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1. Bagg A: Malleable immunoglobulin genes and hematopathology - the good, the bad, and the ugly: a paper from the 2007 William Beaumont hospital symposium on molecular pathology. J Mol Diagn; 2008 Sep;10(5):396-410
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  • An appreciation of the various mechanisms involved in the numerous physiological pathways affecting the immunoglobulin genes, and hence antibody molecules, is central to an understanding of B-cell development vis-à-vis the generation of immunological diversity.
  • In addition, recognition of how such genetic changes with good intentions can turn bad has fostered increasing insights into the pathogenesis of B-cell lymphomas and leukemias.
  • [MeSH-major] Gene Rearrangement, B-Lymphocyte, Heavy Chain / genetics. Genes, Immunoglobulin / genetics. Lymphoma, B-Cell / pathology. Lymphoma, T-Cell / pathology

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  • (PMID = 18687793.001).
  • [ISSN] 1525-1578
  • [Journal-full-title] The Journal of molecular diagnostics : JMD
  • [ISO-abbreviation] J Mol Diagn
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / Immunoglobulin Heavy Chains
  • [Number-of-references] 95
  • [Other-IDs] NLM/ PMC2518734
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2. Prima V, Gore L, Caires A, Boomer T, Yoshinari M, Imaizumi M, Varella-Garcia M, Hunger SP: Cloning and functional characterization of MEF2D/DAZAP1 and DAZAP1/MEF2D fusion proteins created by a variant t(1;19)(q23;p13.3) in acute lymphoblastic leukemia. Leukemia; 2005 May;19(5):806-13
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  • [Title] Cloning and functional characterization of MEF2D/DAZAP1 and DAZAP1/MEF2D fusion proteins created by a variant t(1;19)(q23;p13.3) in acute lymphoblastic leukemia.
  • We analyzed the TS-2 acute lymphoblastic leukemia (ALL) cell line that contains a t(1;19)(q23;p13.3) but lacks E2A-PBX1 fusion typically present in leukemias with this translocation.
  • MEF2D is a member of the MEF2 family of DNA binding proteins that activate transcription of genes involved in control of muscle cell differentiation, and signaling pathways that mediate response to mitogenic signals and survival of neurons and T-lymphocytes.
  • [MeSH-major] Chromosomes, Human, Pair 1 / genetics. Chromosomes, Human, Pair 19 / genetics. DNA-Binding Proteins / physiology. Oncogene Proteins, Fusion / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. RNA-Binding Proteins / physiology. Transcription Factors / physiology
  • [MeSH-minor] Cell Line, Tumor. Cloning, Molecular. DNA / metabolism. Humans. MADS Domain Proteins. MEF2 Transcription Factors. Molecular Sequence Data. Myogenic Regulatory Factors. RNA / metabolism. Translocation, Genetic

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  • (PMID = 15744350.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Databank-accession-numbers] GENBANK/ AY681493/ AY681494
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DAZAP1 protein, human; 0 / DAZAP1-MEF2D fusion protein, human; 0 / DNA-Binding Proteins; 0 / MADS Domain Proteins; 0 / MEF2 Transcription Factors; 0 / MEF2D protein, human; 0 / MEF2D-DAZAP1 fusion protein, human; 0 / Myogenic Regulatory Factors; 0 / Oncogene Proteins, Fusion; 0 / RNA-Binding Proteins; 0 / Transcription Factors; 63231-63-0 / RNA; 9007-49-2 / DNA
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3. Murmann AE, Gao J, Encinosa M, Gautier M, Peter ME, Eils R, Lichter P, Rowley JD: Local gene density predicts the spatial position of genetic loci in the interphase nucleus. Exp Cell Res; 2005 Nov 15;311(1):14-26
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  • Specific chromosomal translocations are hallmarks of many human leukemias.
  • The gene density within a 2 Mbp window was found to be a better predictor for the relative positioning of a genomic locus within the cell nucleus than the gene density of entire chromosomes.
  • Analysis of the position of MLL, AF4, AF6 and AF9 in cell lines carrying chromosomal translocations involving these genes revealed that the position of the normal genes was different from that of the fusion genes, and this was again consistent with the changes in local gene density within a 2 Mbp window.
  • Thus, alterations in gene density directly at translocation junctions could explain the change in the position of affected genes in leukemia cells.
  • [MeSH-major] Interphase / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Oncogene Proteins, Fusion / genetics
  • [MeSH-minor] Animals. Bone Marrow Cells. Cell Nucleus. Chromosome Aberrations. Female. Histone-Lysine N-Methyltransferase. Humans. In Situ Hybridization, Fluorescence. Male. Muntjacs / genetics. Translocation, Genetic

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  • (PMID = 16202404.001).
  • [ISSN] 0014-4827
  • [Journal-full-title] Experimental cell research
  • [ISO-abbreviation] Exp. Cell Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 40046; United States / NCI NIH HHS / CA / CA 84405
  • [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 / MLL protein, human; 0 / MLL-AF4 fusion protein, human; 0 / MLL-AF9 fusion protein, human; 0 / MLL-ELL fusion protein, human; 0 / MLL-ENL oncoprotein, human; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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4. Lefranc MP: IMGT, the international ImMunoGeneTics information system: a standardized approach for immunogenetics and immunoinformatics. Immunome Res; 2005 Sep 20;1:3
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • IMGT is a high quality integrated knowledge resource specialized in immunoglobulins (IG), T cell receptors (TR), major histocompatibility complex (MHC) of human and other vertebrates, and related proteins of the immune system (RPI) of any species which belong to the immunoglobulin superfamily (IgSF) and to the MHC superfamily (MhcSF).
  • IMGT is the international reference in immunogenetics and immunoinformatics for medical research (repertoire analysis of the IG antibody sites and of the TR recognition sites in autoimmune and infectious diseases, AIDS, leukemias, lymphomas, myelomas), veterinary research (IG and TR repertoires in farm and wild life species), genome diversity and genome evolution studies of the adaptive immune responses, biotechnology related to antibody engineering (single chain Fragment variable (scFv), phage displays, combinatorial libraries, chimeric, humanized and human antibodies), diagnostics (detection and follow up of residual diseases) and therapeutical approaches (grafts, immunotherapy, vaccinology).

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  • (PMID = 16305737.001).
  • [ISSN] 1745-7580
  • [Journal-full-title] Immunome research
  • [ISO-abbreviation] Immunome Res
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC1312312
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5. Koschmieder S, Rosenbauer F, Steidl U, Owens BM, Tenen DG: Role of transcription factors C/EBPalpha and PU.1 in normal hematopoiesis and leukemia. Int J Hematol; 2005 Jun;81(5):368-77
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  • [Title] Role of transcription factors C/EBPalpha and PU.1 in normal hematopoiesis and leukemia.
  • A block in normal differentiation is a major contributing factor in the development of solid tumors and leukemias.
  • Cells from patients with acute myeloid leukemia (AML) frequently harbor mutated or dysregulated transcription factor genes, suggesting their involvement in leukemogenesis.
  • The implications of these findings for the study of hematopoiesis in the future as well as novel approaches to more disease-specific therapies are discussed.
  • [MeSH-major] Hematopoiesis. Leukemia / genetics. Transcription Factors / physiology

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  • (PMID = 16158816.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / HL56745; United States / NCI NIH HHS / CA / P01 CA72009
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Activating Transcription Factor 2; 0 / Cyclic AMP Response Element-Binding Protein; 0 / Proto-Oncogene Proteins; 0 / Trans-Activators; 0 / Transcription Factors; 0 / proto-oncogene protein Spi-1
  • [Number-of-references] 91
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6. Alston RD, Geraci M, Eden TO, Moran A, Rowan S, Birch JM: Changes in cancer incidence in teenagers and young adults (ages 13 to 24 years) in England 1979-2003. Cancer; 2008 Nov 15;113(10):2807-15
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  • RESULTS: Incidence rates of leukemias, lymphomas, central nervous system, bone, and germ cell tumors; melanoma; and carcinomas of the thyroid, ovary, cervix, and colon/rectum increased over time (all P < .01); whereas the incidence of carcinomas of the stomach and bladder decreased (both P < .01).

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  • (PMID = 18846564.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Grant] United Kingdom / Cancer Research UK / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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7. Ryan DP, Sunde M, Kwan AH, Marianayagam NJ, Nancarrow AL, Vanden Hoven RN, Thompson LS, Baca M, Mackay JP, Visvader JE, Matthews JM: Identification of the key LMO2-binding determinants on Ldb1. J Mol Biol; 2006 May 26;359(1):66-75
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  • The overexpression of LIM-only protein 2 (LMO2) in T-cells, as a result of chromosomal translocations, retroviral insertion during gene therapy, or in transgenic mice models, leads to the onset of T-cell leukemias.
  • The delineation of this region reveals some specific differences when compared to the equivalent LMO4:Ldb1 interaction that hold promise for the development of reagents to specifically bind LMO2 in the treatment of leukemia.
  • [MeSH-minor] Adaptor Proteins, Signal Transducing. Animals. Homeodomain Proteins / chemistry. Homeodomain Proteins / genetics. Homeodomain Proteins / metabolism. Humans. LIM Domain Proteins. LIM-Homeodomain Proteins. Mice. Models, Molecular. Protein Binding. Proto-Oncogene Proteins. Recombinant Fusion Proteins / chemistry. Recombinant Fusion Proteins / genetics. Recombinant Fusion Proteins / metabolism. T-Lymphocytes / metabolism. Transcription Factors / chemistry. Transcription Factors / genetics. Transcription Factors / metabolism. Two-Hybrid System Techniques

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  • (PMID = 16616188.001).
  • [ISSN] 0022-2836
  • [Journal-full-title] Journal of molecular biology
  • [ISO-abbreviation] J. Mol. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / DNA-Binding Proteins; 0 / Homeodomain Proteins; 0 / LDB1 protein, human; 0 / LHX1 protein, human; 0 / LIM Domain Proteins; 0 / LIM-Homeodomain Proteins; 0 / LMO2 protein, human; 0 / LMO4 protein, human; 0 / Lmo2 protein, mouse; 0 / Metalloproteins; 0 / Proto-Oncogene Proteins; 0 / Recombinant Fusion Proteins; 0 / Transcription Factors
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8. Efferth T, Giaisi M, Merling A, Krammer PH, Li-Weber M: Artesunate induces ROS-mediated apoptosis in doxorubicin-resistant T leukemia cells. PLoS One; 2007;2(8):e693
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  • [Title] Artesunate induces ROS-mediated apoptosis in doxorubicin-resistant T leukemia cells.
  • Artesunate (ART), a powerful anti-malarial herbal compound, has been shown to inhibit growth of various tumor cell lines in vitro and of xenografted Kaposi's sarcoma in mice in vivo.
  • METHODOLOGY AND PRINCIPAL FINDINGS: In this study, we used T-cell leukemias as a model system to study the molecular mechanisms of ART-induced apoptosis.
  • To investigate drug sensitivity and resistance, we chose a Doxorubicin-resistant leukemia cell line and investigated the killing effect of ART on these cells.
  • Therefore, ART can overcome the Doxorubicin-resistance and induce the Doxorubicin-resistant leukemia cells to undergo apoptosis.
  • We also show that ART can synergize with Doxorubicin to enhance apoptotic cell death in leukemic T cells.
  • [MeSH-minor] Acetylcysteine / pharmacology. Animals. Cell Line, Tumor / drug effects. Drug Screening Assays, Antitumor. Free Radical Scavengers / pharmacology. Humans. Leukemia / drug therapy. Leukemia / metabolism. Leukemia / pathology. Mice. Oxidation-Reduction

