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1. Kolmannskog S, Flaegstad T, Helgestad J, Hellebostad M, Zeller B, Glomstein A: [Childhood acute lymphoblastic leukemia in Norway 1992-2000]. Tidsskr Nor Laegeforen; 2007 May 31;127(11):1493-5
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  • [Title] [Childhood acute lymphoblastic leukemia in Norway 1992-2000].
  • BACKGROUND: Acute lymphoblastic leukemia is the most common malignancy in childhood.
  • Four of 6 infants with acute lymphoblastic leukemia and all 4 with mature B-cell leukemia are alive.
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / epidemiology
  • [MeSH-minor] Adolescent. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child. Child, Preschool. Disease-Free Survival. Female. Humans. Infant. Male. Neoplasm Recurrence, Local. Norway / epidemiology. Risk Factors. Stem Cell Transplantation. Treatment Outcome


2. De Keersmaecker K, Graux C, Odero MD, Mentens N, Somers R, Maertens J, Wlodarska I, Vandenberghe P, Hagemeijer A, Marynen P, Cools J: Fusion of EML1 to ABL1 in T-cell acute lymphoblastic leukemia with cryptic t(9;14)(q34;q32). Blood; 2005 Jun 15;105(12):4849-52
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  • [Title] Fusion of EML1 to ABL1 in T-cell acute lymphoblastic leukemia with cryptic t(9;14)(q34;q32).
  • The BCR-ABL1 fusion kinase is frequently associated with chronic myeloid leukemia and B-cell acute lymphoblastic leukemia but is rare in T-cell acute lymphoblastic leukemia (T-ALL).
  • [MeSH-major] Chromosomes, Human, Pair 14. Chromosomes, Human, Pair 9. Cyclin-Dependent Kinase Inhibitor p16 / genetics. Fusion Proteins, bcr-abl / chemistry. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Leukemia, T-Cell / pathology. Oncogene Proteins, Fusion / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic
  • [MeSH-minor] Adolescent. Base Sequence. Benzamides. Blotting, Western. Cell Line. Cell Survival. DNA, Complementary / metabolism. DNA-Binding Proteins / metabolism. Female. Gene Deletion. Genes, abl. Humans. Imatinib Mesylate. In Situ Hybridization, Fluorescence. Karyotyping. Microtubules / metabolism. Milk Proteins / metabolism. Mitogen-Activated Protein Kinase 1 / metabolism. Mitogen-Activated Protein Kinase 3 / metabolism. Models, Genetic. Molecular Sequence Data. Open Reading Frames. Phenotype. Phosphorylation. Piperazines / pharmacology. Polymerase Chain Reaction. Protein Kinase Inhibitors / pharmacology. Protein Structure, Tertiary. Protein-Tyrosine Kinases / metabolism. Pyrimidines / pharmacology. Recombinant Fusion Proteins / metabolism. Retroviridae. Reverse Transcriptase Polymerase Chain Reaction. STAT5 Transcription Factor. Signal Transduction. Time Factors. Trans-Activators / metabolism

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  • (PMID = 15713800.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzamides; 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / DNA, Complementary; 0 / DNA-Binding Proteins; 0 / EML1-ABL1 fusion protein, human; 0 / Milk Proteins; 0 / Oncogene Proteins, Fusion; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / Recombinant Fusion Proteins; 0 / STAT5 Transcription Factor; 0 / Trans-Activators; 0 / abl-bcr fusion protein, human; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3
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3. Cui W, Kong NR, Ma Y, Amin HM, Lai R, Chai L: Differential expression of the novel oncogene, SALL4, in lymphoma, plasma cell myeloma, and acute lymphoblastic leukemia. Mod Pathol; 2006 Dec;19(12):1585-92
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  • [Title] Differential expression of the novel oncogene, SALL4, in lymphoma, plasma cell myeloma, and acute lymphoblastic leukemia.
  • Previously, we reported that SALL4 was constitutively expressed in acute myeloid leukemia and SALL4 transgenic mice developed acute myeloid leukemia.
  • In this study, we aimed to survey SALL4 protein expression in benign and neoplastic hematopoietic tissues in addition to acute myeloid leukemia using immunostaining with a polyclonal anti-SALL4 antibody.
  • Reverse transcription-polymerase chain reaction was also performed to detect SALL4 mRNA expression on eight precursor B-cell lymphoblastic leukemia/lymphomas, 10 benign hematopoietic tissues, and seven hematopoietic cancer cell lines.
  • Of the benign tissues, SALL4 expression was detectable only in CD34+ hematopoietic stem/progenitor cells (2/2 at protein level, 3/3 at RNA level).
  • In neoplastic tissues, only precursor B-cell lymphoblastic leukemia/lymphomas had detectable SALL4 (12/16 at protein level, 7/8 at RNA level), similar to that observed in acute myeloid leukemia.
  • Of the seven cell lines examined, only those derived from acute myeloid leukemia and precursor B-cell lymphoblastic leukemia/lymphomas were positive.
  • The persistence of SALL4 expression in leukemic blasts in precursor B-cell lymphoblastic leukemia/lymphomas resembles to what we observed in acute myeloid leukemia, and correlates with the maturation arrest of these cells.
  • We have shown in our previous study that the constitutive expression of SALL4 in mice can lead to acute myeloid leukemia development.
  • The similar expression pattern of SALL4 in acute myeloid leukemia and B-cell lymphoblastic leukemia/lymphomas suggests that these two disease entities may share similar biological features and/or mechanisms of leukemogenesis.
  • More definite studies to investigate the role of SALL4 in the pathogenesis of B-cell lymphoblastic leukemia/lymphomas are needed in the future to address this question.
  • [MeSH-major] Gene Expression Regulation, Neoplastic. Lymphoma / genetics. Plasmacytoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Transcription Factors / genetics
  • [MeSH-minor] Antigens, CD34 / metabolism. Biomarkers, Tumor / metabolism. Cell Line, Tumor. Cell Separation. Flow Cytometry. Hematopoietic Stem Cells / metabolism. Hematopoietic Stem Cells / pathology. Humans. Immunoenzyme Techniques. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 16998462.001).
  • [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
  • [Grant] United States / NIDDK NIH HHS / DK / K08 DK063220
  • [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 / Antigens, CD34; 0 / Biomarkers, Tumor; 0 / RNA, Messenger; 0 / SALL4 protein, human; 0 / Transcription Factors
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4. Lin TL, Wang QH, Brown P, Peacock C, Merchant AA, Brennan S, Jones E, McGovern K, Watkins DN, Sakamoto KM, Matsui W: Self-renewal of acute lymphocytic leukemia cells is limited by the Hedgehog pathway inhibitors cyclopamine and IPI-926. PLoS One; 2010 Dec 28;5(12):e15262
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  • [Title] Self-renewal of acute lymphocytic leukemia cells is limited by the Hedgehog pathway inhibitors cyclopamine and IPI-926.
  • Recent data suggests that Hh signaling plays a role in normal B-cell development, and we hypothesized that Hh signaling may be important in precursor B-cell acute lymphocytic leukemia (B-ALL).
  • We found that the expression of Hh pathway components was common in human B-ALL cell lines and clinical samples.

