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1. Ikezoe T, Nishioka C, Tasaka T, Yang Y, Komatsu N, Togitani K, Koeffler HP, Taguchi H: The antitumor effects of sunitinib (formerly SU11248) against a variety of human hematologic malignancies: enhancement of growth inhibition via inhibition of mammalian target of rapamycin signaling. Mol Cancer Ther; 2006 Oct;5(10):2522-30
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • We studied antitumor effects of receptor tyrosine kinase inhibitor sunitinib (formerly SU11248) against a variety of hematologic malignancies including the following leukemias: eosinophilic (EOL-1), acute myeloid (THP-1, U937, Kasumi-1), biphenotypic (MV4-11), acute lymphoblastic (NALL-1, Jurkat, BALL-2, PALL-1, PALL-2), blast crisis of chronic myeloid (KU812, Kcl-22, K562), and adult T-cell (MT-1, MT-2, MT-4), as well as non-Hodgkin's lymphoma (KS-1, Dauji, Akata) and multiple myeloma (U266).
  • In addition, sunitinib inhibited the proliferation of freshly isolated leukemia cells from patients possessing mutations in FLT3 gene.
  • Interestingly, rapamycin analogue RAD001 enhanced the ability of sunitinib to inhibit the proliferation of leukemia cells and down-regulate levels of mammalian target of rapamycin effectors p70 S6 kinase and eukaryotic initiation factor 4E-binding protein 1 in these cells.
  • Taken together, sunitinib may be useful for treatment of individuals with leukemias possessing activation mutation of tyrosine kinase, and the combination of sunitinib and RAD001 represents a promising novel treatment strategy.
  • [MeSH-minor] Adaptor Proteins, Signal Transducing / antagonists & inhibitors. Adaptor Proteins, Signal Transducing / biosynthesis. Apoptosis. Cell Line, Tumor. Cell Proliferation / drug effects. Drug Synergism. Everolimus. Humans. Leukemia / metabolism. Leukemia / pathology. Mutation. Phosphoproteins / antagonists & inhibitors. Phosphoproteins / biosynthesis. Receptor Protein-Tyrosine Kinases / genetics. Ribosomal Protein S6 Kinases, 70-kDa / antagonists & inhibitors. Ribosomal Protein S6 Kinases, 70-kDa / biosynthesis. Signal Transduction. Sirolimus / analogs & derivatives. Sirolimus / pharmacology. TOR Serine-Threonine Kinases

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  • (PMID = 17041096.001).
  • [ISSN] 1535-7163
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Antineoplastic Agents; 0 / EIF4EBP1 protein, human; 0 / Indoles; 0 / Phosphoproteins; 0 / Pyrroles; 0 / sunitinib; 9HW64Q8G6G / Everolimus; EC 2.7.- / Protein Kinases; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.11.1 / Ribosomal Protein S6 Kinases, 70-kDa; W36ZG6FT64 / Sirolimus
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2. 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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  • [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

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  • Guide to Pharmacology. gene/protein/disease-specific - Aurora kinase (Aur) family - overview and references .
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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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3. Vales A, Kondo R, Aichberger KJ, Mayerhofer M, Kainz B, Sperr WR, Sillaber C, Jäger U, Valent P: Myeloid leukemias express a broad spectrum of VEGF receptors including neuropilin-1 (NRP-1) and NRP-2. Leuk Lymphoma; 2007 Oct;48(10):1997-2007
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Myeloid leukemias express a broad spectrum of VEGF receptors including neuropilin-1 (NRP-1) and NRP-2.
  • We have examined the expression of five VEGF receptors (VEGR1/Flt-1, VEGFR2/KDR, Flt-4, neuropilin-1 = NRP-1, NRP-2) in leukemic cells obtained from patients with acute myeloid leukemia (n = 28), chronic myeloid leukemia (n = 14), chronic eosinophilic leukemia (n = 3), chronic myelomonocytic leukemia (n = 9), or mast cell leukemia/systemic mastocytosis (n = 3) as well as in respective cell lines.
  • In most patients, leukemic cells expressed NRP-1 mRNA and NRP-2 mRNA independent of the type of disease.
  • By contrast, transcripts for Flt-1, KDR, and Flt-4 were expressed variably without a clear correlation to the type of leukemia.
  • In conclusion, neoplastic cells in myeloid leukemias frequently express VEGFR including NRP-1 and NRP-2.
  • [MeSH-major] Gene Expression Regulation, Leukemic. Leukemia, Myeloid / genetics. Leukemia, Myeloid / metabolism. Neovascularization, Pathologic. Neuropilin-1 / biosynthesis. Neuropilin-2 / biosynthesis. Receptors, Vascular Endothelial Growth Factor / biosynthesis