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  • (PMID = 17668070.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Antimalarials; 0 / Artemisinins; 0 / Free Radical Scavengers; 0 / Reactive Oxygen Species; 60W3249T9M / artesunate; 80168379AG / Doxorubicin; WYQ7N0BPYC / Acetylcysteine
  • [Other-IDs] NLM/ PMC1933253
  • [General-notes] NLM/ Original DateCompleted: 20070806
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9. Tsiftsoglou AS, Bonovolias ID, Tsiftsoglou SA: Multilevel targeting of hematopoietic stem cell self-renewal, differentiation and apoptosis for leukemia therapy. Pharmacol Ther; 2009 Jun;122(3):264-80
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  • [Title] Multilevel targeting of hematopoietic stem cell self-renewal, differentiation and apoptosis for leukemia therapy.
  • Human leukemias are considered clonal hematological malignancies initiated by chromosomal aberrations or epigenetic alterations occurring at the level of either pluripotent hematopoietic stem cells (HSCs) or early multipotent progenitors (MPPs).
  • Future therapies of leukemias require identification of molecular targets involved in hematopoiesis under normal and leukemic conditions and detailed understanding of the interactions between normal hematopoietic and leukemic cells within the bone marrow micro-environment.
  • This review presents the basic aspects of hematopoiesis and highlights multilevel exploitable targets for leukemia therapy.
  • These include HSC niche components, signaling pathways (SCF/c-kit-R, EPO-R-JAK2/STAT, Wnt, Notch, HOX), inducer-receptor interactions, superfine chromatin structure modifications, fused transcription factors, microRNAs and signaling of cell death through the Bcl-2 apoptotic switch (BH3-only proteins).
  • The classes of therapeutics developed or being under development to eradicate human leukemias include novel antimetabolites, DNA hypomethylating agents, histone deacetylation inhibitors (HDACIs), retinoids and other inducers of differentiation, targeted monoclonal antibodies raised against cell surface proteins, pro-apoptotic receptor agonists (PARAs), BH3 peptidomimetics, cell cycle inhibitors, siRNAs and perhaps microRNAs.
  • Some of these agents induce terminal differentiation while others promote cell cycle arrest and apoptosis in leukemia cells.
  • [MeSH-major] Apoptosis / drug effects. Cell Differentiation / drug effects. Drug Delivery Systems / methods. Hematopoietic Stem Cells / drug effects. Hematopoietic Stem Cells / pathology. Leukemia / drug therapy

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  • (PMID = 19306896.001).
  • [ISSN] 1879-016X
  • [Journal-full-title] Pharmacology & therapeutics
  • [ISO-abbreviation] Pharmacol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 225
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10. Sun XL, Fang MY, Jiang F, Jing Y: [Immunologic classification used in typing of 68 cases of acute leukemias]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2006 Feb;14(1):39-41
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  • [Title] [Immunologic classification used in typing of 68 cases of acute leukemias].
  • To evaluate the significance of immunologic classification for typing of acute leukemia (AL).
  • In conclusion, immunologic classification can improve the accuracy in acute leukemia diagnosis.
  • The diagnosis of some special AL, such as acute unidentified leukemia (AUL), AML-M(0) and so on, must rely on immunologic classification.

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  • (PMID = 16584588.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD14; 0 / Antigens, CD34; 0 / Antigens, CD7; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD33 protein, human; 0 / Sialic Acid Binding Ig-like Lectin 3; EC 3.4.11.2 / Antigens, CD13
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11. Nishida S, Hosen N, Shirakata T, Kanato K, Yanagihara M, Nakatsuka S, Hoshida Y, Nakazawa T, Harada Y, Tatsumi N, Tsuboi A, Kawakami M, Oka Y, Oji Y, Aozasa K, Kawase I, Sugiyama H: AML1-ETO rapidly induces acute myeloblastic leukemia in cooperation with the Wilms tumor gene, WT1. Blood; 2006 Apr 15;107(8):3303-12
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  • [Title] AML1-ETO rapidly induces acute myeloblastic leukemia in cooperation with the Wilms tumor gene, WT1.
  • AML1-ETO, a chimeric gene frequently detected in acute myelogenous leukemia (AML), inhibits the differentiation of myeloid progenitors by suppressing genes associated with myeloid differentiation and increases the replating ability of clonogenic myeloid progenitors.
  • The Wilms tumor gene (WT1), which has been identified as the gene responsible for Wilms tumor, is expressed at high levels in almost all human leukemias.
  • [MeSH-major] Cell Differentiation / genetics. Cell Transformation, Neoplastic / genetics. Core Binding Factor Alpha 2 Subunit / genetics. Leukemia, Myeloid, Acute / genetics. Myeloid Progenitor Cells / metabolism. Oncogene Proteins, Fusion / genetics. WT1 Proteins / genetics

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  • (PMID = 16380455.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / WT1 Proteins
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12. Parikh C, Subrahmanyam R, Ren R: Oncogenic NRAS, KRAS, and HRAS exhibit different leukemogenic potentials in mice. Cancer Res; 2007 Aug 1;67(15):7139-46
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  • RAS proteins are small GTPases that play a central role in transducing signals that regulate cell proliferation, survival, and differentiation.
  • The mechanism underlying the different frequencies of RAS isoforms mutated in myeloid leukemia is not known.
  • We found that all three RAS oncogenes have the ability to induce myeloid leukemias, yet have distinct leukemogenic strengths and phenotypes.

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  • (PMID = 17671181.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / HL083515-02; United States / NHLBI NIH HHS / HL / R01 HL083515; United States / NHLBI NIH HHS / HL / HL083515; United States / NHLBI NIH HHS / HL / R01 HL083515-02
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS84018; NLM/ PMC2662707
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13. Mello MR, Metze K, Adam RL, Pereira FG, Magalhães MG, Machado CG, Lorand-Metze I: Phenotypic subtypes of acute lymphoblastic leukemia associated with different nuclear chromatin texture. Anal Quant Cytol Histol; 2008 Apr;30(2):92-8
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  • [Title] Phenotypic subtypes of acute lymphoblastic leukemia associated with different nuclear chromatin texture.
  • OBJECTIVE: To determine if phenotypic subtypes of acute lymphoblastic leukemia (ALL) are associated with different nuclear textures.
  • B-precursor ALL was further subdivided by European Group for the Immunological Classification of Leukemias criteria.
  • CONCLUSION: ALL of B- or T-origin presented significant differences in nuclear texture features, probably reflecting different molecular events associated with cell differentiation, gene methylation pattern, apoptosis, and lineage-specific functional events.

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  • (PMID = 18561745.001).
  • [ISSN] 0884-6812
  • [Journal-full-title] Analytical and quantitative cytology and histology
  • [ISO-abbreviation] Anal. Quant. Cytol. Histol.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Chromatin
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14. Malempati S, Tibbitts D, Cunningham M, Akkari Y, Olson S, Fan G, Sears RC: Aberrant stabilization of c-Myc protein in some lymphoblastic leukemias. Leukemia; 2006 Sep;20(9):1572-81
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  • [Title] Aberrant stabilization of c-Myc protein in some lymphoblastic leukemias.
  • Overexpression of the c-Myc oncoprotein is observed in a large number of hematopoietic malignancies, and transgenic animal models have revealed a potent role for c-Myc in the generation of leukemias and lymphomas.
  • We examined whether aberrant protein stabilization could be a mechanism of c-Myc overexpression in leukemia cell lines and in primary bone marrow samples from pediatric acute lymphoblastic leukemia (ALL) patients.
  • We found that c-Myc protein half-life was prolonged in the majority of leukemia cell lines and bone marrow samples tested.
  • There were no mutations in the c-myc gene in any of the leukemia cell lines that could account for increased c-Myc stability.
  • However, abnormal phosphorylation at two conserved sites, Threonine 58 and Serine 62, was observed in leukemia cell lines with stabilized c-Myc.
  • Moreover, stabilized c-Myc from the ALL cell lines showed decreased affinity for glycogen synthase kinase3beta, the kinase that phosphorylates c-Myc at Threonine 58 and facilitates its degradation.

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  • (PMID = 16855632.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA100855-02; United States / NCI NIH HHS / CA / CA086957-05; United States / NCI NIH HHS / CA / R01 CA100855; United States / NCI NIH HHS / CA / CA100855-02; United States / NCI NIH HHS / CA / K01 CA086957; United States / NCI NIH HHS / CA / K01 CA086957-05
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins c-myc; 2ZD004190S / Threonine; 452VLY9402 / Serine; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.1 / glycogen synthase kinase 3 beta; EC 2.7.11.26 / Glycogen Synthase Kinase 3; EC 3.4.25.1 / Proteasome Endopeptidase Complex; EC 3.4.99.- / ATP dependent 26S protease
  • [Other-IDs] NLM/ NIHMS42996; NLM/ PMC2322939
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15. Thomas X, Cannas G: Leukemia stem cells and new strategies to overcome resistance to therapy. Curr Stem Cell Res Ther; 2010 Sep;5(3):277-86
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  • [Title] Leukemia stem cells and new strategies to overcome resistance to therapy.
  • Acute leukemias are the result of aberrant hematopoietic processes initiated by rare leukemia stem cells that have maintained or acquired the capacity of indefinite proliferation through accumulated mutations and/or epigenetic changes.
  • The most likely view of hematopoietic cell lineage organization is that of complex reactive or adaptative systems.
  • The properties of leukemia stem cells indicate that current chemotherapy will not be effective.
  • Furthermore, recent advances indicate that stem cell microenvironment directly affects cell fate decisions.
  • Because they are quiescent, leukemia stem cells do not respond to cell cycle-specific cytotoxic agents used in treating leukemia, which contribute to treatment failure.
  • New strategies are required that specifically target the malignant stem cell population.
  • [MeSH-major] Drug Resistance, Neoplasm / physiology. Leukemia / physiopathology. Leukemia / therapy. Neoplastic Stem Cells / physiology
  • [MeSH-minor] Cancer Vaccines. Cell Cycle. Cell Differentiation. Cell Lineage. Environment

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  • (PMID = 20528758.001).
  • [ISSN] 2212-3946
  • [Journal-full-title] Current stem cell research & therapy
  • [ISO-abbreviation] Curr Stem Cell Res Ther
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United Arab Emirates
  • [Chemical-registry-number] 0 / Cancer Vaccines
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16. Thomas X, Campos L, Le QH, Guyotat D: Heat shock proteins and acute leukemias. Hematology; 2005 Jun;10(3):225-35
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  • [Title] Heat shock proteins and acute leukemias.
  • HSPs have also been implicated in the resistance of leukemia cells to potential therapeutic agents.
  • HSPs were shown highly expressed by acute myeloid leukemia (AML) cells as well as by acute lymphoblastic leukemia (ALL) cells.
  • [MeSH-major] Antineoplastic Agents / metabolism. Gene Expression Regulation, Leukemic / drug effects. HSP90 Heat-Shock Proteins / metabolism. Neoplasm Proteins / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Rifabutin / analogs & derivatives

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  • (PMID = 16019471.001).
  • [ISSN] 1024-5332
  • [Journal-full-title] Hematology (Amsterdam, Netherlands)
  • [ISO-abbreviation] Hematology
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzoquinones; 0 / HSP90 Heat-Shock Proteins; 0 / Lactams, Macrocyclic; 0 / Neoplasm Proteins; 1W306TDA6S / Rifabutin; 4GY0AVT3L4 / tanespimycin
  • [Number-of-references] 122
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17. Meleshko AN, Movchan LV, Belevtsev MV, Savitskaja TV: Relative expression of different Ikaros isoforms in childhood acute leukemia. Blood Cells Mol Dis; 2008 Nov-Dec;41(3):278-83
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  • [Title] Relative expression of different Ikaros isoforms in childhood acute leukemia.
  • Previous studies demonstrated that human leukemias are heterogeneous for Ikaros expression.
  • We detected eight major isoforms and several minor mutant isoforms in most patients with acute lymphoblastic and myeloid leukemia and in healthy donors, but the relative level of expression varied.
  • We found a negative association between the Ikaros ratio and myeloid coexpression in B-cell ALL, the most prominent was for CD15.
  • [MeSH-major] Gene Expression Regulation, Neoplastic. Ikaros Transcription Factor / genetics. Leukemia / genetics
  • [MeSH-minor] Adolescent. Cell Line. Child. Child, Preschool. Gene Expression. Humans. Infant. Infant, Newborn. Mutant Proteins. Protein Isoforms / genetics. Protein Isoforms / metabolism. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 18675565.001).
  • [ISSN] 1096-0961
  • [Journal-full-title] Blood cells, molecules & diseases
  • [ISO-abbreviation] Blood Cells Mol. Dis.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Mutant Proteins; 0 / Protein Isoforms; 148971-36-2 / Ikaros Transcription Factor
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18. Gindina TL, Mamaev NN, Zubaĭdullina SR, Kondakova EV: [Acute lymphoblastic leukemias with translocations (1;19)(q23;p13): a description of 3 new cases and a review of the literature]. Ter Arkh; 2010;82(11):63-7
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  • [Title] [Acute lymphoblastic leukemias with translocations (1;19)(q23;p13): a description of 3 new cases and a review of the literature].
  • AIM: To discuss the specific features of the cytogenetics and clinical manifestations of acute lymphoblastic leukemias (ALL) with balanced and unbalanced translocations (1;19)(q23; p13).
  • p13) is characteristic for patients of different age groups, mainly for those with pre-B cell ALL.
  • [MeSH-major] Chromosomes, Human, Pair 1 / ultrastructure. Chromosomes, Human, Pair 19 / ultrastructure. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic