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  • (PMID = 21203400.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / R01 HL075826; United States / NCI NIH HHS / CA / P01 CA015396; United States / NCI NIH HHS / CA / R01 CA127574; United States / NCI NIH HHS / CA / R01CA127574; United States / NCI NIH HHS / CA / R01 CA127574-05; United States / NHLBI NIH HHS / HL / HL83077; United States / NHLBI NIH HHS / HL / HL75826; United States / NHLBI NIH HHS / HL / R01 HL083077; United States / NHLBI NIH HHS / HL / T32 HL086345; United States / NCI NIH HHS / CA / P01CA15396
  • [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 / Antigens, CD19; 0 / Antigens, CD34; 0 / Antineoplastic Agents; 0 / Hedgehog Proteins; 0 / IPI-926; 0 / Receptors, G-Protein-Coupled; 0 / SMO protein, human; 0 / Veratrum Alkaloids; EC 1.2.1.3 / Aldehyde Dehydrogenase; ZH658AJ192 / cyclopamine
  • [Other-IDs] NLM/ PMC3011010
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5. Lapucci A, Lulli M, Amedei A, Papucci L, Witort E, Di Gesualdo F, Bertolini F, Brewer G, Nicolin A, Bevilacqua A, Schiavone N, Morello D, Donnini M, Capaccioli S: zeta-Crystallin is a bcl-2 mRNA binding protein involved in bcl-2 overexpression in T-cell acute lymphocytic leukemia. FASEB J; 2010 Jun;24(6):1852-65
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  • [Title] zeta-Crystallin is a bcl-2 mRNA binding protein involved in bcl-2 overexpression in T-cell acute lymphocytic leukemia.
  • The human antiapoptotic bcl-2 gene has been discovered in t(14;18) B-cell leukemias/lymphomas because of its overexpression caused at a transcriptional control level by the bcl-2/IgH fusion gene.
  • An increased Bcl-2 level observed in normal phytohemagglutinin (PHA)-activated T lymphocytes, acute lymphatic leukemia (ALL) T-cell lines, and T cells of patients with leukemia in comparison with normal non-PHA-activated T lymphocytes was concomitant with an increase in zeta-crystallin level.
  • The specific association of zeta-crystallin with the bcl-2 ARE was significantly enhanced in T cells of patients with ALL, which accounts for the higher stability of bcl-2 mRNA and suggests a possible contribution of zeta-crystallin to bcl-2 overexpression occurring in this leukemia.
  • [MeSH-major] 3' Untranslated Regions / physiology. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Proto-Oncogene Proteins c-bcl-2 / metabolism. RNA, Messenger / metabolism. zeta-Crystallins / metabolism
  • [MeSH-minor] Blotting, Western. Cytoplasm / drug effects. Cytoplasm / metabolism. Female. Gene Expression Regulation. Humans. Immunoprecipitation. Male. Middle Aged. Phytohemagglutinins. RNA, Small Interfering / pharmacology. Reverse Transcriptase Polymerase Chain Reaction. Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization. T-Lymphocytes / drug effects. T-Lymphocytes / pathology

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  • (PMID = 20103721.001).
  • [ISSN] 1530-6860
  • [Journal-full-title] FASEB journal : official publication of the Federation of American Societies for Experimental Biology
  • [ISO-abbreviation] FASEB J.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA052443; United States / NCI NIH HHS / CA / R01 CA052443; United States / NCI NIH HHS / CA / R01 CA052443-16
  • [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 / 3' Untranslated Regions; 0 / Phytohemagglutinins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 0 / zeta-Crystallins
  • [Other-IDs] NLM/ PMC2874474
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6. Emerenciano M, Koifman S, Pombo-de-Oliveira MS: Acute leukemia in early childhood. Braz J Med Biol Res; 2007 Jun;40(6):749-60
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  • [Title] Acute leukemia in early childhood.
  • Acute leukemia in early childhood is biologically and clinically distinct.
  • The particular characteristics of this malignancy diagnosed during the first months of life have provided remarkable insights into the etiology of the disease.
  • The pro-B, CD10 negative immunophenotype is typically found in infant acute leukemia, and the most common genetic alterations are the rearrangements of the MLL gene.
  • The Brazilian Collaborative Study Group of Infant Acute Leukemia has found that mothers exposed to dipyrone, pesticides and hormones had an increased chance to give birth to babies with infant acute leukemia [OR = 1.48 (95%CI = 1.05-2.07), OR = 2.27 (95%CI = 1.56-3.31) and OR = 9.08 (95%CI = 2.95-27.96)], respectively.
  • This review aims to summarize recent clues that have facilitated the elucidation of the biology of early childhood leukemias, with emphasis on infant acute leukemia in the Brazilian population.

