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1. Yang J, Ikezoe T, Nishioka C, Tasaka T, Taniguchi A, Kuwayama Y, Komatsu N, Bandobashi K, Togitani K, Koeffler HP, Taguchi H, Yokoyama A: AZD1152, a novel and selective aurora B kinase inhibitor, induces growth arrest, apoptosis, and sensitization for tubulin depolymerizing agent or topoisomerase II inhibitor in human acute leukemia cells in vitro and in vivo. Blood; 2007 Sep 15;110(6):2034-40
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] AZD1152, a novel and selective aurora B kinase inhibitor, induces growth arrest, apoptosis, and sensitization for tubulin depolymerizing agent or topoisomerase II inhibitor in human acute leukemia cells in vitro and in vivo.
  • We have recently shown that hematopoietic malignant cells including those from acute myeloid leukemia (AML) and acute lymphoblastic leukemia (ALL) aberrantly expressed Aurora A and B kinases, and ZM447439, a potent inhibitor of Aurora kinases, effectively induced growth arrest and apoptosis of a variety of leukemia cells.
  • The present study explored the effect of AZD1152, a highly selective inhibitor of Aurora B kinase, on various types of human leukemia cells.
  • AZD1152 inhibited the proliferation of AML lines (HL-60, NB4, MOLM13), ALL line (PALL-2), biphenotypic leukemia (MV4-11), acute eosinophilic leukemia (EOL-1), and the blast crisis of chronic myeloid leukemia K562 cells with an IC50 ranging from 3 nM to 40 nM, as measured by thymidine uptake on day 2 of culture.
  • Taken together, AZD1152 is a promising new agent for treatment of individuals with leukemia.
  • The combined administration of AZD1152 and conventional chemotherapeutic agent to patients with leukemia warrants further investigation.
  • [MeSH-major] Antibiotics, Antineoplastic / pharmacology. Apoptosis / drug effects. Cell Proliferation / drug effects. Leukemia / drug therapy. Organophosphates / pharmacology. Protein-Serine-Threonine Kinases / antagonists & inhibitors. Quinazolines / pharmacology. Tubulin Modulators / pharmacology
  • [MeSH-minor] Animals. Aurora Kinase A. Aurora Kinase B. Aurora Kinases. Case-Control Studies. Cell Cycle / drug effects. Colony-Forming Units Assay. Daunorubicin / pharmacology. Drug Synergism. Drug Therapy, Combination. Drug Tolerance. Enzyme Inhibitors / pharmacology. Female. Flow Cytometry. Humans. Immunoblotting. Mice. Mice, Inbred BALB C. Thymidine / metabolism. Transplantation, Heterologous. Vincristine / pharmacology

  • MedlinePlus Health Information. consumer health - Leukemia.
  • Guide to Pharmacology. gene/protein/disease-specific - Aurora kinase (Aur) family - overview and references .
  • Guide to Pharmacology. gene/protein/disease-specific - aurora kinase A - data and references .
  • Guide to Pharmacology. gene/protein/disease-specific - aurora kinase B - data and references .
  • Hazardous Substances Data Bank. DAUNORUBICIN .
  • Hazardous Substances Data Bank. VINCRISTINE .
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  • (PMID = 17495131.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 2-((3-((4-((5-(2-((3-fluorophenyl)amino)-2-oxoethyl)-1H-pyrazol-3-yl)amino)quinazolin-7-yl)oxy)propyl)(ethyl)amino)ethyl dihydrogen phosphate; 0 / Antibiotics, Antineoplastic; 0 / Enzyme Inhibitors; 0 / Organophosphates; 0 / Quinazolines; 0 / Tubulin Modulators; 5J49Q6B70F / Vincristine; EC 2.7.11.1 / AURKB protein, human; EC 2.7.11.1 / Aurka protein, mouse; EC 2.7.11.1 / Aurkb protein, mouse; EC 2.7.11.1 / Aurora Kinase A; EC 2.7.11.1 / Aurora Kinase B; EC 2.7.11.1 / Aurora Kinases; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; VC2W18DGKR / Thymidine; ZS7284E0ZP / Daunorubicin
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2. Valent P: Pathogenesis, classification, and therapy of eosinophilia and eosinophil disorders. Blood Rev; 2009 Jul;23(4):157-65
SciCrunch. KEGG: Data: Disease Annotation .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pathogenesis, classification, and therapy of eosinophilia and eosinophil disorders.
  • Myeloid neoplasms typically presenting with eosinophilia include chronic myeloid leukemia, chronic eosinophilic leukemia (CEL), other myeloproliferative neoplasms, some acute leukemias, advanced mast cell disorders, and rare forms of myelodysplastic syndromes.
  • Treatment of hypereosinophilic patients depends on the variant of disease, presence of end organ damage, molecular targets, and the overall situation in each case.
  • In a group of patients, oncogenic tyrosine kinases (TK) such as FIP1L1/PDGFRA, can be employed as therapeutic targets by using imatinib or other TK-blocking agents.
  • [MeSH-major] Eosinophilia / diagnosis. Eosinophilia / drug therapy. Eosinophils / metabolism. Myeloproliferative Disorders / complications

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  • (PMID = 19246139.001).
  • [ISSN] 1532-1681
  • [Journal-full-title] Blood reviews
  • [ISO-abbreviation] Blood Rev.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cytokines
  • [Number-of-references] 74
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