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  • (PMID = 21381353.001).
  • [ISSN] 0040-3660
  • [Journal-full-title] Terapevticheskiĭ arkhiv
  • [ISO-abbreviation] Ter. Arkh.
  • [Language] rus
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Russia (Federation)
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19. Walsh SH, Rosenquist R: Immunoglobulin gene analysis of mature B-cell malignancies: reconsideration of cellular origin and potential antigen involvement in pathogenesis. Med Oncol; 2005;22(4):327-41
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  • [Title] Immunoglobulin gene analysis of mature B-cell malignancies: reconsideration of cellular origin and potential antigen involvement in pathogenesis.
  • Mature B-cell malignancies stem from B cells transformed at various developmental stages, accounting for the wide range of heterogeneous features observed in the different disease entities.
  • Analysis of the immunoglobulin (Ig) genes can facilitate the identification of the normal B-cell counterpart of lymphomas and leukemias, as Ig genes acquire somatic hypermutation in germinal centers during the immune response to antigen.
  • Therefore, lymphomas that derive from a naïve, pregerminal center B cell lack somatic hypermutation in the clonal Ig gene, whereas germinal center-derived lymphomas, such as diffuse large B-cell lymphoma and follicular lymphoma, display somatic hypermutation of their Ig genes.
  • Furthermore, biases in the Ig variable heavy chain gene repertoire in B-cell malignancies can indicate a possible antigenic influence in pathogenesis.
  • Much work has been accomplished in the past decade to characterize the Ig genes in different lymphoma entities, and the separation of chronic lymphocytic leukemia into two prognostic subgroups in the late 1990s based on the presence or absence of somatic hypermutation led to investigations of Ig genes in larger cohorts of previously uncharacterized entities, such as mantle cell lymphoma.
  • This review will briefly discuss relevant aspects of normal B-cell development, and then focus on what can be ascertained from Ig studies of newly characterized entities, mantle cell lymphoma, hairy cell leukemia, lymphoplasmacytic lymphoma/ Waldenström's macroglobulinemia, and splenic marginal zone lymphoma, from the point of view of cellular origin and variable heavy chain gene restrictions as a sign of antigen involvement.
  • The recent evidence that an alternative pathway of gaining somatic hypermutation might exist is also considered, and the implications this has for understanding the cellular origin of B-cell malignancies.
  • [MeSH-major] B-Lymphocyte Subsets / immunology. Leukemia, B-Cell / genetics. Lymphoma, B-Cell / genetics

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  • (PMID = 16260850.001).
  • [ISSN] 1357-0560
  • [Journal-full-title] Medical oncology (Northwood, London, England)
  • [ISO-abbreviation] Med. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 115
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20. Sinnett D, N'Diaye N, Labuda D, Krajinovic M: [Genetic determinants of childhood leukemia]. Bull Cancer; 2006 Sep;93(9):857-65
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  • [Title] [Genetic determinants of childhood leukemia].
  • [Transliterated title] Les déterminants génétiques de la leucémie de l'enfant.
  • Little is known about the etiology of this heterogeneous group of diseases despite the fact they constitute the major cause of death by disease among this population.
  • Because of its relatively high prevalence, most of the work done in pediatric oncogenetics has been focused on leukemias, particularly acute lymphoblastic leukemia (ALL).
  • Although it is now well accepted that genetic variations play a significant role in determining individual's cancer susceptibility, few studies have explored genetic susceptibility to childhood leukemia with respect to common polymorphisms.
  • 1) cellular growth and differentiation, 2) DNA replication and repair, 3) metabolism of carcinogens, 4) apoptosis, 5) oxidative stress response and 6) cell cycle.
  • We also observed that, at least at some loci, the parental genetics might be important in predicting the risk of cancer in this pediatric model of a complex disease.
  • Taken together, these results indicate that the investigation of a single enzyme and/or a single genotype might not be sufficient to explain the etiology of childhood leukemia because of the complexity of the environment and that of the inter-individual variability in cancer susceptibility.
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Adolescent. Carcinogens / metabolism. Child. Cytochrome P-450 Enzyme System / genetics. Cytochrome P-450 Enzyme System / metabolism. Environment. Female. Folic Acid / metabolism. Genetic Predisposition to Disease. Glutathione Transferase / genetics. Glutathione Transferase / metabolism. Humans. Male. Maternal Exposure / adverse effects. Oxidative Stress. Paternal Exposure / adverse effects

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  • (PMID = 16980228.001).
  • [ISSN] 1769-6917
  • [Journal-full-title] Bulletin du cancer
  • [ISO-abbreviation] Bull Cancer
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Carcinogens; 9035-51-2 / Cytochrome P-450 Enzyme System; 935E97BOY8 / Folic Acid; EC 2.5.1.18 / Glutathione Transferase
  • [Number-of-references] 65
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21. Ravandi F, Estrov Z: Eradication of leukemia stem cells as a new goal of therapy in leukemia. Clin Cancer Res; 2006 Jan 15;12(2):340-4
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  • [Title] Eradication of leukemia stem cells as a new goal of therapy in leukemia.
  • Leukemias have traditionally been classified and treated on the basis of phenotypic characteristics, such as morphology and cell-surface markers, and, more recently, cytogenetic aberrations.
  • The leukemia cell population is functionally heterogeneous: it consists of leukemia stem cells (LSC) and mature leukemia cells that differentiate abnormally to varying extents.
  • Because they are quiescent, LSCs do not respond to cell cycle-specific cytotoxic agents used to treat leukemia and so contribute to treatment failure.
  • Recent data suggest that mature leukemia cells may acquire LSC characteristics, thereby evading chemotherapeutic treatment and sustaining the disease.
  • Ongoing research is likely to reveal the molecular mechanisms responsible for LSC characteristics and lead to novel strategies for eradicating leukemia.
  • [MeSH-major] Hematopoietic Stem Cells. Leukemia / therapy. Neoplastic Stem Cells

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  • (PMID = 16428470.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 85
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22. Hatina J, Schulz WA, Fischer J, Wahl J, Debatin KM, Beltinger C: [Tumour stem cells--a new concept in tumour biology]. Dtsch Med Wochenschr; 2007 Aug;132(31-32):1629-32
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  • An increasing number of tumours with tumour stem cells has been identified by now, including breast, brain, colon and prostate cancers, as well as leukemias.
  • [MeSH-minor] Animals. Antineoplastic Agents / pharmacology. Bone Marrow. Cell Differentiation. Humans

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  • (PMID = 17654417.001).
  • [ISSN] 1439-4413
  • [Journal-full-title] Deutsche medizinische Wochenschrift (1946)
  • [ISO-abbreviation] Dtsch. Med. Wochenschr.
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 9
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23. Rosenbauer F, Koschmieder S, Steidl U, Tenen DG: Effect of transcription-factor concentrations on leukemic stem cells. Blood; 2005 Sep 1;106(5):1519-24
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  • Increasing evidence suggests that leukemias are sustained by leukemic stem cells.
  • The involvement of a small group of key transcription factors into this process was suggested by their frequent mutation or down-regulation in patients with acute myeloid leukemia (AML).
  • Recent findings in mice with hypomorphic transcription-factor genes demonstrated that leukemic stem-cell formation in AML could directly be caused by reduced transcription-factor activity beyond a critical threshold.
  • Here, we discuss the effects of transcription-factor concentrations on hematopoiesis and leukemia, with a focus on the regulation of transcription-factor gene expression as a major mechanism that alters critical threshold levels during blood development and cancer.

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  • (PMID = 15914558.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA72009; United States / NCI NIH HHS / CA / R01 CA88046
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Transcription Factors
  • [Number-of-references] 76
  • [Other-IDs] NLM/ PMC1895222
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24. Mondrala S, Eastmond DA: Topoisomerase II inhibition by the bioactivated benzene metabolite hydroquinone involves multiple mechanisms. Chem Biol Interact; 2010 Mar 19;184(1-2):259-68
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  • Previous work from our laboratory and others has demonstrated that bioactive benzene metabolites are capable of inhibiting topoII in isolated enzyme and cell culture systems.
  • An increase in cleavable complex formation as well as the inhibition of enzymatic activity at the closed clamp and other stages of the catalytic cycle in bone marrow cells would likely result in DNA breakage, the formation of chromosomal aberrations, and could potentially result in leukemia-associated chromosomal translocations, similar to those seen in leukemias induced by the bisdioxopiperazine type of catalytic topoII inhibitors.

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  • [Copyright] Copyright (c) 2009 Elsevier Ireland Ltd. All rights reserved.
  • (PMID = 20034485.001).
  • [ISSN] 1872-7786
  • [Journal-full-title] Chemico-biological interactions
  • [ISO-abbreviation] Chem. Biol. Interact.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Hydroquinones; 0 / Topoisomerase II Inhibitors; 123-31-9 / hydroquinone; 9007-49-2 / DNA; EC 5.99.1.3 / DNA Topoisomerases, Type II; J64922108F / Benzene
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25. Rossi JG, Felice MS, Bernasconi AR, Ribas AE, Gallego MS, Somardzic AE, Alfaro EM, Alonso CN: Acute leukemia of dendritic cell lineage in childhood: incidence, biological characteristics and outcome. Leuk Lymphoma; 2006 Apr;47(4):715-25
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  • [Title] Acute leukemia of dendritic cell lineage in childhood: incidence, biological characteristics and outcome.
  • CD4+ CD56+ malignancies have only recently been related to dendritic cell (DC) lineage.
  • Considering that leukemias in childhood and in adults are different diseases, we describe three pediatric cases to help compare the biological characteristics, immunophenotype, clinical features, treatment response and incidence of this disease in both age groups.
  • From a total 1363 new patients with acute leukemia (AL), we report three cases with blasts of French - American - British L2 morphology, an absence of the most specific markers for myeloid, T or B lineage and lacking CD34, which led us to evaluate the blasts with an extensive panel of antibodies, including those related to the other putative pathways of lymphoid differentation: natural killer and DC.
  • All three children showed good response to acute lymphoblastic leukemia (ALL) protocols, achieving complete remission even when one of the patients relapsed and received an allogeneic transplant.
  • We emphasize the importance of including antibodies for DC lineage in cases of CD34(-) unclassifiable AL to further characterize these rare cases (0.22%), considering that the tumor cell affiliation to DC lineage relies exclusively on immunophenotypic criteria.
  • [MeSH-major] Dendritic Cells / cytology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / epidemiology
  • [MeSH-minor] Adolescent. Antigens, CD34 / biosynthesis. Cell Lineage. Child. Female. Humans. Immunophenotyping. In Situ Hybridization, Fluorescence. Incidence. Leukocytes, Mononuclear / metabolism. Male. Remission Induction. Treatment Outcome

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  • (PMID = 16690531.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD34
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26. O'Malley DP, Kim YS, Perkins SL, Baldridge L, Juliar BE, Orazi A: Morphologic and immunohistochemical evaluation of splenic hematopoietic proliferations in neoplastic and benign disorders. Mod Pathol; 2005 Dec;18(12):1550-61
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  • We compared the morphologic and immunohistochemical features of splenic hematopoietic proliferations seen in neoplastic myeloid disorders (eg chronic myeloproliferative disorders, myelodysplastic/myeloproliferative disorders and acute myeloid leukemias) to extramedullary hematopoiesis seen in a variety of reactive conditions.
  • Neoplastic hematopoietic proliferations in chronic myeloproliferative disorders are characterized by trilineage hematopoiesis with significant dysplasia in all cell lineages.
  • Acute myeloid leukemia showed an increase in immature forms, which were highlighted by immunohistochemistry.
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Biomarkers, Tumor / metabolism. Cell Proliferation. Child. Child, Preschool. Humans. Middle Aged

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  • (PMID = 16118626.001).
  • [ISSN] 0893-3952
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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27. Weber JM, Calvi LM: Notch signaling and the bone marrow hematopoietic stem cell niche. Bone; 2010 Feb;46(2):281-5
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  • [Title] Notch signaling and the bone marrow hematopoietic stem cell niche.
  • Notch signaling is important throughout development and also appears to play a critical role in cellular maturation and differentiation of osteoblastic cells and hematopoietic cells as disregulation can lead to bone loss and leukemias, respectively.