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  • (PMID = 17581672.001).
  • [ISSN] 0100-879X
  • [Journal-full-title] Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas
  • [ISO-abbreviation] Braz. J. Med. Biol. Res.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Brazil
  • [Chemical-registry-number] 0 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
  • [Number-of-references] 60
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7. Lucas DM, Edwards RB, Lozanski G, West DA, Shin JD, Vargo MA, Davis ME, Rozewski DM, Johnson AJ, Su BN, Goettl VM, Heerema NA, Lin TS, Lehman A, Zhang X, Jarjoura D, Newman DJ, Byrd JC, Kinghorn AD, Grever MR: The novel plant-derived agent silvestrol has B-cell selective activity in chronic lymphocytic leukemia and acute lymphoblastic leukemia in vitro and in vivo. Blood; 2009 May 7;113(19):4656-66
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  • [Title] The novel plant-derived agent silvestrol has B-cell selective activity in chronic lymphocytic leukemia and acute lymphoblastic leukemia in vitro and in vivo.
  • Therapeutic options for advanced B-cell acute lymphoblastic leukemia (ALL) and chronic lymphocytic leukemia (CLL) are limited.
  • Available treatments can also deplete T lymphocytes, leaving patients at risk of life-threatening infections.
  • In the National Cancer Institute cell line screen, the structurally unique natural product silvestrol produces an unusual pattern of cytotoxicity that suggests activity in leukemia and selectivity for B cells.
  • We investigated silvestrol efficacy using primary human B-leukemia cells, established B-leukemia cell lines, and animal models.
  • In vivo, silvestrol causes significant B-cell reduction in Emu-Tcl-1 transgenic mice and significantly extends survival of 697 xenograft severe combined immunodeficient (SCID) mice without discernible toxicity.
  • These data indicate silvestrol has efficacy against B cells in vitro and in vivo and identify translational inhibition as a potential therapeutic target in B-cell leukemias.

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  • (PMID = 19190247.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U19 CA052956; United States / NCI NIH HHS / CA / P01CA125066; United States / NCI NIH HHS / CA / P01 CA125066; United States / NCI NIH HHS / CA / P01 CA081534; United States / NCI NIH HHS / CA / CA52956
  • [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 / Mcl1 protein, mouse; 0 / Myeloid Cell Leukemia Sequence 1 Protein; 0 / Proto-Oncogene Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / RNA, Messenger; 0 / Reactive Oxygen Species; 0 / Tcl1 protein, mouse; 0 / Triterpenes; 0 / silvestrol
  • [Other-IDs] NLM/ PMC2680369
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8. Zhu L, Wang HX, Lui J, Yan HM, Xue M: [Acute leukemia relapse of donor origin in two cases after haploidentical bone marrow transplantation]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2006 Apr;14(2):400-2
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Acute leukemia relapse of donor origin in two cases after haploidentical bone marrow transplantation].
  • To investigate the leukemia relapse of AL patients after HLA haploidentical bone marrow transplantation (HLA HBMT), 2 relapsed leukemia patients received HLA HBMT were studied, peripheral blood simples and bone marrow smear were examined, morphologic change of bone marrow cells was observed, while the HLA genotype and chromosome karyotye were analyzed by PCR and routine G-banding methods, respectively.
  • The results indicated that the two cases were diagnosed primarily as acute lymphocytic leukemia (common cell subtype) and acute megakaryocytic leukemia, in which chromosome abnormalities or activation of protooncogene in leukemic cells were observed.
  • The complete hematopuietie reconstitution of donor origin was obtained in these 2 cases after HLA HBMT, but the leukemic cells in these 2 leukemia patients were confirmed to be donor origin after relapse, their blood groups and HLA genotype were found to be originated from donor.
  • These 2 relapsed leukemia patients were diagnosed as acute lymphocytic leukemia (B cell subtype) and acute megakaryocytic leukemia.
  • It is suggested that high-dose of immunosuppressive agents used in transplantation may contribute to leukemia relapse of donor origin in these patients.
  • Abnormalities in hematopoietic microenvironment may be also involved in the leukemia development.
  • Donor-cell leukemia after allogeneic hematopoietic stem cell transplantation can be an ideal model to investigate the related events in human leukemogenesis.

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  • (PMID = 16638225.001).
  • [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] Case Reports; English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / HLA Antigens
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9. Miao K, Li J, Qiu H, Zhang R, Chen L, Wu H, Wang R, Zhang J: The chromosomal translocation (11;14) (p13; q11) in acute B-Cell lymphocytic leukemia. Onkologie; 2010;33(7):385-7
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  • [Title] The chromosomal translocation (11;14) (p13; q11) in acute B-Cell lymphocytic leukemia.
  • BACKGROUND: Cytogenetic abnormalities are the most important independent prognostic factors of acute leukemia and imply the potential molecular mechanism of the disease.
  • Translocation (11;14)(p13;q11) has been predominantly found in T-cell acute lymphocytic leukemia (ALL) but is rare in B-cell ALL.
  • CASE REPORT: We present the case of a 30-year-old male patient, who presented with symptomatic anemia, thrombocytopenia and leukocytosis.
  • CONCLUSIONS: Translocation (11;14) (p13;q11) in B-cell ALL is rare, but it is worth exploring the molecular mechanisms and discovering the prognostic value in more B-cell ALL patients.
  • [MeSH-major] Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 14 / genetics. Leukemia, B-Cell / genetics. Translocation, Genetic / genetics
  • [MeSH-minor] Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Chromosome Aberrations. Chromosome Banding. Disease Progression. Humans. Immunophenotyping. In Situ Hybridization, Fluorescence. Karyotyping. Male. Prognosis. Remission Induction