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  • (PMID = 17917967.001).
  • [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 / Neuropilin-2; 0 / RNA, Messenger; 144713-63-3 / Neuropilin-1; EC 2.7.10.1 / Receptors, Vascular Endothelial Growth Factor
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4. Valent P: Pathogenesis, classification, and therapy of eosinophilia and eosinophil disorders. Blood Rev; 2009 Jul;23(4):157-65
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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.
  • [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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6. Vega F, Medeiros LJ, Davuluri R, Cromwell CC, Alkan S, Abruzzo LV: t(8;13)-positive bilineal lymphomas: report of 6 cases. Am J Surg Pathol; 2008 Jan;32(1):14-20
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  • Approximately 75% of EMS patients present with or develop precursor T-cell lymphoblastic lymphoma, and most subsequently develop acute myeloid leukemia.
  • Histologically, each tumor was composed of 2 distinct cellular components: small to medium-sized T cells with scant cytoplasm that resembled lymphoblasts, and larger immature-appearing cells with more abundant eosinophilic cytoplasm that resembled myeloblasts, a subset of which expressed myeloid antigens.
  • We believe that these bilineal neoplasms of mixed T-cell and myeloid lineages, which present as lymphoma, are analogous to bilineal leukemias.

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  • (PMID = 18162765.001).
  • [ISSN] 0147-5185
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD
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7. Cools J: Identification and characterization of novel oncogenes in chronic eosinophilic leukemia and T-cell acute lymphoblastic leukemia. Verh K Acad Geneeskd Belg; 2010;72(1-2):55-70
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  • [Title] Identification and characterization of novel oncogenes in chronic eosinophilic leukemia and T-cell acute lymphoblastic leukemia.
  • Insights into these mechanisms may help us to design novel strategies to treat leukemia.
  • Sorafenib was originally developed as a BRAF inhibitor, but our work demonstrates that sorafenib can also be used to treat FIP1L1-PDGFRA positive leukemia, demonstrating that new therapies to treat rare leukemias may be simply found by testing drugs that are already in use for the treatment of other diseases.
  • [MeSH-major] Hypereosinophilic Syndrome / genetics. Nuclear Pore Complex Proteins / genetics. Oncogene Proteins, Fusion / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Receptor, Platelet-Derived Growth Factor alpha / genetics. mRNA Cleavage and Polyadenylation Factors / genetics

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  • (PMID = 20726440.001).
  • [ISSN] 0302-6469
  • [Journal-full-title] Verhandelingen - Koninklijke Academie voor Geneeskunde van België
  • [ISO-abbreviation] Verh. K. Acad. Geneeskd. Belg.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Belgium
  • [Chemical-registry-number] 0 / Benzenesulfonates; 0 / FIP1L1-PDGFRA fusion protein, human; 0 / NUP214 protein, human; 0 / Nuclear Pore Complex Proteins; 0 / Oncogene Proteins; 0 / Oncogene Proteins, Fusion; 0 / Phenylurea Compounds; 0 / Protein Kinase Inhibitors; 0 / Pyridines; 0 / mRNA Cleavage and Polyadenylation Factors; 25X51I8RD4 / Niacinamide; 9ZOQ3TZI87 / sorafenib; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha
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