6 [12477049.001]
  • [Cites] Cancer Treat Res. 2002;112:27-47 [12481710.001]
  • [Cites] Biochem Cell Biol. 1998;76(5):761-70 [10353709.001]
  • (PMID = 16333246.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Equilibrative Nucleoside Transporter 1; 0 / RNA, Messenger; 0 / SLC29A1 protein, human; 04079A1RDZ / Cytarabine
  • [Other-IDs] NLM/ PMC2361532
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3. Leid JG, Steeber DA, Tedder TF, Jutila MA: Antibody binding to a conformation-dependent epitope induces L-selectin association with the detergent-resistant cytoskeleton. J Immunol; 2001 Apr 15;166(8):4899-907
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  • Here we report that a conformational change in L-selectin, induced by an anti-lectin domain mAb (LAM1-116) and recognized by another mAb directed to a conserved epitope on L-selectin (EL-246), predisposed L-selectin to cytoskeletal association.
  • This effect was due to direct binding of the mAb, not to overt signaling events, and was specific to LAM1-116.
  • In the presence of LAM1-116, EL-246 induced cytoskeletal association of L-selectin in the absence of Ab cross-linking as visualized by L-selectin staining after low dose detergent treatment of the cells.
  • [MeSH-minor] Animals. Benzoquinones. Cattle. Cell Fractionation. Cell Line. Cyanogen Bromide. Cytoplasm / genetics. Cytoplasm / immunology. E-Selectin / genetics. E-Selectin / metabolism. Enzyme Inhibitors / pharmacology. Genistein / pharmacology. Humans. Immunoglobulin Fab Fragments / pharmacology. Lactams, Macrocyclic. Leukocytes / chemistry. Leukocytes / drug effects. Leukocytes / enzymology. Leukocytes / immunology. Mice. Microspheres. P-Selectin / genetics. P-Selectin / metabolism. Polyethylene Glycols / pharmacology. Precipitin Tests. Protein Conformation / drug effects. Protein Structure, Tertiary / genetics. Protein-Tyrosine Kinases / antagonists & inhibitors. Quinones / pharmacology. Recombinant Proteins / immunology. Recombinant Proteins / metabolism. Rifabutin / analogs & derivatives. Sheep. Solubility. Staining and Labeling. Transfection. Up-Regulation / drug effects. Up-Regulation / immunology

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  • (PMID = 11290767.001).
  • [ISSN] 0022-1767
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] eng
  • [Grant] United States / NIAID NIH HHS / AI / R01AI47671-03
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; 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 / Antibodies, Monoclonal; 0 / Benzoquinones; 0 / Detergents; 0 / E-Selectin; 0 / Enzyme Inhibitors; 0 / Epitopes; 0 / Immunoglobulin Fab Fragments; 0 / Lactams, Macrocyclic; 0 / P-Selectin; 0 / Quinones; 0 / Recombinant Proteins; 126880-86-2 / L-Selectin; 1W306TDA6S / Rifabutin; 30IQX730WE / Polyethylene Glycols; 70563-58-5 / herbimycin; 9036-19-5 / Nonidet P-40; DH2M523P0H / Genistein; EC 2.7.10.1 / Protein-Tyrosine Kinases; OS382OHJ8P / Cyanogen Bromide
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4. Druhan LJ, Ai J, Massullo P, Kindwall-Keller T, Ranalli MA, Avalos BR: Novel mechanism of G-CSF refractoriness in patients with severe congenital neutropenia. Blood; 2005 Jan 15;105(2):584-91
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  • Severe congenital neutropenia (SCN) is a rare disease diagnosed at or soon after birth, characterized by a myeloid maturation arrest in the bone marrow, ineffective neutrophil production, and recurrent infections.
  • In the subset of patients with SCN transforming to acute myeloid leukemia (AML), mutations that truncate the cytoplasmic tail of the G-CSF receptor (G-CSFR) have been detected.
  • Here, we report a novel mutation in the extracellular portion of the G-CSFR within the WSXWS motif in a patient with SCN without AML who was refractory to G-CSF treatment.
  • Expression of the mutant receptor in either myeloid or lymphoid cells was shown to alter subcellular trafficking of the wild-type (WT) G-CSFR by constitutively heterodimerizing with it.
  • [MeSH-major] Granulocyte Colony-Stimulating Factor / therapeutic use. Neutropenia / drug therapy. Neutropenia / genetics. Neutrophils / drug effects. Receptors, Granulocyte Colony-Stimulating Factor / genetics
  • [MeSH-minor] Adult. Cells, Cultured. Dimerization. Drug Resistance. Female. Gene Expression. Humans. Infant, Newborn. Ligands. Male. Parents. Point Mutation. Signal Transduction / drug effects. Signal Transduction / immunology