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  • [Copyright] Copyright 2010 S. Karger AG, Basel.
  • (PMID = 20631486.001).
  • [ISSN] 1423-0240
  • [Journal-full-title] Onkologie
  • [ISO-abbreviation] Onkologie
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Switzerland
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10. Catusse J, Wollner S, Leick M, Schröttner P, Schraufstätter I, Burger M: Attenuation of CXCR4 responses by CCL18 in acute lymphocytic leukemia B cells. J Cell Physiol; 2010 Nov;225(3):792-800
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  • [Title] Attenuation of CXCR4 responses by CCL18 in acute lymphocytic leukemia B cells.
  • Elevated levels of CCL18 have been described in various diseases including childhood acute lymphocytic leukemia (ALL) but its functions remain poorly characterized.
  • CXCL12 is a pivotal chemokine for hematopoiesis and B cell homing processes.
  • We demonstrate that CCL18 interferes with CXCL12-mediated pre-B ALL cell activation.
  • CXCL12-induced calcium mobilization, chemotaxis, pseudo-emperipolesis and cellular proliferation could be significantly reduced by CCL18 in pre-B ALL cell lines.
  • [MeSH-major] Chemokines, CC / metabolism. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / immunology. Precursor Cells, B-Lymphoid / immunology. Receptors, CXCR4 / metabolism. Signal Transduction
  • [MeSH-minor] Animals. Apoptosis. COS Cells. Calcium Signaling. Cell Line, Tumor. Cell Proliferation. Cercopithecus aethiops. Chemokine CXCL12 / metabolism. Chemotaxis, Leukocyte. Estradiol / metabolism. Estrogen Antagonists / pharmacology. Humans. Ligands. Lymphocyte Activation. Receptors, Estrogen. Receptors, G-Protein-Coupled / antagonists & inhibitors. Receptors, G-Protein-Coupled / genetics. Receptors, G-Protein-Coupled / metabolism. Recombinant Proteins / metabolism. Transfection

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  • [Copyright] © 2010 Wiley-Liss, Inc.
  • (PMID = 20568229.001).
  • [ISSN] 1097-4652
  • [Journal-full-title] Journal of cellular physiology
  • [ISO-abbreviation] J. Cell. Physiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CCL18 protein, human; 0 / CXCL12 protein, human; 0 / CXCR4 protein, human; 0 / Chemokine CXCL12; 0 / Chemokines, CC; 0 / Estrogen Antagonists; 0 / GPER protein, human; 0 / Ligands; 0 / Receptors, CXCR4; 0 / Receptors, Estrogen; 0 / Receptors, G-Protein-Coupled; 0 / Recombinant Proteins; 4TI98Z838E / Estradiol
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11. Gobbi G, Mirandola P, Malinverno C, Sponzilli I, Carubbi C, Ricci F, Binazzi R, Basso G, Giuliani-Piccari G, Ramazzotti G, Pasquantonio G, Cocco L, Vitale M: Aberrant expression of B203.13 antigen in acute lymphoid leukemia of B-cell origin. Int J Oncol; 2008 Aug;33(2):371-4
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  • [Title] Aberrant expression of B203.13 antigen in acute lymphoid leukemia of B-cell origin.
  • The B203.13 monoclonal antibody was developed by immunizing mice with the B/monocyte biphenotypic cell line B1b.
  • During normal hematopoiesis B203.13 is expressed on a fraction of CD34+ cells, while on mature cells it is only present on B-lymphocytes.
  • We tested this antibody as a marker of childhood B-acute lymphoblastic leukemia (B-ALL).
  • The CD10(+)/B203.13(+) phenotype was specific to B-ALL, since CD10(+)/CD20(+) cells from common acute lymphoblastic leukemia (c-ALL) did not express B203.13.
  • We concluded that the use of B203.13 in association with CD10 and CD20 provides meaningful information for distinguishing normal residual B-cells from leukemic B-lymphoblasts and that recurrence of a CD10(+)/B203.13(+) phenotype after transplantation may be a very early relapse indicator of early B-acute lymphoblastic leukemia.
  • [MeSH-major] Antigens, Neoplasm / biosynthesis. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / metabolism

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  • (PMID = 18636158.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antigens, CD20; 0 / Antigens, Neoplasm; EC 3.4.24.11 / Neprilysin
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12. Vanura K, Vrsalovic MM, Le T, Marculescu R, Kusec R, Jäger U, Nadel B: V(D)J targeting mistakes occur at low frequency in acute lymphoblastic leukemia. Genes Chromosomes Cancer; 2009 Aug;48(8):725-36
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  • [Title] V(D)J targeting mistakes occur at low frequency in acute lymphoblastic leukemia.
  • Translocations of proto-oncogenes to the B-cell or T-cell antigen receptor loci in acute T- or B-cell leukemia and lymphoma have been, in most cases, accredited to V(D)J or switch recombination depending on the location of the breakpoint at the receptor locus.
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Proto-Oncogenes / genetics. Recombination, Genetic. Translocation, Genetic. VDJ Recombinases / metabolism
  • [MeSH-minor] Adaptor Proteins, Signal Transducing. Animals. Cells, Cultured. DNA Breaks. DNA-Binding Proteins / genetics. Fibroblasts. Genes, T-Cell Receptor. Homeodomain Proteins / genetics. LIM Domain Proteins. Lymphocyte Specific Protein Tyrosine Kinase p56(lck) / genetics. Metalloproteins / genetics. Mice. Receptors, Antigen, B-Cell / genetics. TCF Transcription Factors / genetics. Transcription Factor 7-Like 1 Protein

