[X] Close
You are about to erase all the values you have customized, search history, page format, etc.
Click here to RESET all values       Click here to GO BACK without resetting any value
Items 1 to 22 of about 22
1. 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
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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

  • Hazardous Substances Data Bank. CYTARABINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [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
  •  go-up   go-down


2. 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
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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.

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • Hazardous Substances Data Bank. CYTARABINE .
  • Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .
  • Hazardous Substances Data Bank. PREDNISOLONE .
  • Hazardous Substances Data Bank. VINCRISTINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


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
Hazardous Substances Data Bank. POLYETHYLENE GLYCOL MONO(OCTYLPHENYL) ETHER .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Antibody binding to a conformation-dependent epitope induces L-selectin association with the detergent-resistant cytoskeleton.
  • 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

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. GENISTEIN .
  • Hazardous Substances Data Bank. CYANOGEN BROMIDE .
  • Hazardous Substances Data Bank. RIFABUTIN .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


Advertisement
4. Sperr WR, Hauswirth AW, Florian S, Ohler L, Geissler K, Valent P: Human leukaemic stem cells: a novel target of therapy. Eur J Clin Invest; 2004 Aug;34 Suppl 2:31-40
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Acute myeloid leukaemia (AML) is a life-threatening haematopoietic disease that is characterized by clonal growth and the accumulation of myelopoietic progenitor cells.
  • Although AML cells only have a limited potential to undergo differentiation and maturation, each AML clone is organized in a hierarchical manner similar to normal haematopoiesis.
  • Recent data have shown that each AML clone consists of leukaemic stem cells and their progeny, and that AML stem cells differ from more mature cells in several aspects, including survival and target antigen profiles.
  • Most importantly, AML stem cells, but not their progeny, have the capacity to repopulate haematopoietic tissues with leukaemias in NOD/SCID mice.
  • Furthermore, AML stem cells are thought to be responsible for the infinite growth of leukaemias in patients with AML.
  • The phenotypic properties of AML stem cells have also been described.
  • In most cases, these cells are detectable within the CD34+, CD38-, Lin-, CD123+ subpopulation of AML cells.
  • Because of their AML-initiating and -renewing capacity and their unique phenotype, which includes several molecular targets of drug therapy, AML stem cells have recently been proposed as novel important target cell populations in the context of curative therapies.
  • The present article gives an overview of our knowledge about AML stem cells, their phenotype, and their role as a 'therapy-target' in new concepts to treat and to cure patients with AML.
  • [MeSH-major] Genetic Therapy / methods. Leukemia, Myeloid / therapy. Neoplastic Stem Cells

  • MedlinePlus Health Information. consumer health - Genes and Gene Therapy.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15291804.001).
  • [ISSN] 0014-2972
  • [Journal-full-title] European journal of clinical investigation
  • [ISO-abbreviation] Eur. J. Clin. Invest.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 108
  •  go-up   go-down


5. 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
Genetic Alliance. consumer health - Tuberculosis.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


6. 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

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


7. Leung J, Pang A, Yuen WH, Kwong YL, Tse EW: Relationship of expression of aquaglyceroporin 9 with arsenic uptake and sensitivity in leukemia cells. Blood; 2007 Jan 15;109(2):740-6
Hazardous Substances Data Bank. ALL-TRANS-RETINOIC ACID .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Relationship of expression of aquaglyceroporin 9 with arsenic uptake and sensitivity in leukemia cells.
  • Arsenic trioxide (As2O3) is highly efficacious in acute promyelocytic leukemia (APL).
  • In 10 of 11 myeloid and lymphoid leukemia lines, quantitative polymerase chain reaction (Q-PCR) and Western blotting showed that AQP9 expression correlated positively with As2O3-induced cytotoxicity.
  • Similarly, the chronic myeloid leukemia line K562 expressed low levels of AQP9 and was As2O3 insensitive.
  • Pretreatment of the myeloid leukemia line HL-60 with all-trans retinoic acid (ATRA) up-regulated AQP9, leading to a significantly increased arsenic uptake and As2O3-induced cytotoxicity on incubation with As2O3, which might explain the synergism between ATRA and As2O3.
  • Q-PCR showed that primary APL cells expressed AQP9 significantly (2-3 logs) higher than other acute myeloid leukemias (AMLs), which might explain their exquisite As2O3 sensitivity.
  • However, APL and AML with maturation expressed comparable AQP9 levels, suggesting that AQP9 expression was related to granulocytic maturation.
  • [MeSH-major] Aquaporins / metabolism. Arsenicals / pharmacology. Leukemia, Myeloid / metabolism. Leukemia, Promyelocytic, Acute / drug therapy. Leukemia, Promyelocytic, Acute / metabolism. Oxides / pharmacology
  • [MeSH-minor] Acute Disease. Cell Line, Tumor. Cell Proliferation / drug effects. Gene Expression Profiling. Humans. K562 Cells. Point Mutation. Reverse Transcriptase Polymerase Chain Reaction / methods. Sensitivity and Specificity. Tretinoin / pharmacology. Up-Regulation / drug effects