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  • [Copyright] (c) 2009 Elsevier Inc. All rights reserved.
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  • (PMID = 19679213.001).
  • [ISSN] 1873-2763
  • [Journal-full-title] Bone
  • [ISO-abbreviation] Bone
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / DK076876-01A2; United States / NIDDK NIH HHS / DK / K08 DK064381; United States / NIDDK NIH HHS / DK / R01 DK 076876; United States / NIDDK NIH HHS / DK / R01 DK081843; United States / NIDDK NIH HHS / DK / DK081843-01A1; United States / NIDDK NIH HHS / DK / R01 DK076876-01A2; United States / NIDDK NIH HHS / DK / R01 DK081843-01A1; United States / NIDDK NIH HHS / DK / R01 DK076876; United States / NIDDK NIH HHS / DK / R21 DK069563; United States / NIAMS NIH HHS / AR / T32 AR05345903
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptors, Notch
  • [Number-of-references] 73
  • [Other-IDs] NLM/ NIHMS146505; NLM/ PMC3073451
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28. Lefranc MP, Giudicelli V, Kaas Q, Duprat E, Jabado-Michaloud J, Scaviner D, Ginestoux C, Clément O, Chaume D, Lefranc G: IMGT, the international ImMunoGeneTics information system. Nucleic Acids Res; 2005 Jan 1;33(Database issue):D593-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The international ImMunoGeneTics information system (IMGT) (http://imgt.cines.fr), created in 1989, by the Laboratoire d'ImmunoGenetique Moleculaire LIGM (Universite Montpellier II and CNRS) at Montpellier, France, is a high-quality integrated knowledge resource specializing in the immunoglobulins (IGs), T cell receptors (TRs), major histocompatibility complex (MHC) of human and other vertebrates, and related proteins of the immune systems (RPI) that belong to the immunoglobulin superfamily (IgSF) and to the MHC superfamily (MhcSF).
  • IMGT is used in medical research (autoimmune diseases, infectious diseases, AIDS, leukemias, lymphomas, myelomas), veterinary research, biotechnology related to antibody engineering (phage displays, combinatorial libraries, chimeric, humanized and human antibodies), diagnostics (clonalities, detection and follow up of residual diseases) and therapeutical approaches (graft, immunotherapy and vaccinology).
  • [MeSH-minor] Animals. Database Management Systems. Databases, Nucleic Acid. Databases, Protein. Genes, Immunoglobulin. Genes, T-Cell Receptor. Genomics. Humans. Internationality. Major Histocompatibility Complex. Protein Conformation. Systems Integration. Vertebrates / genetics. Vertebrates / immunology

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  • (PMID = 15608269.001).
  • [ISSN] 1362-4962
  • [Journal-full-title] Nucleic acids research
  • [ISO-abbreviation] Nucleic Acids Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC540019
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29. Wayne AS, Baird K, Egeler RM: Hematopoietic stem cell transplantation for leukemia. Pediatr Clin North Am; 2010 Feb;57(1):1-25
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  • [Title] Hematopoietic stem cell transplantation for leukemia.
  • Leukemia represents the most common pediatric malignancy, accounting for approximately 30% of all cancers in children less than 20 years of age.
  • Most children diagnosed with leukemia are cured without hematopoietic stem cell transplantation (HSCT), but for some high-risk subgroups, allogeneic HSCT plays an important role in their therapeutic approach.
  • The characteristics of these high-risk subgroups and the role of HSCT in childhood leukemias are discussed.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation / methods. Leukemia / surgery

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  • (PMID = 20307709.001).
  • [ISSN] 1557-8240
  • [Journal-full-title] Pediatric clinics of North America
  • [ISO-abbreviation] Pediatr. Clin. North Am.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / Z99 CA999999; United States / Intramural NIH HHS / / ZIC BC010596-06; United States / Intramural NIH HHS / / ZIC SC010353-10
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 169
  • [Other-IDs] NLM/ NIHMS181181; NLM/ PMC2913522
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30. Kaledin VI, Il'nitskaia SI, Baginskaia NV, Kholodar' AV, Obut TA: [Effect of phenobarbital and thyroxine on hepatocarcinogenesis initiated in mice by nitrosoethylurea and diethylnitrosamine]. Ross Fiziol Zh Im I M Sechenova; 2005 Dec;91(12):1481-91
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  • 29.4% of male and 42.1% of female ICR mice who had received nitrosoethylurea died of leukemia within 3-6 months after the carcinogen treatment.
  • There was no case of leukemia in mice treated with diethylnitrosamine.
  • Phenobarbital and thyroxine did not affect development of either leukemias or lung adenomas.

  • Hazardous Substances Data Bank. Phenobarbital .
  • Hazardous Substances Data Bank. LEVOTHYROXINE .
  • Hazardous Substances Data Bank. N-NITROSODIETHYLAMINE .
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  • (PMID = 16493929.001).
  • [ISSN] 0869-8139
  • [Journal-full-title] Rossiiskii fiziologicheskii zhurnal imeni I.M. Sechenova
  • [ISO-abbreviation] Ross Fiziol Zh Im I M Sechenova
  • [Language] RUS
  • [Publication-type] Comparative Study; English Abstract; Journal Article
  • [Publication-country] Russia (Federation)
  • [Chemical-registry-number] 0 / Alkylating Agents; 0 / Hypnotics and Sedatives; 3IQ78TTX1A / Diethylnitrosamine; P8M1T4190R / Ethylnitrosourea; Q51BO43MG4 / Thyroxine; YQE403BP4D / Phenobarbital
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31. Yan M, Himoudi N, Pule M, Sebire N, Poon E, Blair A, Williams O, Anderson J: Development of cellular immune responses against PAX5, a novel target for cancer immunotherapy. Cancer Res; 2008 Oct 01;68(19):8058-65
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  • PAX5 is a member of the PAX family of developmental transcription factors with an important role in B-cell development.
  • Its expression in normal adult tissue is limited to the hemopoietic system, but it is aberrantly expressed in a number of solid cancers and leukemias where it functions as an oncogene.
  • We generated high-avidity CTL clones from these lines capable of killing cells pulsed with <1 nmol/L of TLP and killing a range of PAX5-expressing malignant cell lines. I.v. injection of an anti-PAX5 CTL clone into immunodeficient mice bearing s.c. human tumors resulted in specific growth inhibition of PAX5-expressing tumors.
  • This knowledge can be used for the therapeutic generation of CTL lines or the cloning of high-avidity T-cell receptor genes for use in adoptive immunotherapy.
  • [MeSH-minor] Animals. Cell Proliferation. Chemotaxis, Leukocyte / immunology. Complement C5 / genetics. Genes, RAG-1 / physiology. Humans. Immunity, Cellular / physiology. Interleukin Receptor Common gamma Subunit / genetics. K562 Cells. Mice. Mice, Knockout. T-Lymphocytes / immunology. T-Lymphocytes / transplantation. Tumor Cells, Cultured. Xenograft Model Antitumor Assays

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  • (PMID = 18829564.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G0501935; United Kingdom / Cancer Research UK / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Complement C5; 0 / Interleukin Receptor Common gamma Subunit; 0 / PAX5 Transcription Factor; 0 / PAX5 protein, human
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32. Kim YR, Eom HS, Min CK, Lee S, Chung NG, Yoo NJ, Lee SH: Analysis of NOTCH1 extracellular juxtamembrane expansion mutations in acute leukemias and multiple myelomas. APMIS; 2009 Feb;117(2):147-8
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  • [Title] Analysis of NOTCH1 extracellular juxtamembrane expansion mutations in acute leukemias and multiple myelomas.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Multiple Myeloma / genetics. Mutation. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Receptor, Notch1 / genetics

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  • (PMID = 19239437.001).
  • [ISSN] 1600-0463
  • [Journal-full-title] APMIS : acta pathologica, microbiologica, et immunologica Scandinavica
  • [ISO-abbreviation] APMIS
  • [Language] eng
  • [Publication-type] Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / NOTCH1 protein, human; 0 / Receptor, Notch1
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33. Nasedkina TV, Guseva NA, Gra OA, Mityaeva ON, Chudinov AV, Zasedatelev AS: Diagnostic microarrays in hematologic oncology: applications of high- and low-density arrays. Mol Diagn Ther; 2009;13(2):91-102
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  • Different applications of biochips in the field of hematologic oncology include analysis of chromosomal translocations in leukemias, diagnostics of T-cell lymphomas, and pharmacogenetics.
  • [MeSH-minor] Biomarkers, Tumor / analysis. Chromosome Aberrations. Gene Rearrangement. Genes, T-Cell Receptor gamma. Humans. Leukemia / diagnosis. Leukemia / genetics. Leukemia / metabolism. Polymorphism, Single Nucleotide

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  • (PMID = 19537844.001).
  • [ISSN] 1177-1062
  • [Journal-full-title] Molecular diagnosis & therapy
  • [ISO-abbreviation] Mol Diagn Ther
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] New Zealand
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Number-of-references] 102
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34. Karp JE, Ricklis RM, Balakrishnan K, Briel J, Greer J, Gore SD, Smith BD, McDevitt MA, Carraway H, Levis MJ, Gandhi V: A phase 1 clinical-laboratory study of clofarabine followed by cyclophosphamide for adults with refractory acute leukemias. Blood; 2007 Sep 15;110(6):1762-9
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  • [Title] A phase 1 clinical-laboratory study of clofarabine followed by cyclophosphamide for adults with refractory acute leukemias.
  • Clofarabine has shown impressive response rates in patients with acute leukemias.
  • Based on these clinical and laboratory observations, we designed a mechanism-based combination protocol with clofarabine and cyclophosphamide for patients with relapsed acute leukemias.
  • At dose level 1 (20 mg/m(2) clofarabine + cyclophosphamide, 6 patients) and dose level 0 (10 mg/m(2) clofarabine + cyclophosphamide, 12 patients) overall response rates were 50% and 30%, respectively, with responses in 4 (67%) of 6 patients with refractory acute lymphoblastic leukemia.

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  • (PMID = 17562873.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00293410
  • [Grant] United States / NCI NIH HHS / CA / R01 CA057629; United States / NCI NIH HHS / CA / CA57629
  • [Publication-type] Clinical Trial, Phase I; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adenine Nucleotides; 0 / Arabinonucleosides; 0 / H2AFX protein, human; 0 / Histones; 762RDY0Y2H / clofarabine; 8N3DW7272P / Cyclophosphamide
  • [Other-IDs] NLM/ PMC1976362
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35. Widlak P, Garrard WT: Roles of the major apoptotic nuclease-DNA fragmentation factor-in biology and disease. Cell Mol Life Sci; 2009 Jan;66(2):263-74
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  • [Title] Roles of the major apoptotic nuclease-DNA fragmentation factor-in biology and disease.
  • Here we review the recent literature that has uncovered new insight into DFF's regulation, and both its positive and negative roles in human disease.
  • Cells from mice deficient in DFF still undergo apoptotic death without significant cell-autonomous DNA degradation.
  • Negative aspects of DFF expression include contributing to susceptibility to acquire systemic lupus erythematosus, to chromosomal translocations that result in mixed lineage leukemias, and in the possible spreading of oncogenes and HIV due to horizontal gene transfer.
  • [MeSH-minor] Animals. Enzyme Activation. Gene Transfer, Horizontal. Genetic Predisposition to Disease. Humans. Leukemia, Myeloid, Acute / chemically induced. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / metabolism. Lupus Erythematosus, Systemic / genetics. Mutation. Neoplasms / genetics. Neoplasms / metabolism. Protein Subunits / chemistry. Protein Subunits / genetics. Protein Subunits / metabolism