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  • (PMID = 19455608.001).
  • [ISSN] 1098-2264
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / DNA-Binding Proteins; 0 / Homeodomain Proteins; 0 / LIM Domain Proteins; 0 / Lmo2 protein, mouse; 0 / Metalloproteins; 0 / Receptors, Antigen, B-Cell; 0 / TCF Transcription Factors; 0 / Tcf7l1 protein, mouse; 0 / Tlx1 protein, mouse; 0 / Transcription Factor 7-Like 1 Protein; EC 2.7.10.2 / Lymphocyte Specific Protein Tyrosine Kinase p56(lck); EC 2.7.7.- / VDJ Recombinases
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13. Kraigher-Krainer E, Lackner H, Sovinz P, Schwinger W, Benesch M, Urban C: Numb chin syndrome as initial manifestation in a child with acute lymphoblastic leukemia. Pediatr Blood Cancer; 2008 Sep;51(3):426-8
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  • [Title] Numb chin syndrome as initial manifestation in a child with acute lymphoblastic leukemia.
  • We report on an 11-year-old male who presented with NCS as initial manifestation of acute lymphoblastic leukemia of B-cell type.
  • [MeSH-major] Chin / pathology. Hypesthesia / etiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology

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  • [Copyright] (c) 2008 Wiley-Liss, Inc.
  • (PMID = 18506757.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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14. Song JH, Schnittke N, Zaat A, Walsh CS, Miller CW: FBXW7 mutation in adult T-cell and B-cell acute lymphocytic leukemias. Leuk Res; 2008 Nov;32(11):1751-5
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  • [Title] FBXW7 mutation in adult T-cell and B-cell acute lymphocytic leukemias.
  • Engineered FBXW7 null cells display cell cycle and chromosome stability defects.
  • Mutations of FBXW7 have been found in human colorectal, ovarian, endometrial tumors and T-cell acute lymphocytic leukemias.
  • Prompted by these findings we have examined acute myeloid leukemia, non-Hodgkin's lymphoma, T-cell acute lymphocytic leukemia, B-cell acute lymphocytic leukemia and adult T-cell leukemia DNA for mutations of the FBXW7 gene.
  • As expected, mutations were found in T-cell acute lymphocytic leukemias.
  • However mutations of FBXW7 were also found in four of 118 B-cell acute lymphocytic leukemias and one of 24 adult T-cell leukemia samples.
  • These observations suggest that disruption of FBXW7 has a role in several forms of lymphocytic leukemias and not exclusively T-cell acute lymphocytic leukemia.
  • [MeSH-major] Burkitt Lymphoma / genetics. Cell Cycle Proteins / genetics. F-Box Proteins / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Lymphoma, Non-Hodgkin / genetics. Mutation / genetics. Ubiquitin-Protein Ligases / genetics

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  • (PMID = 18485478.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / F-Box Proteins; EC 6.3.2.19 / FBXW7 protein, human; EC 6.3.2.19 / Ubiquitin-Protein Ligases
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15. Saxena A, Rai A, Raina V, Seth T, Mitra DK: Expression of CD13/aminopeptidase N in precursor B-cell leukemia: role in growth regulation of B cells. Cancer Immunol Immunother; 2010 Jan;59(1):125-35
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of CD13/aminopeptidase N in precursor B-cell leukemia: role in growth regulation of B cells.
  • Expression of cell surface CD13 in acute B-cell leukemia (ALL-B) is often viewed, as an aberrant expression of a myeloid lineage marker.
  • Here, we attempted to study the stage specific expression of CD13 on ALL-B blasts and understand its role in leukemogenesis as pertaining to stage of B-cell ontogeny.
  • Among 68 cases of early B-cell ALL, 22 cases with distinct immunophenotype was identified as immature B-cell ALL.
  • This strongly indicates leukemogenesis at an early stage of B-cell development.
  • We also identified, the existence of a subpopulation of cells with remarkably similar phenotype in non-leukemic marrow from healthy subjects (expressing CD10, CD19, CD22, CD24, Tdt together with the co-expression of CD13).
  • By blocking their cell surface CD13 in leukemic blasts with monoclonal antibody we were able to inhibit their proliferation.
  • CD13 may thus be an important target for novel molecular therapy of early stage acute B-cell leukemia.
  • [MeSH-major] Antigens, CD13 / immunology. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / immunology. Precursor Cells, B-Lymphoid / immunology
  • [MeSH-minor] Adolescent. Adult. Aged. Cell Proliferation. Child. Child, Preschool. Female. Humans. Male. Middle Aged. Young Adult