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  • (PMID = 15353486.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA16058; United States / NCI NIH HHS / CA / CA75226; United States / NCI NIH HHS / CA / CA82859
  • [Publication-type] Case Reports; Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Ligands; 0 / Receptors, Granulocyte Colony-Stimulating Factor; 143011-72-7 / Granulocyte Colony-Stimulating Factor
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5. Srivastava MD, Ambrus JL: Effect of 1,25(OH)2 Vitamin D3 analogs on differentiation induction and cytokine modulation in blasts from acute myeloid leukemia patients. Leuk Lymphoma; 2004 Oct;45(10):2119-26
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  • [Title] Effect of 1,25(OH)2 Vitamin D3 analogs on differentiation induction and cytokine modulation in blasts from acute myeloid leukemia patients.
  • In acute myeloid leukemia (AML), cell proliferation and differentiation are uncoupled, causing a maturation block.
  • We investigated 1alpha, 25(OH)2 Vitamin D3 and 5 of its more potent analogs with reduced calcium resorbing activity for differentiation of blast cells from AML (FAB M1) patients, compared to TPA.
  • Vitamin D3 and its analogs can induce differentiation of primary cells from AML patients in vitro, but may need to be combined with other agents for terminal differentiation of blasts and effective therapy in vivo.
  • [MeSH-major] Calcitriol / analogs & derivatives. Cell Differentiation / drug effects. Cytokines / antagonists & inhibitors. Granulocyte Precursor Cells / drug effects. Leukemia, Myeloid, Acute / pathology
  • [MeSH-minor] Acute Disease. Cell Adhesion. Cells, Cultured. Dose-Response Relationship, Drug. Humans. Interleukin-6 / antagonists & inhibitors. Interleukin-8 / antagonists & inhibitors. Structure-Activity Relationship


6. Merhi F, Auger J, Rendu F, Bauvois B: Allium compounds, dipropyl and dimethyl thiosulfinates as antiproliferative and differentiating agents of human acute myeloid leukemia cell lines. Biologics; 2008 Dec;2(4):885-95
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  • [Title] Allium compounds, dipropyl and dimethyl thiosulfinates as antiproliferative and differentiating agents of human acute myeloid leukemia cell lines.
  • The beneficial effects appear related to the organosulfur products generated upon processing of Allium.
  • Leukemia cells from patients with acute myeloid leukemia (AML) display high proliferative capacity and have a reduced capacity of undergoing apoptosis and maturation.
  • Whether the sulfur-containing molecules thiosulfinates (TS), diallyl TS (All(2)TS), dipropyl TS (Pr(2)TS) and dimethyl TS (Me(2)TS), are able to exert chemopreventative activity against AML is presently unknown.
  • The present study was an evaluation of proliferation, cytotoxicity, differentiation and secretion of AML cell lines (U937, NB4, HL-60, MonoMac-6) in response to treatment with these TS and their related sulfides (diallylsulfide, diallyl disulfide, dipropyl disulfide, dimethyl disulfide).
  • As assessed by flow cytometry, ELISA, gelatin zymogaphy and RT-PCR, we showed that Pr(2)TS and Me(2)TS, but not All(2)TS and sulfides, 1) inhibited cell proliferation in dose- and time-dependent manner and this process was neither due to cytotoxicity nor apoptosis, 2) induced macrophage maturation, and 3) inhibited the levels of secreted MMP-9 (protein and activity) and TNF-alpha protein, without altering mRNA levels.
  • By establishing for the first time that Pr(2)TS and Me(2)TS affect proliferation, differentiation and secretion of leukemic cell lines, this study provides the opportunity to explore the potential efficiency of these molecules in AML.