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  • (PMID = 18810317.001).
  • [ISSN] 1420-9071
  • [Journal-full-title] Cellular and molecular life sciences : CMLS
  • [ISO-abbreviation] Cell. Mol. Life Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Protein Subunits; EC 3.1.- / Deoxyribonucleases; EC 3.1.- / caspase-activated deoxyribonuclease
  • [Number-of-references] 118
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36. Spinello I, Quaranta MT, Pasquini L, Pelosi E, Petrucci E, Pagliuca A, Castelli G, Mariani G, Diverio D, Foà R, Testa U, Labbaye C: PLZF-mediated control on c-kit expression in CD34(+) cells and early erythropoiesis. Oncogene; 2009 Jun 11;28(23):2276-88
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  • The promyelocytic leukemia zinc-finger protein (PLZF) is a transcription factor and c-kit is a receptor tyrosine kinase associated with human disease, particularly in hematopoietic cells.
  • The inverse correlation between PLZF and c-kit expression was found in normal CD34(+)38(+/-) hematopoietic progenitor/stem cells and in acute myeloid leukemias of M0/M1 French-American-British subtypes, suggesting that the control of PLZF on c-kit expression may be crucial at the level of the stem cell/progenitor compartment.
  • [MeSH-minor] Antigens, CD38 / metabolism. Blotting, Western. Cell Line. Cell Proliferation. Electrophoretic Mobility Shift Assay. Flow Cytometry. Fluorescent Antibody Technique. Gene Expression Regulation, Neoplastic. Humans. K562 Cells. Leukemia / genetics. Leukemia / metabolism. Leukemia / pathology. Luciferases / genetics. Luciferases / metabolism. MicroRNAs / genetics. MicroRNAs / metabolism. Microscopy, Phase-Contrast. RNA, Messenger / genetics. RNA, Messenger / metabolism. RNA, Small Interfering / genetics. Reverse Transcriptase Polymerase Chain Reaction. Transfection

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  • (PMID = 19421145.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Kruppel-Like Transcription Factors; 0 / MIRN221 microRNA, human; 0 / MIRN222 microRNA, human; 0 / MicroRNAs; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 147855-37-6 / ZBTB16 protein, human; EC 1.13.12.- / Luciferases; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit; EC 3.2.2.5 / Antigens, CD38
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37. Fragoso R, Pereira T, Wu Y, Zhu Z, Cabeçadas J, Dias S: VEGFR-1 (FLT-1) activation modulates acute lymphoblastic leukemia localization and survival within the bone marrow, determining the onset of extramedullary disease. Blood; 2006 Feb 15;107(4):1608-16
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  • [Title] VEGFR-1 (FLT-1) activation modulates acute lymphoblastic leukemia localization and survival within the bone marrow, determining the onset of extramedullary disease.
  • The presence of persistent circulating leukemia cells, or engrafted into extramedullary tissues, is a bad prognostic factor for patients with acute leukemia.
  • However, little is known about the mechanisms that regulate the exit of leukemia cells from the bone marrow (BM) microenvironment.
  • We reveal that vascular endothelial growth factor receptor 1 (FLT-1) modulates acute leukemia distribution within the BM, along VEGF and PlGF gradients, regulating leukemia survival and exit into the peripheral circulation.
  • FLT-1 activation on acute lymphoblastic leukemia (ALL) cells results in cell migration and proliferation in vitro, whereas in vivo FLT-1-overexpressing cells accumulate in the BM epiphysis of nonobese diabetic-severe combined immunodeficient (NOD-SCID) recipients and are detected in circulation 2 weeks after inoculation.
  • In turn, FLT-1 neutralization affects leukemia localization (now in the BM diaphysis), increases leukemia apoptosis, and impedes the exit of ALL cells, prolonging the survival of inoculated mice.
  • We demonstrate further that FLT-1-induced cell migration involves actin polymerization and lipid raft formation.
  • FLT-1 targeting on subsets of acute leukemias may delay the onset of extramedullary disease, which may be advantageous in combinatorial therapeutic settings.
  • [MeSH-major] Bone Marrow / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology. Vascular Endothelial Growth Factor Receptor-1 / genetics

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  • [ErratumIn] Blood. 2006 Apr 15;107(8):3057
  • (PMID = 16249383.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Complementary; EC 2.7.10.1 / FLT1 protein, human; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-1
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38. Ekiz HA, Baran Y: Therapeutic applications of bioactive sphingolipids in hematological malignancies. Int J Cancer; 2010 Oct 1;127(7):1497-506
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  • Sphingolipids are sphingosine-based lipid molecules that have important functions in cellular signal transduction and in a variety of cellular processes including proliferation, differentiation, programmed cell death (apoptosis) and responses to stressful conditions.
  • They have a major impact on determination of the cell fate by contributing to the cell survival or cell death through apoptosis.
  • Despite the number of carbon atoms in the fatty acid chain changes the physiological role; ceramides generally exert suppressive roles on the cell proliferation.
  • As they have significant impacts particularly on the cell death and survival, bioactive sphingolipids have a great potential to be targets in cancer therapy.
  • This review compiles the current knowledge in this area for enlightening the therapeutic potentials of bioactive sphingolipids in various leukemias.
  • [MeSH-minor] Cell Death / drug effects. Cell Survival / drug effects. Ceramides / physiology. Ceramides / therapeutic use. Homeostasis. Humans. Sphingosine / physiology

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  • (PMID = 20503271.001).
  • [ISSN] 1097-0215
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Ceramides; 0 / Sphingolipids; NGZ37HRE42 / Sphingosine
  • [Number-of-references] 136
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39. Faber J, Krivtsov AV, Stubbs MC, Wright R, Davis TN, van den Heuvel-Eibrink M, Zwaan CM, Kung AL, Armstrong SA: HOXA9 is required for survival in human MLL-rearranged acute leukemias. Blood; 2009 Mar 12;113(11):2375-85
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  • [Title] HOXA9 is required for survival in human MLL-rearranged acute leukemias.
  • Leukemias that harbor translocations involving the mixed lineage leukemia gene (MLL) possess unique biologic characteristics and often have an unfavorable prognosis.
  • Gene expression analyses demonstrate a distinct profile for MLL-rearranged leukemias with consistent high-level expression of select Homeobox genes, including HOXA9.
  • Here, we investigated the effects of HOXA9 suppression in MLL-rearranged and MLL-germline leukemias using RNA interference.
  • Gene expression profiling after HOXA9 suppression demonstrated co-down-regulation of a program highly expressed in human MLL-AML and murine MLL-leukemia stem cells, including HOXA10, MEIS1, PBX3, and MEF2C.
  • We demonstrate that HOXA9 depletion in 17 human AML/ALL cell lines (7 MLL-rearranged, 10 MLL-germline) induces proliferation arrest and apoptosis specifically in MLL-rearranged cells (P = .007).
  • Moreover, mice transplanted with HOXA9-depleted t(4;11) SEMK2 cells revealed a significantly lower leukemia burden, thus identifying a role for HOXA9 in leukemia survival in vivo.
  • Our data indicate an important role for HOXA9 in human MLL-rearranged leukemias and suggest that targeting HOXA9 or downstream programs may be a novel therapeutic option.

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  • (PMID = 19056693.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA066996; United States / NCI NIH HHS / CA / P01 CA66996
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / Homeodomain Proteins; 0 / MLL protein, human; 0 / Nuclear Proteins; 0 / RNA, Small Interfering; 0 / homeobox protein HOXA9; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; 150826-18-9 / AFF1 protein, human; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
  • [Other-IDs] NLM/ PMC2656267
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40. Lee SH, Jeong EG, Yoo NJ, Lee SH: Mutational analysis of NOTCH1, 2, 3 and 4 genes in common solid cancers and acute leukemias. APMIS; 2007 Dec;115(12):1357-63
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  • [Title] Mutational analysis of NOTCH1, 2, 3 and 4 genes in common solid cancers and acute leukemias.
  • Recent studies reported a high incidence of gain-of-function mutations of the NOTCH1 gene in T-cell acute lymphoblastic leukemias (ALL).
  • To see whether NOTCH1 mutation occurs in other malignancies, we analyzed NOTCH1 for the detection of somatic mutations in 334 malignancies, including 48 lung, 48 breast, 48 colorectal and 48 gastric carcinomas, and 142 acute leukemias (105 acute myelogenous leukemias, 32 B-ALLs and 4 T-ALLs) by single-strand conformation polymorphism assay.
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. DNA Mutational Analysis. DNA Primers. Humans. Middle Aged. Mutation. Polymerase Chain Reaction. Polymorphism, Single-Stranded Conformational. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 18184405.001).
  • [ISSN] 0903-4641
  • [Journal-full-title] APMIS : acta pathologica, microbiologica, et immunologica Scandinavica
  • [ISO-abbreviation] APMIS
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / DNA Primers; 0 / NOTCH2 protein, human; 0 / NOTCH3 protein, human; 0 / NOTCH4 protein, human; 0 / Proto-Oncogene Proteins; 0 / Receptor, Notch1; 0 / Receptor, Notch2; 0 / Receptors, Notch
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41. Chiaretti S, Ritz J, Foa R: Genomic analysis in lymphoid leukemias. Rev Clin Exp Hematol; 2005 Jun;9(1):E3
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  • [Title] Genomic analysis in lymphoid leukemias.
  • Important biological insights have been revealed by this technique in several tumors: in acute lymphoblastic leukemia (ALL), these studies have allowed to identify specific patterns associated with known molecular abnormalities, as well as with phenotypic characteristics and with different prognostic features.
  • In chronic lymphocytic leukemia (CLL), this approach has helped to dissect that this disease is a single entity with distinct variants that are characterized by a diverse IgVH mutational status, that can be discriminated by a small set of genes, has allowed to define a similarity between this disease and memory B cells and has also led to hypothesize that CLL cells from IgVH unmutated patients may be continuously stimulated in vivo, thus showing a gene profile that is reminiscent of the B cell receptor.
  • In multiple myeloma (MM), gene expression profiles has provided insights into the disease and has offered the opportunity of stratifying patients according to the degree of aggressiveness of the disease.
  • [MeSH-major] Genomics / methods. Leukemia, Lymphoid / genetics

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  • (PMID = 16027105.001).
  • [ISSN] 1825-151X
  • [Journal-full-title] Reviews in clinical and experimental hematology
  • [ISO-abbreviation] Rev Clin Exp Hematol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Italy
  • [Number-of-references] 140
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42. Went PT, Zimpfer A, Pehrs AC, Sabattini E, Pileri SA, Maurer R, Terracciano L, Tzankov A, Sauter G, Dirnhofer S: High specificity of combined TRAP and DBA.44 expression for hairy cell leukemia. Am J Surg Pathol; 2005 Apr;29(4):474-8
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  • [Title] High specificity of combined TRAP and DBA.44 expression for hairy cell leukemia.
  • Because of marrow fibrosis, bone marrow aspirations are often nonconclusive in patients with hairy cell leukemia (HCL).
  • DBA.44 reactivity was especially frequent in follicular lymphomas (46%), whereas tartrate-resistant acid phosphatase (TRAP) expression was often seen in mantle cell lymphomas (57%), primary mediastinal large B-cell lymphomas (54%), and chronic lymphocytic leukemia/small lymphocytic lymphoma (41%).
  • A combined DBA.44/TRAP positivity was seen in only 3% of non-HCL non-Hodgkin lymphomas, including cases of diffuse large B-cell lymphomas, follicular lymphomas, chronic lymphatic leukemia/small lymphocytic leukemias, and mantle cell lymphomas.
  • [MeSH-major] Acid Phosphatase / metabolism. Antibodies, Monoclonal / metabolism. Isoenzymes / metabolism. Leukemia, Hairy Cell / metabolism. Lymphoma, Non-Hodgkin / metabolism

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  • (PMID = 15767800.001).
  • [ISSN] 0147-5185
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Validation Studies
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Isoenzymes; EC 3.1.3.- / tartrate-resistant acid phosphatase; EC 3.1.3.2 / Acid Phosphatase
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43. Gefen N, Binder V, Zaliova M, Linka Y, Morrow M, Novosel A, Edry L, Hertzberg L, Shomron N, Williams O, Trka J, Borkhardt A, Izraeli S: Hsa-mir-125b-2 is highly expressed in childhood ETV6/RUNX1 (TEL/AML1) leukemias and confers survival advantage to growth inhibitory signals independent of p53. Leukemia; 2010 Jan;24(1):89-96
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  • [Title] Hsa-mir-125b-2 is highly expressed in childhood ETV6/RUNX1 (TEL/AML1) leukemias and confers survival advantage to growth inhibitory signals independent of p53.
  • The levels of chr 21 miRNAs were quantified by qRT-PCR in four types of childhood acute lymphoblastic leukemia (ALL) characterized by either numerical (trisomy or tetrasomy) or structural abnormalities of chr 21.
  • Suprisingly, high expression of the hsa-mir-125b-2 cluster, consisting of three miRNAs, was identified in leukemias with the structural ETV6/RUNX1 abnormality and not in ALLs with trisomy 21.
  • Conversely, knockdown of the endogenous miR-125b in the ETV6/RUNX1 leukemia cell line REH increased apoptosis after Doxorubicin and Staurosporine treatments.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / physiology. MicroRNAs / analysis. Oncogene Proteins, Fusion / physiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / mortality. Tumor Suppressor Protein p53 / physiology