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  • (PMID = 19562339.001).
  • [ISSN] 1432-0851
  • [Journal-full-title] Cancer immunology, immunotherapy : CII
  • [ISO-abbreviation] Cancer Immunol. Immunother.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] EC 3.4.11.2 / Antigens, CD13
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16. Bhatia S, Kaul D, Varma N: Potential tumor suppressive function of miR-196b in B-cell lineage acute lymphoblastic leukemia. Mol Cell Biochem; 2010 Jul;340(1-2):97-106
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  • [Title] Potential tumor suppressive function of miR-196b in B-cell lineage acute lymphoblastic leukemia.
  • Keeping in view the fact that genes coding microRNAs (miRNAs) have been found to be localized in chromosomal regions susceptible to genetic translocations, this study was addressed to identify and characterize the miRNAs that are present near/within the regions involved in genetic translocations characteristic of B-cell acute lymphoblastic leukemia (B-cell ALL).
  • Out of six such identified miRNAs miR-196b was not only found to be significantly down-regulated in both EB-3 cell line as well as B-cell ALL patients as compared to that found in the corresponding controls, but also had the inherent capacity to down-regulate the highly expressed c-myc gene, a consequence of genetic translocation characteristic of EB-3 cells at both transcriptional and translational level.
  • Also down-regulation of c-myc gene was accompanied by decreased expressions of c-myc effector genes coding for hTERT, Bcl-2, and AATF.
  • Based upon these results, we propose for the first time that miR-196b has the inherent capacity to down-regulate the overamplified c-myc gene recognized as a common pathognomonic feature leading to cancer in general and B-cell ALL in particular.
  • Hence miR-196b can be assigned with the tumor suppressor function and can be of therapeutic importance in paving the way toward the treatment of B-cell ALL.
  • [MeSH-major] Gene Expression Regulation, Leukemic. Genes, Tumor Suppressor. MicroRNAs / metabolism. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Algorithms. Apoptosis / genetics. Apoptosis Regulatory Proteins / genetics. Case-Control Studies. Cell Line, Tumor. Cell Proliferation. Computational Biology. Down-Regulation. Humans. Proto-Oncogene Proteins c-bcl-2 / genetics. Proto-Oncogene Proteins c-myc / genetics. Repressor Proteins / genetics. Telomerase / genetics. Transcription, Genetic. Transfection

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  • (PMID = 20549547.001).
  • [ISSN] 1573-4919
  • [Journal-full-title] Molecular and cellular biochemistry
  • [ISO-abbreviation] Mol. Cell. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / AATF protein, human; 0 / Apoptosis Regulatory Proteins; 0 / MIRN196 microRNA, human; 0 / MYC protein, human; 0 / MicroRNAs; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Proto-Oncogene Proteins c-myc; 0 / Repressor Proteins; EC 2.7.7.49 / TERT protein, human; EC 2.7.7.49 / Telomerase
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17. Ghavamzadeh A, Allahyari A, Alimoghaddam K, Karimi A, Shamshiri A, Abolhasani R, Manookian A, Asadi M, Khatami F: Outpatient versus inpatient autologous stem cell transplantation for malignant hematologic disorders. J Clin Oncol; 2009 May 20;27(15_suppl):7042
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  • [Title] Outpatient versus inpatient autologous stem cell transplantation for malignant hematologic disorders.
  • : 7042 Background: High-dose chemotherapy with autologous stem cell support is utilized for the treatment of a variety of malignancies including Hodgkin/non-Hodgkins lymphoma and acute leukemias.
  • The aim of this study was to compare the time of engraftment and mortality rate and cost of neutropenic treatment in outpatient versus inpatient autologous stem cell transplantation (SCT).
  • They received conditioning regimen (CEAM for NHL and HL, busulfan and etoposide for AML) and stem cell infusion in hospital.
  • The day after SCT, outpatient group were discharged and followed by outpatient SCT team, and to be re-hospitalized in case of febrile neutropenia, after sepsis workup and performing chest x-ray, they were received the first dose of antibiotic in hospital and treatment continued in home.

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  • (PMID = 27961405.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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18. Tong W, Stevenson W, Cortes J, Needham L, Brotherton D, Davidson A, Drummond A, Garcia-Manero G: In vitro and in vivo anti-leukemia activity of CHR-2845, a cell-targeted HDAC inhibitor for use in monocytic leukemia. J Clin Oncol; 2009 May 20;27(15_suppl):e14579
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  • [Title] In vitro and in vivo anti-leukemia activity of CHR-2845, a cell-targeted HDAC inhibitor for use in monocytic leukemia.
  • : e14579 Background: Histone deacetylase inhibitors alter gene expression and induce apoptosis in a wide range of cancer cells including those derived from human leukemias.
  • METHODS: We studied the in vitro and in vivo anti-leukemia activity of CHR-2845 using cell proliferation assay, annexin V binding assay, cell cycle analysis, western blot and in vitro primary leukemia cell culture.
  • RESULTS: Both U937 and THP1 cells express high levels of hCE-1 whereas the myeloid cell line, HL60, does not.
  • In comparison to vorinostat, CHR-2845 showed increased anti-proliferative potency (IC<sub>50</sub>) against monocytic cell lines (THP1, 30 nM vs 700 nM and U937, 30 nM vs 475 nM), compared to a myeloid cell line (HL60, 700nM vs 470 nM).
  • In a broad panel of leukemic cell lines, the potency of CHR-2845 over vorinostat correlated completely with hCE-1 expression.
  • In monocytic cell lines, CHR-2845 induced more apoptosis than vorinostat (THP1: 45±5% vs 11±1% and U937: 23±14% vs 6±1%), as measured by flow cytometry using Annexin V.
  • Biochemical assessment of histone H3 and H4 protein acetylation by Western blot also indicateed that CHR-2845 is at least 10 times more potent than vorinostat in monocytic cell lines but not in HL-60 cells.
  • We also studied the anti-leukemia activity of CHR-2845 in primary leukemia cells from 8 patients with acute or chronic myelomonocytic leukemia.
  • CONCLUSIONS: These results indicated that CHR-2845 has potential to be efficacious in the treatment of patients with monocytic leukemia.