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  • [Cites] Cell Biol Toxicol. 2004 Jul;20(4):253-60 [15499972.001]
  • [Cites] Cardiovasc Hematol Agents Med Chem. 2006 Jan;4(1):33-52 [16529548.001]
  • [Cites] Blood Rev. 2006 Mar;20(2):71-82 [16185796.001]
  • [Cites] Mutat Res. 2004 Nov 2;555(1-2):121-31 [15476856.001]
  • [Cites] Nat Rev Immunol. 2004 Aug;4(8):617-29 [15286728.001]
  • [Cites] Lancet Neurol. 2003 Dec;2(12):747-56 [14636780.001]
  • [Cites] Crit Rev Oncol Hematol. 2004 May;50(2):87-100 [15157658.001]
  • [Cites] J Biol Chem. 2004 Apr 23;279(17):17772-84 [14754893.001]
  • [Cites] Leukemia. 2004 Feb;18(2):227-32 [14671638.001]
  • [Cites] Acta Haematol. 2004;111(1-2):107-23 [14646349.001]
  • [Cites] Cancer Res. 2003 Oct 15;63(20):6825-37 [14583480.001]
  • [Cites] J Nutr. 2003 Jul;133(7):2171-5 [12840173.001]
  • [Cites] Blood. 2003 Jun 15;101(12):4667-79 [12623839.001]
  • [Cites] J Chromatogr A. 2003 Mar 28;991(1):69-75 [12703902.001]
  • [Cites] Leukemia. 2002 Oct;16(10):2062-71 [12357358.001]
  • [Cites] Life Sci. 2002 Jun 14;71(4):411-9 [12044841.001]
  • [Cites] Leukemia. 2002 May;16(5):791-8 [11986939.001]
  • [Cites] J Hematother Stem Cell Res. 2002 Feb;11(1):33-47 [11847002.001]
  • [Cites] Acta Haematol. 2001;106(4):190-207 [11815717.001]
  • [Cites] Biochem Pharmacol. 2002 Jan 1;63(1):41-7 [11754872.001]
  • [Cites] J Biol Chem. 2001 Nov 30;276(48):45491-6 [11585813.001]
  • [Cites] J Immunol Methods. 2002 Jan 1;259(1-2):55-64 [11730841.001]
  • [Cites] Thromb Haemost. 2001 Nov;86(5):1284-91 [11816719.001]
  • [Cites] J Clin Invest. 2001 Sep;108(6):851-9 [11560954.001]
  • [Cites] Blood. 2001 Jun 15;97(12):3919-24 [11389035.001]
  • [Cites] Arch Intern Med. 2001 Mar 26;161(6):813-24 [11268223.001]
  • [Cites] J Nutr. 2001 Mar;131(3s):1058S-60S [11238816.001]
  • [Cites] Cancer Res. 2001 Jan 1;61(1):2-7 [11196162.001]
  • [Cites] J Nutr. 2006 Mar;136(3 Suppl):827S-831S [16484574.001]
  • [Cites] J Nutr. 2006 Mar;136(3 Suppl):716S-725S [16484550.001]
  • [Cites] J Biol Chem. 2005 Dec 16;280(50):41487-93 [16219763.001]
  • [Cites] Mol Cancer Ther. 2005 Sep;4(9):1388-98 [16170031.001]
  • [Cites] Crit Rev Food Sci Nutr. 2004;44(6):479-88 [15615431.001]
  • [Cites] Stem Cells Dev. 2004 Oct;13(5):484-95 [15588506.001]
  • [Cites] Eur J Immunol. 1999 Sep;29(9):3009-16 [10508275.001]
  • [Cites] Blood. 1999 Sep 15;94(6):1971-8 [10477726.001]
  • [Cites] Leukemia. 1999 Jun;13(6):835-42 [10360369.001]
  • [Cites] Leuk Res. 1998 Jun;22(6):537-47 [9678720.001]
  • [Cites] Drug Metabol Drug Interact. 2000;17(1-4):51-79 [11201304.001]
  • [Cites] Biochem Pharmacol. 2000 Nov 15;60(10):1475-83 [11020449.001]
  • [Cites] Int J Cancer. 2000 Jun 15;86(6):768-76 [10842189.001]
  • [Cites] Biochim Biophys Acta. 2000 Mar 27;1470(2):M55-62 [10722927.001]
  • [Cites] Leuk Res. 2008 Feb;32(2):315-22 [17561254.001]
  • [Cites] Cancer. 2008 Feb 1;112(3):572-80 [18085638.001]
  • [Cites] Platelets. 2007 Nov;18(7):481-90 [17852771.001]
  • [Cites] Oncologist. 2007;12 Suppl 2:14-21 [18039635.001]
  • [Cites] Haematologica. 2007 Sep;92(9):1224-9 [17666366.001]
  • [Cites] Curr Oncol Rep. 2007 Sep;9(5):337-44 [17706161.001]
  • [Cites] Leukemia. 2007 Aug;21(8):1605 [17637714.001]
  • [Cites] Cancer Metastasis Rev. 2006 Mar;25(1):9-34 [16680569.001]
  • [Cites] Cell Death Differ. 2006 May;13(5):748-58 [16498458.001]
  • [Cites] J Chromatogr A. 2006 Apr 21;1112(1-2):3-22 [16388813.001]
  • [Cites] J Nutr. 2006 Mar;136(3 Suppl):810S-812S [16484570.001]
  • [Cites] Carcinogenesis. 2006 Mar;27(3):533-40 [16169930.001]
  • [Cites] J Cell Biochem Suppl. 1997;27:106-12 [9591200.001]
  • [Cites] Blood. 1997 Mar 15;89(6):1870-5 [9058706.001]
  • [Cites] Biochim Biophys Acta. 1996 Jan 17;1315(1):15-20 [8611641.001]
  • [Cites] Carcinogenesis. 1996 Apr;17(4):669-73 [8625476.001]
  • [Cites] J Exp Med. 1995 Nov 1;182(5):1545-56 [7595224.001]
  • [Cites] Blood. 1994 Jul 1;84(1):294-302 [7517212.001]
  • [Cites] J Cell Sci. 1993 Apr;104 ( Pt 4):991-9 [8314909.001]
  • [Cites] Leuk Res. 1991;15(6):409-18 [1861527.001]
  • [Cites] Blood. 1991 Mar 1;77(5):1080-6 [1995093.001]
  • [Cites] Blood. 1987 Nov;70(5):1233-44 [3311197.001]
  • [Cites] Blood. 1990 Feb 1;75(3):626-32 [2153423.001]
  • [Cites] J Immunol. 1990 Feb 15;144(4):1311-6 [2105994.001]
  • (PMID = 19707466.001).
  • [ISSN] 1177-5475
  • [Journal-full-title] Biologics : targets & therapy
  • [ISO-abbreviation] Biologics
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] New Zealand
  • [Other-IDs] NLM/ PMC2727902
  • [Keywords] NOTNLM ; acute myeloid leukemia / differentiation / matrix metalloproteinase-9 / proliferation / thiosulfinate
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7. Herry A, Douet-Guilbert N, Guéganic N, Morel F, Le Bris MJ, Berthou C, De Braekeleer M: Del(5q) and MLL amplification in homogeneously staining region in acute myeloblastic leukemia: a recurrent cytogenetic association. Ann Hematol; 2006 Apr;85(4):244-9
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  • [Title] Del(5q) and MLL amplification in homogeneously staining region in acute myeloblastic leukemia: a recurrent cytogenetic association.
  • We report here a 71 year-old female presenting with acute myeloblastic leukemia (FAB-M1) after treatment of essential thrombocythemia with Vercyte.
  • Twenty-one cases, including ours, of myelodysplastic syndromes and acute myelogenous leukemia with MLL amplification present in hsr or dmin were found in the literature.
  • Most of these patients shared some characteristics: they were old, they had de novo acute myeloid leukemia (AML) with a complex karyotype and a short survival, 90% of them having also a del(5q).
  • Therefore, the simultaneous presence of MLL amplification and del(5q) appears to be a nonrandom association that could be the signature of AML in elderly patients with a poor prognosis.
  • [MeSH-major] Chromosome Deletion. Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 5 / genetics. Chromosomes, Human, Pair 7 / genetics. Gene Amplification. Leukemia, Myeloid, Acute / genetics. Myeloid-Lymphoid Leukemia Protein / genetics
  • [MeSH-minor] 6-Mercaptopurine / therapeutic use. Aged. Cytogenetic Analysis. Fatal Outcome. Female. Histone-Lysine N-Methyltransferase. Humans. In Situ Hybridization, Fluorescence / methods. Karyotyping. Pipobroman / therapeutic use. Prognosis. Sensitivity and Specificity. Thrombocytosis / diagnosis. Thrombocytosis / drug therapy