  • Hazardous Substances Data Bank. ARSENIC TRIOXIDE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16968895.001).
  • [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 / AQP9 protein, human; 0 / Aquaporins; 0 / Arsenicals; 0 / Oxides; 5688UTC01R / Tretinoin; S7V92P67HO / arsenic trioxide
  •  go-up   go-down


8. 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
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Sulphated galactocerebroside (sulphatide) has been established as a ligand for L-selectin and shown to trigger intracellular signals in human neutrophils.
  • We have found that sulphatide activated transcription factor NF-kappa B in human neutrophils in a concentration-dependent manner whereas non-sulphated galactocerebroside did not demonstrate such an effect.
  • 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

  • Hazardous Substances Data Bank. CHYMOTRYPSIN .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


9. 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
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Ischemia/reperfusion (I/R) injury appears to be a significant neutrophil-dependent component and may be ameliorated by blocking leukocyte-endothelial adhesion.
  • 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

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


10. 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
Hazardous Substances Data Bank. VIDARABINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • Hazardous Substances Data Bank. CYTARABINE .
  • Hazardous Substances Data Bank. THIOGUANINE .
  • Hazardous Substances Data Bank. DAUNORUBICIN .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


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
Genetic Alliance. consumer health - Bronchiolitis Obliterans.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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

  • Genetic Alliance. consumer health - Transplantation.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


12. Fujii S, Miyata A, Kikuchi T, Kibata M: [An elderly case of acute myelocytic leukemia complicated with bleeding gastric angiodysplasia, successfully treated with topical endoscopic polidocanol injection]. Nihon Ronen Igakkai Zasshi; 2004 May;41(3):334-8
Hazardous Substances Data Bank. DODECYL ALCOHOL, ETHOXYLATED .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [An elderly case of acute myelocytic leukemia complicated with bleeding gastric angiodysplasia, successfully treated with topical endoscopic polidocanol injection].
  • A 72-year-old man with acute myelocytic leukemia (AML) suffered relapsing massive bleeding from gastric angiodysplasia.
  • He had hypercellular (nucleated cell count 42 x 10(4)/microl) bone marrow with 90% myeloblasts, and AML (FAB: M1) was diagnosed.
  • In July, his AML relapsed and he was treated mainly by transfusion therapy.
  • In this case, topical injection of polidocanol was an effective procedure for the massive bleeding from it even in an elderly patient with the complication of thrombocytopenia due to AML.
  • [MeSH-major] Angiodysplasia / complications. Gastrointestinal Hemorrhage / drug therapy. Leukemia, Myeloid, Acute / complications. Polyethylene Glycols / administration & dosage. Stomach Diseases / complications


13. 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
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • Hazardous Substances Data Bank. 1,25-DIHYDROXYCHOLECALCIFEROL .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15370259.001).
  • [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
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cytokines; 0 / Interleukin-6; 0 / Interleukin-8; FXC9231JVH / Calcitriol
  •  go-up   go-down