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  • (PMID = 27963654.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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19. Larson RA: Three new drugs for acute lymphoblastic leukemia: nelarabine, clofarabine, and forodesine. Semin Oncol; 2007 Dec;34(6 Suppl 5):S13-20
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  • [Title] Three new drugs for acute lymphoblastic leukemia: nelarabine, clofarabine, and forodesine.
  • The search for more effective and safer anti-leukemia therapies has led to the identification of several new agents that show activity against specific types of acute lymphoblastic leukemia (ALL).
  • Of these, nelarabine has shown clinically meaningful benefit in patients with T-cell ALL, with overall response rates ranging from 33% to 60%, the induction of durable complete remissions, and an overall 1-year survival rate of 28% in adults.
  • Clofarabine has also shown promising clinical activity in pediatric patients, with an overall response rate of 30%, and some patients are able to proceed to allogeneic hematopoietic cell transplantation.
  • Forodesine is the most recent novel agent, with a unique mechanism that has shown single-agent activity in relapsed and refractory T- and B-cell leukemias and cutaneous lymphomas.
  • The rationale, pharmacology, and clinical experience to date with these agents in the treatment of patients with refractory acute leukemia are reviewed, with a highlight on ALL.
  • [MeSH-major] Adenine Nucleotides / pharmacology. Antineoplastic Agents / pharmacology. Arabinonucleosides / pharmacology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Purine Nucleosides / pharmacology. Purine-Nucleoside Phosphorylase / drug effects. Pyrimidinones / pharmacology

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  • (PMID = 18086342.001).
  • [ISSN] 0093-7754
  • [Journal-full-title] Seminars in oncology
  • [ISO-abbreviation] Semin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adenine Nucleotides; 0 / Antineoplastic Agents; 0 / Arabinonucleosides; 0 / Purine Nucleosides; 0 / Pyrimidinones; 426X066ELK / forodesine; 60158CV180 / nelarabine; 762RDY0Y2H / clofarabine; EC 2.4.2.1 / Purine-Nucleoside Phosphorylase
  • [Number-of-references] 41
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20. Teachey DT, Felix CA: Development of cold agglutinin autoimmune hemolytic anemia during treatment for pediatric acute lymphoblastic leukemia. J Pediatr Hematol Oncol; 2005 Jul;27(7):397-9
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  • [Title] Development of cold agglutinin autoimmune hemolytic anemia during treatment for pediatric acute lymphoblastic leukemia.
  • Those most often associated with AIHA include chronic lymphocytic leukemia, B-cell lymphomas, and Burkitt-type acute lymphoblastic leukemia (ALL) and are clonal populations of mature B cells.
  • There have been no reports of patients with B-cell precursor ALL who developed AIHA while undergoing chemotherapy, but AIHA has been reported in a few patients with ALL after hematopoietic stem cell transplant.
  • The authors describe a child with B-cell precursor ALL who developed cold agglutinin AIHA during maintenance treatment while in remission after infection with influenza B.
  • [MeSH-major] Agglutinins. Anemia, Hemolytic / chemically induced. Anemia, Hemolytic, Autoimmune / etiology. Antineoplastic Combined Chemotherapy Protocols / adverse effects. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • (PMID = 16012332.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Agglutinins; 0 / Autoantibodies; 0 / Cryoglobulins; 0 / cold agglutinins
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21. Derwich K, Sedek L, Meyer C, Pieczonka A, Dawidowska M, Gaworczyk A, Wachowiak J, Konatkowska B, Witt M, Marschalek R, Szczepański T: Infant acute bilineal leukemia. Leuk Res; 2009 Jul;33(7):1005-8
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  • [Title] Infant acute bilineal leukemia.
  • Most cases of acute leukemia can be assigned to the myeloid, B or T lineage.
  • There are rare cases of acute leukemia, which cannot be clearly classified, because either blasts express antigens of more than one lineage (acute biphenotypic leukemias) or distinct blast populations of two lineages co-exist (acute bilineal leukemias, aBLL).
  • We present a 10-month-old infant with de novo aBLL, characterized by blasts of monocytic and B-cell precursor lineages.
  • Despite poor initial response, both to acute lymphoblastic leukemia (ALL) induction treatment and acute myeloid leukemia induction blocks, the child reached complete clinical remission with minimal residual disease negative status and was transplanted.
  • This case report illustrates that aBLL is a very aggressive type of acute leukemia that should be individually treated and monitored, particularly in children less than 1 year of age.
  • [MeSH-major] B-Lymphocytes / pathology. Leukemia, Biphenotypic, Acute / diagnosis. Leukemia, Myeloid, Acute / diagnosis. Neoplasm, Residual / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis
  • [MeSH-minor] Cell Lineage. Hematopoietic Stem Cell Transplantation. Humans. Infant. Male. Remission Induction. Treatment Outcome

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  • (PMID = 19286255.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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22. Luo SD, Wu Y, Chen JH, Liu HK, Chen YZ: [Gene expression profile of human TGF-beta signal transduction pathway of B cell type acute lymphocytic leukemia]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2008 Aug;16(4):742-5
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  • [Title] [Gene expression profile of human TGF-beta signal transduction pathway of B cell type acute lymphocytic leukemia].
  • This study was aimed to investigate the gene expression profile of TGF-beta signal transduction pathway in B-cell type acute lymphocytic leukemia (B-ALL).
  • The gene expression profiles in B-ALL primary cells and cell lines (NALM6 cells, Raji cells), B-lymphocyte of control were detected by cDNA microarray including 113 different genes in human TGF-beta/BMP signal transduction pathway, and TGF-beta(1) mRNA expression was detected by real time RT-PCR.
  • The B lymphocytes in peripheral blood of heacthy persons sorted by flow cytometry were used as control.
  • The results showed that as compared with B lymphocytes in peripheral blood of heacthy persons, the TGF-beta(1) expression in B-ALL cells, NALM6 cells and Raji cells were down-regulationed, myc and smad1 gene expressions were up-regulated, IL-6, smad 7 gene expressions were down-regulated.
  • It is concluded that TGF-beta signal transduction is abnormal in B-cell type acute lymphocytic leukemia.