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  • (PMID = 16425025.001).
  • [ISSN] 0939-5555
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; 6Q99RDT97R / Pipobroman; E7WED276I5 / 6-Mercaptopurine; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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8. Kremser A, Dressig J, Grabrucker C, Liepert A, Kroell T, Scholl N, Schmid C, Tischer J, Kufner S, Salih H, Kolb HJ, Schmetzer H: Dendritic cells (DCs) can be successfully generated from leukemic blasts in individual patients with AML or MDS: an evaluation of different methods. J Immunother; 2010 Feb-Mar;33(2):185-99
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  • [Title] Dendritic cells (DCs) can be successfully generated from leukemic blasts in individual patients with AML or MDS: an evaluation of different methods.
  • Myeloid-leukemic cells (AML, MDS, CML) can be differentiated to leukemia-derived dendritic cell [DC (DCleu)] potentially presenting the whole leukemic antigen repertoire without knowledge of distinct leukemia antigens and are regarded as promising candidates for a vaccination strategy.
  • We studied the capability of 6 serum-free DC culture methods, chosen according to different mechanisms, to induce DC differentiation in 137 cases of AML and 52 cases of MDS.
  • DC-stimulating substances were cytokines ("standard-medium", "MCM-Mimic", "cytokine-method"), bacterial lysates ("Picibanil"), double-stranded RNA ["Poly (I:C)"] or a cytokine bypass method ("Ca-ionophore").
  • The quality/quantity of DC generated was estimated by flow cytometry studying (co) expressions of "DC"antigens, costimulatory, maturation, and blast-antigens.
  • Comparing these methods on average 15% to 32% DC, depending on methods used, could be obtained from blast-containing mononuclear cells (MNC) in AML/MDS cases with a DC viability of more than 60%.
  • Average results of all culture methods tested were comparable, however not every given case of AML could be differentiated to DC with 1 selected method.
  • [MeSH-major] Cancer Vaccines. Cell Culture Techniques / methods. Dendritic Cells / pathology. Leukemia, Myeloid, Acute / pathology. Myelodysplastic Syndromes / pathology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antigen Presentation / drug effects. Antigens, Differentiation / metabolism. Antigens, Neoplasm / immunology. Antigens, Neoplasm / metabolism. Cell Differentiation / drug effects. Cell Separation. Culture Media, Serum-Free. Cytokines / metabolism. Cytokines / pharmacology. Cytotoxicity, Immunologic. Female. Flow Cytometry. Humans. Male. Middle Aged. Picibanil / pharmacology. Poly I-C / pharmacology. T-Lymphocytes, Cytotoxic / immunology