14. Graf M, Hecht K, Reif S, Pelka-Fleischer R, Pfister K, Schmetzer H: Expression and prognostic value of hemopoietic cytokine receptors in acute myeloid leukemia (AML): implications for future therapeutical strategies. Eur J Haematol; 2004 Feb;72(2):89-106
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression and prognostic value of hemopoietic cytokine receptors in acute myeloid leukemia (AML): implications for future therapeutical strategies.
  • There is evidence to suggest, that those receptors (R) could play a role in leukemia with respect to cell differentiations and its regulation, prognosis, and pathobiology.
  • METHODS: We have studied the expression of CKR on mononuclear bone marrow (BM) cells of 89 patients with acute myeloid leukemia (AML) at first diagnosis, three patients at relapse or with persisting AML and eight healthy probands by fluorescence-activated cell sorting (FACS) analysis using directly fluorescein-conjugated antibodies: CD114 (hG-CSF-R), CD116 (hGM-CSF-R), CD117 (hSCF-R), CD123 (hIL-3-R), CD130 (gp130subunit), CD135 (hFL-R).
  • RESULTS: All investigated CKR were more frequently expressed in AML-samples than in healthy BM-samples, except CD130, which was only expressed on 5-6% of AML-blasts in all and with only one healthy BM-sample being CD130(+).
  • Within the French-American-British (FAB) types we observed a maturation- and lineage (granulocytic/monocytic)-committed expression profile.
  • Monocytic subtypes (FAB-type M4/M5) showed significantly more GM-CSF-R(+) (P = 0.001) and FL-R(+) (P = 0.001) and significantly less stem cell factor-R (SCF-R(+)) (P = 0.02) cases.
  • Highest proportions of G-CSF-R(+) blasts were observed in FAB-type M3.
  • In undifferentiated leukemias (FAB-type M1, M2) high amounts of SCF-R(+), IL-3-R(+), and FL-R(+) blasts could be detected.
  • FL-R was the only CKR, which was positive in FAB-type M0 (n = 2).
  • For clinical evaluation only patients treated by the AML-CG-protocol, were included (n = 53).
  • Patients with more than 32.5% IL-3-R(+) cells also showed a tendency to a lower relapse-free survival probability (P = 0.26), whereas patients with more than 33% GM-CSF-R(+) (P = 0.06) and patients with more than 52% G-CSF-R(+) (P = 0.175) blasts tended to have a higher relapse-free survival probability.
  • CONCLUSION: We can conclude, that CKR-expression in AML is maturation- and lineage-committed and the proportions of especially early acting CKR have influence on relapse-free survival probability of AML-patients, independently of the karyotype.
  • With respect to the individual CKR status the benefit of cytokines as priming agents, as agents to treat neutropenia or to influence the metabolism of chemotherapy can be discussed under new points of view.
  • [MeSH-major] Leukemia, Myeloid, Acute / immunology. Receptors, Cytokine / blood


15. 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
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


16. Smetana K, Pluskalová M, Marinov Y, Hrkal Z: The effect of 5-aminolevulinic acid-based photodynamic treatment (PDT) on nucleoli of leukemic granulocytic precursors represented by K562 blastic cells in vitro. Med Sci Monit; 2004 Nov;10(11):BR405-9
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The effect of 5-aminolevulinic acid-based photodynamic treatment (PDT) on nucleoli of leukemic granulocytic precursors represented by K562 blastic cells in vitro.
  • BACKGROUND: Since photodynamic treatment (PDT) induces apoptosis in individual HL-60 cells originating from early granulocytic precursors of acute myeloid leukemia, the present study was undertaken to provide information on such treatment of K562 cells, which originate from early granulocytic precursors of chronic myeloid leukemia (blastic phase) and carry the bcr/abl fusion gene with anti-apoptotic properties.
  • MATERIAL/METHODS: PDT was based on the 5-aminolevulinic acid treatment of K562 cells, followed by blue light irradiation under conditions which in HL-60 cells induce an apoptotic process without previous terminal maturation.
  • Nuclei and nucleoli were visualized by cytochemical procedures to demonstrate DNA, RNA and silver stained proteins of nucleolus organizer regions (AgNORs).
  • [MeSH-major] Aminolevulinic Acid / pharmacology. Cell Nucleolus / drug effects. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Photosensitizing Agents / pharmacology
  • [MeSH-minor] Apoptosis. Cell Nucleus / drug effects. Cell Nucleus / ultrastructure. Chromatin / ultrastructure. HL-60 Cells. Humans. K562 Cells. Mitosis / drug effects. Necrosis. Stem Cells / drug effects

  • MedlinePlus Health Information. consumer health - Chronic Myeloid Leukemia.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15507844.001).
  • [ISSN] 1234-1010
  • [Journal-full-title] Medical science monitor : international medical journal of experimental and clinical research
  • [ISO-abbreviation] Med. Sci. Monit.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Chromatin; 0 / Photosensitizing Agents; 88755TAZ87 / Aminolevulinic Acid
  •  go-up   go-down


17. 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
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


18. 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
Hazardous Substances Data Bank. PIPOBROMAN .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • Hazardous Substances Data Bank. MERCAPTOPURINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