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  • (PMID = 19890372.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA120772; United States / NCI NIH HHS / CA / R01 CA120772-03
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CDKN1A protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Interleukin-3; 0 / MIRN125 microRNA, human; 0 / MicroRNAs; 0 / Oncogene Proteins, Fusion; 0 / TEL-AML1 fusion protein; 0 / Tumor Suppressor Protein p53
  • [Other-IDs] NLM/ NIHMS158685; NLM/ PMC2811577
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44. Ratei R, Karawajew L, Schabath R, Ehrfeldt A, Grunert F, Ludwig WD: Differential expression of the carcinoembryonic antigen-related cell adhesion molecules panCD66, CD66a, CD66c and of sialyl-Lewis x (CD15s) on blast cells of acute leukemias. Int J Hematol; 2008 Mar;87(2):137-43
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  • [Title] Differential expression of the carcinoembryonic antigen-related cell adhesion molecules panCD66, CD66a, CD66c and of sialyl-Lewis x (CD15s) on blast cells of acute leukemias.
  • Expression of CD66 has been reported to occur on blast cells from children with acute lymphoblastic leukemia (ALL), but little is known about the differential expression pattern of panCD66 and other members of the CD66 family on blast cells from patients with acute myeloid leukemia (AML).
  • We have performed flow cytometry immunophenotyping on blast cells from 28 patients with acute myeloid leukemia (AML), 13 patients with B-cell precursor acute lymphoblastic leukemia (BCP-ALL) and 7 patients with T-ALL using monoclonal antibodies (mAbs) against panCD66 (clone D14HD11), CD66a (clone 4.3.17), CD66c (clone 9A6) and CD15s.
  • Radioimmunotherapeutic strategies targeting CD66 antigens should consider the heterogeneous expression pattern of CD66 molecules in acute leukemias especially in AML where expression is correlated with mature granulomonocytic cells but not with CD34 and CD117 positive progenitor cells.
  • [MeSH-major] Antigens, CD / metabolism. Cell Adhesion Molecules / metabolism. Leukemia, Myeloid, Acute / metabolism. Oligosaccharides / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism

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  • (PMID = 18299959.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / 5-acetylneuraminyl-(2-3)-galactosyl-(1-4)-(fucopyranosyl-(1-3))-N-acetylglucosamine; 0 / Antigens, CD; 0 / CD66 antigens; 0 / CEACAM6 protein, human; 0 / Cell Adhesion Molecules; 0 / GPI-Linked Proteins; 0 / Oligosaccharides
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45. Boyd KE, Xiao YY, Fan K, Poholek A, Copeland NG, Jenkins NA, Perkins AS: Sox4 cooperates with Evi1 in AKXD-23 myeloid tumors via transactivation of proviral LTR. Blood; 2006 Jan 15;107(2):733-41
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  • Myeloid leukemias in AKXD23 mice contain proviral insertions at Evi1, resulting in transcriptional activation.
  • Although Evi1 is clearly involved in leukemia, gene transfer studies in mice with Evi1 fail to cause leukemia, arguing that cooperating events are necessary.

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  • (PMID = 16204320.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / 1F32CA88467-01; United States / NCI NIH HHS / CA / R01 CA81216
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Cytokines; 0 / DNA-Binding Proteins; 0 / Evi1 protein, mouse; 0 / High Mobility Group Proteins; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 0 / SOXC Transcription Factors; 0 / Sox4 protein, mouse; 0 / Trans-Activators; 0 / Transcription Factors
  • [Other-IDs] NLM/ PMC1895620
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46. Lau A, Belanger CL, Winn LM: In utero and acute exposure to benzene: investigation of DNA double-strand breaks and DNA recombination in mice. Mutat Res; 2009 May 31;676(1-2):74-82
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  • Benzene, a ubiquitous pollutant, has been identified as a human leukemogen and early exposure to environmental carcinogens such as benzene has been linked to childhood leukemia.
  • These results demonstrate that in utero exposure increases the frequency of micronuclei and DNA recombination events in hematopoietic tissue of fetal and post-natal mice and may be an initiating event in the etiology of childhood leukemias.
  • Further investigations into different types of DNA damage and repair pathways are warranted to fully elucidate the role of genotoxic mechanisms in the etiology of benzene-induced childhood leukemias.
  • [MeSH-minor] Animals. Bone Marrow / drug effects. Bone Marrow / metabolism. Bone Marrow Cells / drug effects. Cell Nucleus / drug effects. DNA Damage / drug effects. Dose-Response Relationship, Drug. Female. Male. Mice. Mice, Inbred C57BL. Micronuclei, Chromosome-Defective / chemically induced. Mutagenicity Tests. Pregnancy

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  • (PMID = 19486867.001).
  • [ISSN] 0027-5107
  • [Journal-full-title] Mutation research
  • [ISO-abbreviation] Mutat. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Mutagens; 9007-49-2 / DNA; J64922108F / Benzene
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47. Si J, Mueller L, Collins SJ: CaMKII regulates retinoic acid receptor transcriptional activity and the differentiation of myeloid leukemia cells. J Clin Invest; 2007 May;117(5):1412-21
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  • [Title] CaMKII regulates retinoic acid receptor transcriptional activity and the differentiation of myeloid leukemia cells.
  • Retinoic acid receptors (RARs) are members of the nuclear hormone receptor family and regulate the proliferation and differentiation of multiple different cell types, including promyelocytic leukemia cells.
  • Here we describe a biochemical/functional interaction between the Ca(2+)/calmodulin-dependent protein kinases (CaMKs) and RARs that modulates the differentiation of myeloid leukemia cells.
  • In myeloid cell lines, CaMKIIgamma localizes to RAR target sites within myeloid gene promoters but dissociates from the promoter upon retinoic acid-induced myeloid cell differentiation.
  • KN62, a pharmacological inhibitor of the CaMKs, enhances the terminal differentiation of myeloid leukemia cell lines, and this is associated with a reduction in activated (autophosphorylated) CaMKII in the terminally differentiating cells.
  • These observations reveal a significant cross-talk between Ca(2+) and retinoic acid signaling pathways that regulates the differentiation of myeloid leukemia cells, and they suggest that CaMKIIgamma may provide a new therapeutic target for the treatment of certain human myeloid leukemias.

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  • (PMID = 17431504.001).
  • [ISSN] 0021-9738
  • [Journal-full-title] The Journal of clinical investigation
  • [ISO-abbreviation] J. Clin. Invest.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / P50 HL054881; United States / NCI NIH HHS / CA / R01 CA118971; United States / NHLBI NIH HHS / HL / HL 54881; United States / NCI NIH HHS / CA / R01 CA 118971
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptors, Retinoic Acid; 5688UTC01R / Tretinoin; EC 2.7.11.17 / Calcium-Calmodulin-Dependent Protein Kinase Type 2; EC 2.7.11.17 / Calcium-Calmodulin-Dependent Protein Kinases
  • [Other-IDs] NLM/ PMC1847537
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48. Messmer BT, Messmer D, Allen SL, Kolitz JE, Kudalkar P, Cesar D, Murphy EJ, Koduru P, Ferrarini M, Zupo S, Cutrona G, Damle RN, Wasil T, Rai KR, Hellerstein MK, Chiorazzi N: In vivo measurements document the dynamic cellular kinetics of chronic lymphocytic leukemia B cells. J Clin Invest; 2005 Mar;115(3):755-64
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  • [Title] In vivo measurements document the dynamic cellular kinetics of chronic lymphocytic leukemia B cells.
  • Due to its relatively slow clinical progression, B cell chronic lymphocytic leukemia (B-CLL) is classically described as a disease of accumulation rather than proliferation.
  • We used a nonradioactive, stable isotopic labeling method to measure B-CLL cell kinetics in vivo.
  • Those patients with birth rates greater than 0.35% per day were much more likely to exhibit active or to develop progressive disease than those with lower birth rates Thus, B-CLL is not a static disease that results simply from accumulation of long-lived lymphocytes.
  • A correlation between birth rates and disease activity and progression appears to exist, which may help identify patients at risk for worsening disease in advance of clinical deterioration.

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  • (PMID = 15711642.001).
  • [ISSN] 0021-9738
  • [Journal-full-title] The Journal of clinical investigation
  • [ISO-abbreviation] J. Clin. Invest.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA087956; United States / NCI NIH HHS / CA / R01 CA81554; United States / NCRR NIH HHS / RR / M01 RR018535; United States / NCI NIH HHS / CA / R01 CA081554; United States / NCI NIH HHS / CA / R01 CA87956
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 059QF0KO0R / Water; 9007-49-2 / DNA; AR09D82C7G / Deuterium
  • [Other-IDs] NLM/ PMC548318
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49. Rubnitz JE, Gibson B, Smith FO: Acute myeloid leukemia. Pediatr Clin North Am; 2008 Feb;55(1):21-51, ix
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  • [Title] Acute myeloid leukemia.
  • Acute myeloid leukemia (AML) is a heterogeneous group of leukemias that result from clonal transformation of hematopoietic precursors through the acquisition of chromosomal rearrangements and multiple gene mutations.
  • As a result of highly collaborative clinical research by pediatric cooperative cancer groups worldwide, disease-free survival has improved significantly during the past 3 decades.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid, Acute / therapy. Stem Cell Transplantation

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  • (PMID = 18242314.001).
  • [ISSN] 0031-3955
  • [Journal-full-title] Pediatric clinics of North America
  • [ISO-abbreviation] Pediatr. Clin. North Am.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anthracyclines; 04079A1RDZ / Cytarabine
  • [Number-of-references] 229
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50. Ostrowska H, Hempel D, Holub M, Sokolowski J, Kloczko J: Assessment of circulating proteasome chymotrypsin-like activity in plasma of patients with acute and chronic leukemias. Clin Biochem; 2008 Nov;41(16-17):1377-83
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  • [Title] Assessment of circulating proteasome chymotrypsin-like activity in plasma of patients with acute and chronic leukemias.
  • OBJECTIVE: We evaluated whether the proteasomal chymotrypsin-like (ChT-L) activity is increased in plasma of patients with acute lymphoblastic (ALL), acute myeloblastic (AML) and chronic lymphocytic (CLL) leukemias.
  • CONCLUSIONS: Plasma proteasome ChT-L activity can be a useful bio-marker for patients with acute leukemia at the blast stage.
  • [MeSH-major] Chymotrypsin / blood. Leukemia / blood. Proteasome Endopeptidase Complex / blood
  • [MeSH-minor] Adolescent. Adult. Aged. Case-Control Studies. Female. Humans. Hydrolysis / drug effects. L-Lactate Dehydrogenase / blood. Leukemia, Lymphocytic, Chronic, B-Cell / blood. Leukemia, Lymphocytic, Chronic, B-Cell / diagnosis. Leukemia, Myeloid, Acute / blood. Leukemia, Myeloid, Acute / diagnosis. Male. Middle Aged. Oligopeptides / pharmacology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / blood. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Proteasome Inhibitors. Protein Subunits / metabolism. Sodium Dodecyl Sulfate / pharmacology