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  • (PMID = 20139775.001).
  • [ISSN] 1537-4513
  • [Journal-full-title] Journal of immunotherapy (Hagerstown, Md. : 1997)
  • [ISO-abbreviation] J. Immunother.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Differentiation; 0 / Antigens, Neoplasm; 0 / Cancer Vaccines; 0 / Culture Media, Serum-Free; 0 / Cytokines; 24939-03-5 / Poly I-C; 39325-01-4 / Picibanil
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9. McGrattan P, Alexander HD, Humphreys MW, Kettle PJ: Tetrasomy 13 as the sole cytogenetic abnormality in acute myeloid leukemia M1 without maturation. Cancer Genet Cytogenet; 2002 Jun;135(2):192-5
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  • [Title] Tetrasomy 13 as the sole cytogenetic abnormality in acute myeloid leukemia M1 without maturation.
  • We report a case of acute myeloid leukemia (AML) M1 showing a 48,XY,+13,+13 karyotype.
  • Tetrasomy 13 as the sole cytogenetic abnormality has not been reported previously in M1 AML and has only been reported in three other AML cases, all with an immature phenotype and poor outcome.
  • [MeSH-major] Aneuploidy. Chromosomes, Human, Pair 13. Leukemia, Myeloid, Acute / genetics
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cytarabine / administration & dosage. Daunorubicin / administration & dosage. Drug Resistance, Neoplasm. Fatal Outcome. Granulocyte Colony-Stimulating Factor / administration & dosage. Humans. Male. Middle Aged. Thioguanine / administration & dosage. Vidarabine / administration & dosage. Vidarabine / analogs & derivatives

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  • (PMID = 12127406.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; 143011-72-7 / Granulocyte Colony-Stimulating Factor; FA2DM6879K / Vidarabine; FTK8U1GZNX / Thioguanine; ZS7284E0ZP / Daunorubicin; DAT protocol 1; FLAG protocol
  • [Number-of-references] 10
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10. Zhang J, Shen B, Li Y, Sun Y: STAT3 exerts two-way regulation in the biological effects of IL-6 in M1 leukemia cells. Leuk Res; 2001 Jun;25(6):463-72
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  • [Title] STAT3 exerts two-way regulation in the biological effects of IL-6 in M1 leukemia cells.
  • The signal transducer and activator of transcription (STAT) proteins have been implicated in cytokine-regulated proliferation, differentiation and cell survival.
  • Interleukin-6 (IL-6), a pleiotropic cytokine, induces a robust and sustained activation of STAT3 in M1 acute myeloid leukemia cells, which in turn undergo growth arrest, terminal differentiation and apoptosis in response to IL-6.
  • The roles of STAT3 activation in IL-6-mediated responses in M1 cells are not fully understood.
  • We introduced STAT3 antisense cDNA into M1 cells.
  • STAT3 antisense cDNA blocked the expression and IL-6-induced tyrosine phosphorylation and DNA binding of STAT3, and resulted in reduction of both IL-6-induced growth arrest at G(0)/G(1) phase and macrophage differentiation in the M1 transformants.
  • This observation is in accordance with previous reports and confirms that STAT3 plays an essential role in IL-6-induced growth arrest and terminal differentiation in M1 leukemia cells.
  • On the other hand, STAT3 antisense cDNA augmented IL-6-induced apoptosis of M1 cells, which was supported by the cell cycle assay, DNA fragmentation assay and detection of the p17 active fragment of Caspase 3.
  • As proliferation inhibition and differentiation induction stands for a negative signal, while survival maintenance stands for a positive signal, we conclude that STAT3 exerts two-way regulation on the biological effects of IL-6 in M1 leukemia cells.
  • [MeSH-major] DNA-Binding Proteins / physiology. Interleukin-6 / pharmacology. Leukemia, Myeloid, Acute / pathology. Trans-Activators / physiology
  • [MeSH-minor] Animals. Apoptosis / drug effects. Cell Differentiation / drug effects. Cell Division / drug effects. DNA, Antisense / pharmacology. DNA, Complementary / pharmacology. Macrophages / drug effects. Macrophages / physiology. Mice. STAT3 Transcription Factor. Signal Transduction. Tumor Cells, Cultured