19. Bertagnolo V, Brugnoli F, Mischiati C, Sereni A, Bavelloni A, Carini C, Capitani S: Vav promotes differentiation of human tumoral myeloid precursors. Exp Cell Res; 2005 May 15;306(1):56-63
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Vav promotes differentiation of human tumoral myeloid precursors.
  • In T and B cells, it appears crucial for both development and functions, while, in non-lymphoid hematopoietic cells, Vav seems not involved in cell maturation, but rather in the response of mature cells to agonist-dependent proliferation and phagocytosis.
  • We have previously demonstrated that the amount and the tyrosine phosphorylation of Vav are up-regulated in both whole cells and nuclei of tumoral promyelocytes induced to granulocytic maturation by ATRA and that tyrosine-phosphorylated Vav does not display any ATRA-induced GEF activity but contributes to the regulation of PI 3-K activity.
  • In this study, we report that Vav accumulates in nuclei of ATRA-treated APL-derived cells and that the down-modulation of Vav prevents differentiation of tumoral promyelocytes, indicating that it is a key molecule in ATRA-dependent myeloid maturation.
  • On the other hand, the overexpression of Vav induces an increased expression of surface markers of granulocytic differentiation without affecting the maturation-related changes of the nuclear morphology.
  • Consistent with an effect of Vav on the transcriptional machinery, array profiling shows that the inhibition of the Syk-dependent tyrosine phosphorylation of Vav reduces the number of ATRA-induced genes.
  • Our data support the unprecedented notion that Vav plays crucial functions in the maturation process of myeloid cells, and suggest that Vav can be regarded as a potential target for the therapeutic treatment of myeloproliferative disorders.
  • [MeSH-major] Cell Cycle Proteins / physiology. Cell Differentiation / physiology. Myeloid Progenitor Cells / metabolism. Proto-Oncogene Proteins / physiology
  • [MeSH-minor] Cell Line, Tumor. Enzyme Inhibitors / pharmacology. Gene Expression / drug effects. Gene Expression / genetics. Gene Expression / physiology. Gene Expression Regulation, Leukemic / drug effects. Granulocytes / physiology. HL-60 Cells. Humans. Leukemia, Promyelocytic, Acute / genetics. Leukemia, Promyelocytic, Acute / metabolism. Leukemia, Promyelocytic, Acute / pathology. Phosphorylation. Protein-Tyrosine Kinases / antagonists & inhibitors. Protein-Tyrosine Kinases / metabolism. Proto-Oncogene Proteins c-vav. RNA, Small Interfering / genetics. Stilbenes / pharmacology. Transfection. Tretinoin / pharmacology. Tumor Cells, Cultured

  • Hazardous Substances Data Bank. ALL-TRANS-RETINOIC ACID .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15878332.001).
  • [ISSN] 0014-4827
  • [Journal-full-title] Experimental cell research
  • [ISO-abbreviation] Exp. Cell Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / Enzyme Inhibitors; 0 / Proto-Oncogene Proteins; 0 / Proto-Oncogene Proteins c-vav; 0 / RNA, Small Interfering; 0 / Stilbenes; 0 / VAV1 protein, human; 4339-71-3 / 3,3',4,5'-tetrahydroxystilbene; 5688UTC01R / Tretinoin; EC 2.7.10.1 / Protein-Tyrosine Kinases
  •  go-up   go-down


20. 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
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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.
  • Cell numbers decreased to a mean of 71% after 7 d of cytokine-free culture, but increased to 210% in cytokine-supplemented cultures.
  • By immunofluorescence/flow cytometry, there was no significant change in Bcl-2 over 7 d of culture, while Bax increased, particularly in cytokine-free cultures (2.2-fold), which led to a significant decrease in the Bcl-2/Bax ratio.
  • 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

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


21. Lo Nigro L, Schiliro G: Occurrence of a FAB-M1 AML in a child during treatment of APL: emergence of an immature clone or a therapy related-AML? Haematologica; 2002 May;87(5):ELT26
MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Occurrence of a FAB-M1 AML in a child during treatment of APL: emergence of an immature clone or a therapy related-AML?
  • [MeSH-major] Leukemia, Myeloid, Acute / etiology. Leukemia, Promyelocytic, Acute / drug therapy. Neoplasms, Second Primary / etiology
  • [MeSH-minor] Antineoplastic Agents, Alkylating / administration & dosage. Antineoplastic Agents, Alkylating / adverse effects. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Child. Fatal Outcome. Humans. Male

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12010686.001).
  • [ISSN] 0390-6078
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Case Reports; Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating
  •  go-up   go-down


22. 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
Hazardous Substances Data Bank. CYTARABINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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

  • Genetic Alliance. consumer health - Acute Myeloid Leukemia, Adult.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down






Advertisement