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  • (PMID = 18773885.001).
  • [ISSN] 1873-2933
  • [Journal-full-title] Clinical biochemistry
  • [ISO-abbreviation] Clin. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Oligopeptides; 0 / Proteasome Inhibitors; 0 / Protein Subunits; 134381-21-8 / epoxomicin; 368GB5141J / Sodium Dodecyl Sulfate; EC 1.1.1.27 / L-Lactate Dehydrogenase; EC 3.4.21.1 / Chymotrypsin; EC 3.4.25.1 / Proteasome Endopeptidase Complex
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51. de Lima M, Champlin RE, Thall PF, Wang X, Martin TG 3rd, Cook JD, McCormick G, Qazilbash M, Kebriaei P, Couriel D, Shpall EJ, Khouri I, Anderlini P, Hosing C, Chan KW, Andersson BS, Patah PA, Caldera Z, Jabbour E, Giralt S: Phase I/II study of gemtuzumab ozogamicin added to fludarabine, melphalan and allogeneic hematopoietic stem cell transplantation for high-risk CD33 positive myeloid leukemias and myelodysplastic syndrome. Leukemia; 2008 Feb;22(2):258-64
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  • [Title] Phase I/II study of gemtuzumab ozogamicin added to fludarabine, melphalan and allogeneic hematopoietic stem cell transplantation for high-risk CD33 positive myeloid leukemias and myelodysplastic syndrome.
  • We investigated the hypothesis that gemtuzumab ozogamicin (GO), an anti-CD33 immunotoxin would improve the efficacy of fludarabine/melphalan as a preparative regimen for allogeneic hematopoietic stem cell transplantation (HSCT) in a phase I/II trial.
  • GO dose was de-escalated to 2 mg m(-2): 18% had toxicity (n=8) and 82% responded (n=36).
  • [MeSH-major] Aminoglycosides / administration & dosage. Antibodies, Monoclonal / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Hematopoietic Stem Cell Transplantation / methods. Leukemia, Myeloid / therapy. Myelodysplastic Syndromes / therapy
  • [MeSH-minor] Adolescent. Adult. Aged. Antibodies, Monoclonal, Humanized. Antigens, CD. Antigens, Differentiation, Myelomonocytic. Disease-Free Survival. Female. Graft Survival. Humans. Male. Melphalan / administration & dosage. Middle Aged. Remission Induction. Sialic Acid Binding Ig-like Lectin 3. Survival Rate. Transplantation, Homologous. Vidarabine / administration & dosage. Vidarabine / analogs & derivatives

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  • (PMID = 17989720.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase I; Clinical Trial, Phase II; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Aminoglycosides; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD33 protein, human; 0 / Sialic Acid Binding Ig-like Lectin 3; 0 / gemtuzumab; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine; Q41OR9510P / Melphalan
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52. Ross DD, Nakanishi T: Impact of breast cancer resistance protein on cancer treatment outcomes. Methods Mol Biol; 2010;596:251-90
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  • This chapter presents a synopsis of translational clinical studies relating BCRP expression in leukemias, lymphomas, and a variety of solid tumors with clinical outcome.
  • Whether this adverse prognostic effect results from resistance imparted to the cancer cells as the direct result of BCRP efflux of anticancer drugs, or whether BCRP expression (and also Pgp expression - coexpression of these transporters is common among poor risk cancers) serves as indicators of the activity of signaling pathways that enhance cancer cellular proliferation, metastases, genomic instability, enhance drug resistance, and oppose programmed cell death mechanisms is yet unknown.
  • [MeSH-minor] ATP Binding Cassette Transporter, Sub-Family G, Member 2. Animals. Antineoplastic Agents / metabolism. Antineoplastic Agents / therapeutic use. Cell Line, Tumor. Genetic Predisposition to Disease. Humans. Mutation. Neoplastic Stem Cells / metabolism. Polymorphism, Genetic. Treatment Outcome. Xenobiotics / metabolism

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  • (PMID = 19949928.001).
  • [ISSN] 1940-6029
  • [Journal-full-title] Methods in molecular biology (Clifton, N.J.)
  • [ISO-abbreviation] Methods Mol. Biol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ABCG2 protein, human; 0 / ATP Binding Cassette Transporter, Sub-Family G, Member 2; 0 / ATP-Binding Cassette Transporters; 0 / Antineoplastic Agents; 0 / Neoplasm Proteins; 0 / Xenobiotics
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53. Schüz J, Jacobsen R, Olsen JH, Boice JD Jr, McLaughlin JK, Johansen C: Cellular telephone use and cancer risk: update of a nationwide Danish cohort. J Natl Cancer Inst; 2006 Dec 6;98(23):1707-13
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  • Cellular telephone use was not associated with increased risk for brain tumors (SIR = 0.97), acoustic neuromas (SIR = 0.73), salivary gland tumors (SIR = 0.77), eye tumors (SIR = 0.96), or leukemias (SIR = 1.00).
  • [MeSH-major] Cell Phones. Neoplasms / epidemiology


54. Bullinger L, Rücker FG, Kurz S, Du J, Scholl C, Sander S, Corbacioglu A, Lottaz C, Krauter J, Fröhling S, Ganser A, Schlenk RF, Döhner K, Pollack JR, Döhner H: Gene-expression profiling identifies distinct subclasses of core binding factor acute myeloid leukemia. Blood; 2007 Aug 15;110(4):1291-300
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  • [Title] Gene-expression profiling identifies distinct subclasses of core binding factor acute myeloid leukemia.
  • Core binding factor (CBF) leukemias, characterized by either inv(16)/t(16;16) or t(8;21), constitute acute myeloid leukemia (AML) subgroups with favorable prognosis.
  • To improve the molecular characterization we profiled gene expression in a large series (n = 93) of AML patients with CBF leukemia [(inv (16), n = 55; t(8;21), n = 38)].
  • While there was no obvious correlation with fusion gene transcript levels, FLT3 tyrosine kinase domain, KIT, and NRAS mutations, the newly defined inv(16)/t(8;21) subgroup was associated with elevated white blood cell counts and FLT3 internal tandem duplications (P = .011 and P = .026, respectively).
  • In the "favorable" CBF leukemias, antiapoptotic mechanisms and deregulated mTOR signaling and, in the newly defined "unfavorable" subgroup, aberrant MAPK signaling and chemotherapy-resistance mechanisms might play a role.
  • While the leukemogenic relevance of these signatures remains to be validated, their existence nevertheless supports a prognostically relevant biologic basis for the heterogeneity observed in CBF leukemia.
  • [MeSH-major] Biomarkers, Tumor / genetics. Core Binding Factors / genetics. Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Leukemia, Myeloid, Acute / genetics. Mutation / genetics


55. Passegué E, Weisman IL: Leukemic stem cells: where do they come from? Stem Cell Rev; 2005;1(3):181-8
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  • Leukemias can now be viewed as aberrant hematopoietic processes initiated by rare cancer stem cells, or leukemic stem cells (LSCs) that have maintained or reacquired the capacity for indefinite proliferation through accumulated mutations and/or epigenetic changes.
  • Yet, despite their critical importance, much remains to be learned about the developmental origin of LSCs and the mechanisms responsible for their emergence in the course of the disease.
  • Mouse models of human leukemias have provided a unique system to study the mechanisms influencing LSC generation and function, and were recently used to demonstrate that LSCs can arise from both self-renewing hematopoietic stem cells (HSCs) and committed progenitor populations.
  • This striking finding indicates that LSC identity is largely dictated by the nature of the oncogenic events and by how these events perturb essential processes such as self-renewal, proliferation, differentiation, and survival.
  • Such approaches in the mouse are essential for the basic understanding of leukemogenesis and for the conceptual design of novel therapeutic strategies that could lead to improved treatments for human leukemias.
  • [MeSH-major] Cell Differentiation. Cell Proliferation. Hematopoiesis. Hematopoietic Stem Cells / metabolism. Leukemia / metabolism. Neoplastic Stem Cells / metabolism
  • [MeSH-minor] Animals. Cell Survival. Disease Models, Animal. Humans. Mice

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  • (PMID = 17142854.001).
  • [ISSN] 1550-8943
  • [Journal-full-title] Stem cell reviews
  • [ISO-abbreviation] Stem Cell Rev
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA86017
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 65
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56. Sadananda Adiga MN, Chandy S, Ramachandra N, Appaji L, Aruna Kumari BS, Ramaswamy G, Savithri HS, Krishnamoorthy L: Methylenetetrahydrofolate reductase gene polymorphisms and risk of acute lymphoblastic leukemia in children. Indian J Cancer; 2010 Jan-Mar;47(1):40-5
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  • [Title] Methylenetetrahydrofolate reductase gene polymorphisms and risk of acute lymphoblastic leukemia in children.
  • Leukemias are malignancies arising from rapidly proliferating hematopoietic cells having great requirement of DNA synthesis.
  • This case-control study was undertaken to analyze the association of the MTHFR gene polymorphisms 677 C"T and 1298 A"C and the risk of acute lymphoblastic leukemia in children.
  • MATERIALS AND METHODS: Eighty-six patients aged below 15 years with a confirmed diagnosis of acute lymphoblastic leukemia (ALL) and 99 matched controls were taken for this study.
  • [MeSH-major] Genetic Predisposition to Disease. Methylenetetrahydrofolate Reductase (NADPH2) / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 20071789.001).
  • [ISSN] 1998-4774
  • [Journal-full-title] Indian journal of cancer
  • [ISO-abbreviation] Indian J Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
  • [Chemical-registry-number] EC 1.5.1.20 / Methylenetetrahydrofolate Reductase (NADPH2)
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57. Bug G, Ottmann OG: The DAC system and associations with acute leukemias and myelodysplastic syndromes. Invest New Drugs; 2010 Dec;28 Suppl 1:S36-49
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  • [Title] The DAC system and associations with acute leukemias and myelodysplastic syndromes.
  • Imbalances of histone acetyltransferase (HAT) and deacetylase activity (DAC) that result in deregulated gene expression are commonly observed in leukemias.
  • While DACi have shown clear evidence of activity in acute myeloid leukemia, myelodysplastic syndromes and lymphoid malignancies, their precise role in treatment of these different entities remain to be elucidated.
  • Successful development of these compounds as elements of novel targeted treatment strategies for leukemia will require that clinical studies be performed in conjunction with translational research including efforts to identify predictive biomarkers.
  • [MeSH-major] Histone Deacetylases / metabolism. Leukemia, Myeloid, Acute / enzymology. Myelodysplastic Syndromes / enzymology

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  • (PMID = 21153858.001).
  • [ISSN] 1573-0646
  • [Journal-full-title] Investigational new drugs
  • [ISO-abbreviation] Invest New Drugs
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Histone Deacetylase Inhibitors; 5688UTC01R / Tretinoin; EC 3.5.1.98 / Histone Deacetylases
  • [Other-IDs] NLM/ PMC3003828
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58. Tang X, Long C, Wang C, Xiao G: [Expression of DLK1 gene in acute leukemias and its function in erythroid differentiation of K562 cell line]. Zhong Nan Da Xue Xue Bao Yi Xue Ban; 2009 Sep;34(9):886-91
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  • [Title] [Expression of DLK1 gene in acute leukemias and its function in erythroid differentiation of K562 cell line].
  • OBJECTIVE: To determine the expression of DLK1 gene in acute leukemias (AL) and its function in erythroid differentiation of K562 cells.
  • METHODS: We detected the expression of DLK1 gene in 65 different acute leukemia categories (a test group) and 34 normal bone marrow controls (a control group) with RT-PCR.
  • The K562 cell line was induced to erythroid differentiation by hemin.
  • RESULTS: Both leukemia cells and normal marrow cells expressed DLK1.
  • The expression of DLK1 mRNA in patients in the test group was higher than that in the control group (P=0.018), while there was no significance between acute lymphoblastic leukemia and acute myelogenous leukemia (P>0.05).The expression of DLK1 mRNA in the test group at onset had no relation with the WBC and platelet count in the total peripheral blood, and the same was true for blast cell rates in bone marrow cells.The level of DLK1 protein in the test group was higher than that in the control group, which was consistent with the mRNA expression (P=0.042).
  • CONCLUSION: DLK1 gene may be involved in leukemia,but the mRNA level of DLK1 has no relation with some clinical characteristics of AL patients at onset.
  • [MeSH-major] Cell Differentiation / genetics. Cell Transformation, Neoplastic / genetics. Erythroid Cells / pathology. Intercellular Signaling Peptides and Proteins / metabolism. Leukemia / genetics. Membrane Proteins / metabolism
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Case-Control Studies. Child. Child, Preschool. Erythroid Precursor Cells / pathology. Female. Humans. K562 Cells. Male. Middle Aged. RNA, Messenger / genetics. RNA, Messenger / metabolism. Young Adult