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  • (PMID = 11337018.001).
  • [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 / DNA, Antisense; 0 / DNA, Complementary; 0 / DNA-Binding Proteins; 0 / Interleukin-6; 0 / STAT3 Transcription Factor; 0 / Stat3 protein, mouse; 0 / Trans-Activators
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11. Nakade Y, Fujimura M, Ohkura N, Waseda Y, Yamazakis H, Inuzuka K, Ikeda H, Oe H, Nanbu Y, Takamuralo T, Sakai Y, Wada T: [A case of bronchiolitis obliterans caused by allogeneic hematopoietic stem cell transplantation diagnosed with a body plethysmograph]. Rinsho Byori; 2010 Sep;58(9):906-11
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  • A 19-year-old woman with acute myeloid leukemia (M1) was treated with allogeneic hematopoietic stem cell transplantation.
  • She was admitted to the Dept. of Respiratory Medicine at Kanazawa University Hospital, because she complained of progressive obstructive ventilatory impairment.
  • The pathological diagnosis made using biopsied lung, obtained by a right lower partial lobectomy, was constrictive bronchiolitis.
  • [MeSH-major] Bronchiolitis Obliterans / diagnosis. Bronchiolitis Obliterans / etiology. Hematopoietic Stem Cell Transplantation / adverse effects. Plethysmography, Whole Body
  • [MeSH-minor] Adult. Female. Humans. Leukemia, Myeloid, Acute / therapy

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  • (PMID = 20963951.001).
  • [ISSN] 0047-1860
  • [Journal-full-title] Rinsho byori. The Japanese journal of clinical pathology
  • [ISO-abbreviation] Rinsho Byori
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
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12. Skladanowski A, Bozko P, Sabisz M, Larsen AK: Dual inhibition of PI3K/Akt signaling and the DNA damage checkpoint in p53-deficient cells with strong survival signaling: implications for cancer therapy. Cell Cycle; 2007 Sep 15;6(18):2268-75
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  • Natural (intrinsic) resistance of many tumor types to DNA damaging agents is closely associated with their capacity to undergo robust cell cycle arrest in G(2)/M.
  • In this work, we wanted to clarify if inhibition of multiple checkpoint/survival pathways may confer better efficacy in the potentiation of genotoxic agents compared to inhibition of either pathway alone.
  • We compared the influence of UCN-01, which affects both the DNA damage checkpoint and PI3K/Akt-mediated survival signaling, with the PI3K inhibitors wortmannin and LY294002 in p53-deficient M1 acute myeloid leukemia cells treated with the DNA damaging agent cisplatin.
  • Unexpectedly, dual inhibition of both survival and checkpoint signaling by UCN-01, also increased the cytotoxicity of cisplatin, but to a lesser degree than wortmannin or LY294002.
  • Our results elucidate a novel function for PI3K/Akt as a survival factor during DNA damage-induced G(2) arrest and could have important pharmacological consequences for the application of response modulators in p53-deficient tumors with strong survival signaling.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. DNA Damage / physiology. Phosphatidylinositol 3-Kinases / antagonists & inhibitors. Proto-Oncogene Proteins c-akt / antagonists & inhibitors. Signal Transduction / physiology. Tumor Suppressor Protein p53 / deficiency
  • [MeSH-minor] Animals. Cell Cycle / drug effects. Cell Cycle / physiology. Cell Line, Tumor. Cell Survival / drug effects. Cell Survival / genetics. Cell Survival / physiology. Mice. Neoplasms / drug therapy. Neoplasms / enzymology

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  • (PMID = 17890906.001).
  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [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 / Tumor Suppressor Protein p53; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
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13. Baines P, Fisher J, Truran L, Davies E, Hallett M, Hoy T, Burnett AK: The MEK inhibitor, PD98059, reduces survival but does not block acute myeloid leukemia blast maturation in vitro. Eur J Haematol; 2000 Apr;64(4):211-8
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  • [Title] The MEK inhibitor, PD98059, reduces survival but does not block acute myeloid leukemia blast maturation in vitro.
  • The appearance of blasts in acute myeloid leukemia (AML) reflects a shift from cellular processes inducing maturation and cell death to those favouring survival and accumulation.
  • We have monitored changes in the growth factor signalling molecule MAPKinase, in the cytoprotective protein Bcl-2 and in the cell death protein Bax, during maturation of proliferating and non-proliferating AML blasts in vitro.
  • Eighteen AML samples were cultured for 7 d in serum-free medium with or without a supplement of recombinant cytokines comprising c-kit ligand, IL3 and GMCSF.
  • Maturation of AML blasts, as assessed by morphology on Romanowsky-stained slides of 7/18 samples and by changes in surface CD markers on all 18 leukemias, occurred in both the absence and presence of cytokines.
  • Immunoblotting demonstrated that ERK was briefly phosphorylated after seeding AML blasts into culture.
  • PD98059, an inhibitor of MAPKinase kinase (MEK) which activates MAPKinase, inhibited this transient ERK phosphorylation but was unable to block maturation as measured by acquisition of CD15 in samples from 12 patients with low starting numbers of CD15-positive cells.
  • PD98059, however, reduced cell numbers in 7-d liquid culture and, in cytokine-supplemented cultures, this was associated with a 1.3-fold increase in Bcl-2 (p = 0.012) and a 1.4-fold increase in Bax (p = 0.02).
  • The MAPKinase pathway is not required for this maturation, but it does maintain cell viability in the absence or presence of cytokines.
  • A rise in Bcl-2 may not protect AML blasts in the face of elevated Bax.
  • [MeSH-major] Enzyme Inhibitors / pharmacology. Flavonoids / pharmacology. Leukemia, Myeloid / drug therapy. Leukemia, Myeloid / pathology
  • [MeSH-minor] Acute Disease. Adult. Aged. Calcium-Calmodulin-Dependent Protein Kinases / antagonists & inhibitors. Cell Differentiation / drug effects. Cell Survival / drug effects. Female. Humans. Male. Middle Aged. Proto-Oncogene Proteins / metabolism. Proto-Oncogene Proteins c-bcl-2 / metabolism. Signal Transduction / drug effects. Tumor Cells, Cultured. bcl-2-Associated X Protein

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  • (PMID = 10776691.001).
  • [ISSN] 0902-4441
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] DENMARK
  • [Chemical-registry-number] 0 / 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one; 0 / BAX protein, human; 0 / Enzyme Inhibitors; 0 / Flavonoids; 0 / Proto-Oncogene Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / bcl-2-Associated X Protein; EC 2.7.11.17 / Calcium-Calmodulin-Dependent Protein Kinases
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14. Takahashi T, Maruyama Y, Satoh Y, Yoshimoto M, Tsujisaki M: Complex t(8;14;21)(q22;q13;q22), a variant of t(8;21), with t(15;21)(q15;p11) in a patient with acute myelogenous leukemia (M1). Cancer Genet Cytogenet; 2004 Dec;155(2):152-3
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  • [Title] Complex t(8;14;21)(q22;q13;q22), a variant of t(8;21), with t(15;21)(q15;p11) in a patient with acute myelogenous leukemia (M1).
  • [MeSH-major] Chromosomes, Human, Pair 14. Chromosomes, Human, Pair 15. Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8. Genetic Variation. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / prevention & control. Translocation, Genetic
  • [MeSH-minor] Antimetabolites, Antineoplastic / therapeutic use. Core Binding Factor Alpha 2 Subunit. Cytarabine / therapeutic use. Drug Therapy, Combination. Female. Humans. Idarubicin / therapeutic use. Karyotyping. Leukocytes, Mononuclear / chemistry. Middle Aged. Oncogene Proteins, Fusion / genetics. RNA, Messenger / genetics. Reverse Transcriptase Polymerase Chain Reaction. Secondary Prevention. Transcription Factors / genetics

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  • (PMID = 15571802.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Antimetabolites, Antineoplastic; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / RNA, Messenger; 0 / Transcription Factors; 04079A1RDZ / Cytarabine; ZRP63D75JW / Idarubicin
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15. Turutin DV, Kubareva EA, Pushkareva MA, Ullrich V, Sud'ina GF: Activation of NF-kappa B transcription factor in human neutrophils by sulphatides and L-selectin cross-linking. FEBS Lett; 2003 Feb 11;536(1-3):241-5
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  • Sulphated galactocerebroside (sulphatide) has been established as a ligand for L-selectin and shown to trigger intracellular signals in human neutrophils.
  • The activation was inhibitable by pretreatment with primary monoclonal anti-L-selectin antibody (clone LAM1-116).
  • Binding of the primary antibody to L-selectin was insufficient to induce NF-kappa B activation but cross-linking of L-selectin with a secondary antibody was effective. alpha-Chymotrypsin, the agent known to shed L-selectin, activated NF-kappa B by itself.
  • The response to sulphatides was inhibited by jasplakinolide, an actin-polymerising agent known to downregulate surface expression of L-selectin, Fc gamma RIIIb, CD43 and CD44.
  • [MeSH-minor] Antibodies, Monoclonal / pharmacology. Cell Adhesion / drug effects. Chymotrypsin / pharmacology. Electrophoretic Mobility Shift Assay. Humans. Peptides, Cyclic / pharmacology