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  • (PMID = 19779261.001).
  • [ISSN] 1672-7347
  • [Journal-full-title] Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences
  • [ISO-abbreviation] Zhong Nan Da Xue Xue Bao Yi Xue Ban
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / DLK1 protein, human; 0 / Intercellular Signaling Peptides and Proteins; 0 / Membrane Proteins; 0 / RNA, Messenger
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59. Mobasheri MB, Modarressi MH, Shabani M, Asgarian H, Sharifian RA, Vossough P, Shokri F: Expression of the testis-specific gene, TSGA10, in Iranian patients with acute lymphoblastic leukemia (ALL). Leuk Res; 2006 Jul;30(7):883-9
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  • [Title] Expression of the testis-specific gene, TSGA10, in Iranian patients with acute lymphoblastic leukemia (ALL).
  • Testis-specific gene antigen (TSGA10) is expressed in fetus, testis and frequently in human solid cancers and acute leukemias, making it a candidate for immunotherapy and for detection of minimal residual disease (MRD).
  • There is also evidence for potential TSGA10 involvement in cell proliferation.
  • Here we demonstrated expression of TSGA10 by semi-quantitative RT-PCR in 44 (84.6%) out of 52 bone marrow samples and all peripheral blood samples from patients with acute lymphoblastic leukemia (ALL).
  • Presence of TSGA10 expression in ALL may open a window to functional study of mitotic checkpoint proteins in leukemia.
  • RT-PCR of TSGA10 may help in detection of residual clonal cells leading to early diagnosis and better prognostic qualification of the disease.
  • [MeSH-major] Gene Expression Regulation, Leukemic / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Proteins / genetics

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  • (PMID = 16406020.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Databank-accession-numbers] GENBANK/ AI696619/ AW057728/ AW591313/ BE047007/ BF243403
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Proteins; 0 / TSGA10 protein, human
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60. Guerrouahen BS, Futami M, Vaklavas C, Kanerva J, Whichard ZL, Nwawka K, Blanchard EG, Lee FY, Robinson LJ, Arceci R, Kornblau SM, Wieder E, Cayre YE, Corey SJ: Dasatinib inhibits the growth of molecularly heterogeneous myeloid leukemias. Clin Cancer Res; 2010 Feb 15;16(4):1149-58
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  • [Title] Dasatinib inhibits the growth of molecularly heterogeneous myeloid leukemias.
  • PURPOSE: Dasatinib is a dual Src/Abl inhibitor recently approved for Bcr-Abl+ leukemias with resistance or intolerance to prior therapy.
  • Because Src kinases contribute to multiple blood cell functions by triggering a variety of signaling pathways, we hypothesized that their molecular targeting might lead to growth inhibition in acute myeloid leukemia (AML).
  • EXPERIMENTAL DESIGN: We studied growth factor-dependent and growth factor-independent leukemic cell lines, including three cell lines expressing mutants of receptor tyrosine kinases (Flt3 or c-Kit) as well as primary AML blasts for responsiveness to dasatinib.
  • RESULTS: Dasatinib resulted in the inhibition of Src family kinases in all cell lines and blast cells at approximately 1 x 10(-9) mol/L.
  • Cell lines that showed growth inhibition at approximately 1 x 10(-6) mol/L showed a G(1) cell cycle arrest and correlated with accumulation of p21 and p27 protein.

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  • (PMID = 20145167.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA108922; United States / NHLBI NIH HHS / HL / K02 HL003794-06; United States / NCI NIH HHS / CA / R01 CA108922-04; United States / NCI NIH HHS / CA / R01-CA120535; United States / NCI NIH HHS / CA / R01-CA108922; United States / NCI NIH HHS / CA / CA108922-04; United States / NHLBI NIH HHS / HL / HL003794-06; United States / NCI NIH HHS / CA / R01 CA120535; United States / NHLBI NIH HHS / HL / K02 HL003794
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CDKN1A protein, human; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Pyrimidines; 0 / Thiazoles; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit; EC 2.7.10.2 / lyn protein-tyrosine kinase; EC 2.7.10.2 / src-Family Kinases; RBZ1571X5H / Dasatinib
  • [Other-IDs] NLM/ NIHMS163746; NLM/ PMC2988651
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61. Tamura K, Arai H, Ueno E, Saito C, Yagihara H, Isotani M, Ono K, Washizu T, Bonkobara M: Comparison of dendritic cell-mediated immune responses among canine malignant cells. J Vet Med Sci; 2007 Sep;69(9):925-30
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  • [Title] Comparison of dendritic cell-mediated immune responses among canine malignant cells.
  • Dendritic cell (DC) vaccination is one of the most attractive immunotherapies for malignancies in dogs.
  • To examine the differences in DC-mediated immune responses from different types of malignancies in dogs, we vaccinated dogs using autologous DCs pulsed with keyhole limpet hemocyanin (KLH) and cell lysate prepared from squamous cell carcinoma SCC2/88 (SCC-KLH-DC), histiocytic sarcoma CHS-5 (CHS-KLH-DC), or B cell leukemia GL-1 (GL-KLH-DC) in vitro.
  • By contrast, neither CD8 nor CD4 T cell infiltration was found at the DTH challenge site in the dogs vaccinated with CHS-KLH-DC or GL-KLH-DC.
  • These findings may reflect that the efficacy of immune induction by DC vaccination varies among tumor types and that immune responses could be inducible in squamous cell carcinoma.
  • Our results encouraged further investigation of therapeutic vaccination for dogs with advanced squamous cell carcinoma in clinical trials.

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  • (PMID = 17917377.001).
  • [ISSN] 0916-7250
  • [Journal-full-title] The Journal of veterinary medical science
  • [ISO-abbreviation] J. Vet. Med. Sci.
  • [Language] ENG
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Cancer Vaccines
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62. Fullmer A, O'Brien S, Kantarjian H, Jabbour E: Novel therapies for relapsed acute lymphoblastic leukemia. Curr Hematol Malig Rep; 2009 Jul;4(3):148-56
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  • [Title] Novel therapies for relapsed acute lymphoblastic leukemia.
  • The outcome of salvage therapy for relapsed acute lymphoblastic leukemia (ALL) remains poor.
  • Novel strategies under investigation as monotherapy or in combination with chemotherapy improve the treatment of relapsed disease.
  • Nelarabine demonstrates activity as monotherapy in T-cell ALL and is approved by the US Food and Drug Administration.
  • Clofarabine, a second-generation purine analogue approved in pediatric leukemia, has shown activity in adult acute leukemias including ALL and acute myeloid leukemia.
  • The benefit of matched related-donor allogeneic stem cell transplantation is significant for standard-risk ALL but not for high-risk ALL.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Hematopoietic Stem Cell Transplantation / methods. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy

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  • (PMID = 20425428.001).
  • [ISSN] 1558-822X
  • [Journal-full-title] Current hematologic malignancy reports
  • [ISO-abbreviation] Curr Hematol Malig Rep
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 50
  • [Other-IDs] NLM/ NIHMS674650; NLM/ PMC4572835
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63. Duran-Struuck R, Dysko RC: Principles of bone marrow transplantation (BMT): providing optimal veterinary and husbandry care to irradiated mice in BMT studies. J Am Assoc Lab Anim Sci; 2009 Jan;48(1):11-22
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  • Bone marrow transplantation (BMT) is the treatment of choice for many leukemias, solid tumors, and metabolic diseases.
  • We discuss the crucial role of the irradiator for BMT research and the importance of aseptic husbandry practices to lessen the possibility of the irradiator for being a source for disease transmission.

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  • (PMID = 19245745.001).
  • [ISSN] 1559-6109
  • [Journal-full-title] Journal of the American Association for Laboratory Animal Science : JAALAS
  • [ISO-abbreviation] J. Am. Assoc. Lab. Anim. Sci.
  • [Language] ENG
  • [Grant] United States / NCRR NIH HHS / RR / K01 RR024466; United States / NCRR NIH HHS / RR / T32 RR007008; United States / NCRR NIH HHS / RR / K01RR024466; United States / NCRR NIH HHS / RR / T32-RR07008
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] United States
  • [Number-of-references] 112
  • [Other-IDs] NLM/ PMC2694700
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64. Choi J, Foss F: Efficacy of low dose clofarabine in refractory precursor T- acute lymphoblastic leukemia. Yale J Biol Med; 2006 Dec;79(3-4):169-72
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  • [Title] Efficacy of low dose clofarabine in refractory precursor T- acute lymphoblastic leukemia.
  • Refractory T-lymphoblastic leukemia in adults has a poor prognosis in patients who relapse after allogeneic stem cell transplantation, and relatively few new agents have demonstrated activity.
  • We used low dose clofarabine and induced a remission in a patient who relapsed in the skin and marrow after allogeneic transplant and was refractory to nelarabine and report a near complete response, suggesting significant activity for low intermittent dose clofarabine in patients with relapsed T-cell leukemias.
  • [MeSH-major] Adenine Nucleotides / therapeutic use. Arabinonucleosides / therapeutic use. Leukemia-Lymphoma, Adult T-Cell / drug therapy
  • [MeSH-minor] Adult. Bone Marrow Neoplasms / drug therapy. Bone Marrow Neoplasms / secondary. Clinical Trials as Topic. Drug Administration Schedule. Drug Resistance, Neoplasm. Humans. Immunophenotyping. Male. Recurrence. Skin Neoplasms / drug therapy. Skin Neoplasms / secondary. Stem Cell Transplantation. Transplantation, Homologous. Treatment Outcome

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
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  • (PMID = 17940627.001).
  • [ISSN] 1551-4056
  • [Journal-full-title] The Yale journal of biology and medicine
  • [ISO-abbreviation] Yale J Biol Med
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adenine Nucleotides; 0 / Arabinonucleosides; 60158CV180 / nelarabine; 762RDY0Y2H / clofarabine
  • [Other-IDs] NLM/ PMC1994805
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65. Hyde RK, Liu PP: RUNX1 repression-independent mechanisms of leukemogenesis by fusion genes CBFB-MYH11 and AML1-ETO (RUNX1-RUNX1T1). J Cell Biochem; 2010 Aug 1;110(5):1039-45
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  • The core binding factor (CBF) acute myeloid leukemias (AMLs) are a prognostically distinct subgroup that includes patients with the inv(16) and t(8:21) chromosomal rearrangements.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / genetics. Leukemia / genetics. Oncogene Proteins, Fusion / genetics
  • [MeSH-minor] Acute Disease. Gene Expression Regulation, Leukemic. Humans. Leukemia, Myeloid / genetics. Models, Genetic

  • MedlinePlus Health Information. consumer health - Leukemia.
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  • [Copyright] Published 2010 Wiley-Liss, Inc.
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  • (PMID = 20589720.001).
  • [ISSN] 1097-4644
  • [Journal-full-title] Journal of cellular biochemistry
  • [ISO-abbreviation] J. Cell. Biochem.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / ZIA HG000030-16
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / CBFbeta-MYH11 fusion protein; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / RUNX1 protein, human
  • [Other-IDs] NLM/ NIHMS360619; NLM/ PMC3298446
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66. McGrattan P, Logan A, Humphreys M, Bowers M: Jumping translocation in acute monocytic leukemia (M5b) with alternative breakpoint sites in the long arm of donor chromosome 3. Med Oncol; 2010 Sep;27(3):667-72
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  • [Title] Jumping translocation in acute monocytic leukemia (M5b) with alternative breakpoint sites in the long arm of donor chromosome 3.
  • After 20 months a diagnosis of disease transformation to acute monocytic leukemia (M5b) was made.
  • Conventional G-banded analysis of unstimulated peripheral blood cultures detected the proximal 3q1?2 JT clone involving recipient chromosome 10 several weeks after transformation to acute monocytic leukemia.
  • Palliative care was administered until his demise 2.2 months after disease transformation.
  • There have been fewer than 70 cases of acquired JTs reported in the literature, including one myeloproliferative neoplasm and five acute myeloid leukemias involving a single breakpoint site on donor chromosome 3.
  • [MeSH-major] Chromosome Breakpoints. Chromosomes, Human, Pair 3 / genetics. Leukemia, Monocytic, Acute / genetics. Translocation, Genetic
  • [MeSH-minor] Aged, 80 and over. Anemia, Refractory, with Excess of Blasts / genetics. Disease Progression. Humans. Male

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  • (PMID = 19629764.001).
  • [ISSN] 1559-131X
  • [Journal-full-title] Medical oncology (Northwood, London, England)
  • [ISO-abbreviation] Med. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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67. Xiao L, Rasouli P, Ruden DM: Possible effects of early treatments of hsp90 inhibitors on preventing the evolution of drug resistance to other anti-cancer drugs. Curr Med Chem; 2007;14(2):223-32
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  • Hsp90 is an exciting target for anti-cancer drugs because most of the proteins that interact with Hsp90 are known to be in the cell cycle, signaling and chromatin-remodeling pathways.
  • Similarly, in humans