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  • (PMID = 12586371.001).
  • [ISSN] 0014-5793
  • [Journal-full-title] FEBS letters
  • [ISO-abbreviation] FEBS Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Depsipeptides; 0 / Galactosylceramides; 0 / NF-kappa B; 0 / Peptides, Cyclic; 0 / Sulfoglycosphingolipids; 102396-24-7 / jasplakinolide; 126880-86-2 / L-Selectin; EC 3.4.21.- / alpha-chymotrypsin; EC 3.4.21.1 / Chymotrypsin
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16. Yan ZQ, Bolognesi MP, Steeber DA, Tedder TF, Chen LE, Seaber AV, Urbaniak JR: Blockade of L-selectin attenuates reperfusion injury in a rat model. J Reconstr Microsurg; 2000 Apr;16(3):227-33
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  • Using a rat extensor digitorum longus (EDL) muscle model, the present study tested the hypothesis that in vivo administration of the function-blocking monoclonal antibody (mAb) LAM1-116 which recognizes L-selectin, a cell-surface adhesion receptor, could decrease I/R injury.
  • In 46 rats, one EDL served as a normal control and the opposite EDL underwent 3 hr of ischemia followed by 3 hr of reperfusion after pretreatment with LAM1-116 mAb, control IgG, or saline.
  • Myeloperoxidase (MPO) activity showed only a two-fold increase from normal in LAM1-116-treated I/R EDL while a 27-fold increase occurred in the IgG2a and saline groups, with a statistically significant (p < 0.001) difference.
  • A significantly (p < 0.05) lower wet weight ratio, improved fatigue contractile force, and less neutrophil infiltration were found in LAM1-116-treated EDL, when compared to those in control IgG- or saline-treated EDL.
  • The results indicate that blockade of L-selectin by LAM1-116 mAb can effectively reduce neutrophil infiltration in reperfused skeletal muscle, thereby decreasing tissue edema and improving muscle fatigue contractile force.
  • [MeSH-major] Antibodies, Monoclonal / pharmacology. L-Selectin / drug effects. Peroxidase / metabolism. Reperfusion Injury / drug therapy
  • [MeSH-minor] Animals. Disease Models, Animal. Dose-Response Relationship, Drug. Female. Immunoglobulin G / metabolism. Immunoglobulin G / pharmacology. Leukocyte Count / drug effects. Muscle Contraction / drug effects. Muscle, Skeletal / pathology. Organ Size / drug effects. Rats. Rats, Sprague-Dawley. Reference Values. Sensitivity and Specificity

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  • (PMID = 10803628.001).
  • [ISSN] 0743-684X
  • [Journal-full-title] Journal of reconstructive microsurgery
  • [ISO-abbreviation] J Reconstr Microsurg
  • [Language] eng
  • [Grant] United States / NIAID NIH HHS / AI / AI-26872; United States / NHLBI NIH HHS / HL / HL 36046; United States / NHLBI NIH HHS / HL / HL-50985; etc
  • [Publication-type] Comparative Study; Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Immunoglobulin G; 126880-86-2 / L-Selectin; EC 1.11.1.7 / Peroxidase
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17. Mashita T, Shimoda T, Yoshioka H, Takahashi Y, Mitsuda M: A cat with acute myeloblastic leukemia without maturation (M1) treated with combination chemotherapy. J Vet Med Sci; 2006 Jan;68(1):97-101
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  • [Title] A cat with acute myeloblastic leukemia without maturation (M1) treated with combination chemotherapy.
  • Acute myeloblastic leukemia without maturation (M1) was diagnosed according to the FAB classification.

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  • (PMID = 16462128.001).
  • [ISSN] 0916-7250
  • [Journal-full-title] The Journal of veterinary medical science
  • [ISO-abbreviation] J. Vet. Med. Sci.
  • [Language] ENG
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; 5J49Q6B70F / Vincristine; 8N3DW7272P / Cyclophosphamide; 9PHQ9Y1OLM / Prednisolone; EC 1.11.1.7 / Peroxidase
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18. Singh T, Arora DK: Motility and chemotactic response of Pseudomonas fluorescens toward chemoattractants present in the exudate of Macrophomina phaseolina. Microbiol Res; 2001;156(4):343-51
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  • Pseudomonas fluorescens strains (LAM1-hydrophilic) and (LAM2-hydrophobic) showed positive chemotaxis towards attractants (sugars, amino acids, polyols and organic acids) present in the exudate of Macrophomina phaseolina (a soil-borne plant pathogenic fungus).
  • Relative to control, the RCDI values decreased 1.5-fold in amino acids or sugars, and 1.2-fold in polyols or organic acids.
  • [MeSH-major] Basidiomycota / metabolism. Chemotactic Factors / pharmacology. Pseudomonas fluorescens / drug effects
  • [MeSH-minor] Chemotaxis / drug effects. Dose-Response Relationship, Drug. Flagella / drug effects. Signal Transduction. Soil Microbiology

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  • (PMID = 11770852.001).
  • [ISSN] 0944-5013
  • [Journal-full-title] Microbiological research
  • [ISO-abbreviation] Microbiol. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Chemotactic Factors
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