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  • (PMID = 18718051.001).
  • [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 / RNA, Messenger; 0 / Transforming Growth Factor beta
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23. Li LX, Tang YM, Gu WZ, Tang HF, Qian BQ, Shen HQ, Luo CF: [Establishment of animal model with B lineage acute leukemia in nude mice for evaluation of new therapeutic agents]. Zhejiang Da Xue Xue Bao Yi Xue Ban; 2008 Sep;37(5):511-4
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  • [Title] [Establishment of animal model with B lineage acute leukemia in nude mice for evaluation of new therapeutic agents].
  • OBJECTIVE: To establish an acute leukemia animal model for testing new therapeutic agents in vivo.
  • METHODS: Nude mice were intraperitoneally injected with 2 mg cyclophosphamide, 24 h later 5 x 10(6) acute B-cell leukemia Nalm-6 cells was inoculated via the tail vein, then monitored daily.
  • CONCLUSION: B lineage acute leukemia animal model has been successfully established in the nude mice, which is suitable for testing new therapeutic agents.
  • [MeSH-major] Disease Models, Animal. Precursor Cell Lymphoblastic Leukemia-Lymphoma

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  • (PMID = 18925721.001).
  • [ISSN] 1008-9292
  • [Journal-full-title] Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences
  • [ISO-abbreviation] Zhejiang 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] 8N3DW7272P / Cyclophosphamide
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24. Hatakeyama N, Tamura Y, Sahara H, Suzuki N, Suzuki K, Hori T, Mizue N, Torigoe T, Tsutsumi H, Sato N: Induction of autologous CD4- and CD8-mediated T-cell responses against acute lymphocytic leukemia cell line using apoptotic tumor cell-loaded dendritic cells. Exp Hematol; 2006 Feb;34(2):197-207
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  • [Title] Induction of autologous CD4- and CD8-mediated T-cell responses against acute lymphocytic leukemia cell line using apoptotic tumor cell-loaded dendritic cells.
  • OBJECTIVE: Several studies have demonstrated that dendritic cells (DCs) pulsed with tumor lysate or apoptotic tumor cells can elicit effective T-cell responses.
  • We applied this approach to induce HLA class I- and class II-restricted T-cell responses directed against autologous acute lymphocytic leukemia (B-ALL) cell line NH-1.
  • METHODS: Autologous T cells were stimulated by apoptotic tumor cell-loaded DCs generated from a patient with ALL.
  • The stimulated and expanded T cells were isolated into CD8(+) T-cell line and CD4(+) T-cell line, and each of them was examined as to their functions.
  • RESULTS: Both CD8(+) and CD4(+) T-cell lines demonstrated cytotoxicity against NH-1 in an major histocompatibility complex-dependent manner.
  • Finally, we established two independent CD4(+) T-cell clones restricted to HLA-DR.
  • The CD4(+) T-cell line responded strongly to autologous Epstein-Barr virus-transformed lymphoblastoid cell lines (EBV-LCL) but not to autologous normal cells.
  • Furthermore, the T-cell clones also responded to allogeneic EBV-LCLs and B-ALL cell lines in the context of the HLA-DRB1( *)04051 molecule.
  • Interestingly, 293T and COS-7 cells, which had been transfected with the HLA-DRB1( *)04051, were also recognized by T-cell clones.
  • [MeSH-major] CD4-Positive T-Lymphocytes / immunology. CD8-Positive T-Lymphocytes / immunology. Cell Fusion. Dendritic Cells / immunology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology
  • [MeSH-minor] Apoptosis / immunology. Cell Line, Tumor. Cytotoxicity Tests, Immunologic. Epitopes / immunology. Epstein-Barr Virus Nuclear Antigens / immunology. Female. HLA-DR Antigens / classification. HLA-DR Antigens / immunology. Histocompatibility Antigens Class II / immunology. Histocompatibility Antigens Class II / pharmacology. Humans. Infant. Lymphocyte Activation

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  • (PMID = 16459188.001).
  • [ISSN] 0301-472X
  • [Journal-full-title] Experimental hematology
  • [ISO-abbreviation] Exp. Hematol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Epitopes; 0 / Epstein-Barr Virus Nuclear Antigens; 0 / HLA-DR Antigens; 0 / Histocompatibility Antigens Class II
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25. Batinić D, Dubravcić K, Rajić L, Mikulić M, Labar B: [Biphenotypic and bilineal acute leukemias]. Acta Med Croatica; 2008 Oct;62(4):387-90
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  • [Title] [Biphenotypic and bilineal acute leukemias].
  • Human acute leukemias (AL) are classified as myeloid or lymphoid according to cytomorphology and the expression of leukocyte differentiation antigens/CD-markers.
  • However, in the minority of cases leukemic cells express markers of more than one lineage, which has led to the introduction of a new subgroup of acute leukemias termed mixed or biphenotypic acute leukemias (BAL).
  • In an effort to distinguish between BAL and those AL with aberrant expression of markers of other lineage, the European Group for the Immunological Characterization of Acute Leukemias (EGIL) has proposed a scoring system in which CD-markers are assigned a score of 0.5, 1.0 or 2.0, depending on the specificity of a particular antigen for myeloid, B- and/or T-lymphoid lineage, respectively.
  • In addition to BAL in which a single cell population expresses both myeloid and lymphoid differentiation markers, this new group of leukemias also comprises cases that present with two separate blast populations (acute bilineal leukemia, aBLL).
  • In general, BAL accounts for less than 5% of all AL cases, whereas aBLL is a rare disease constituting 1%-2% of AL cases that contains B- or T-lymphoid along with myeloid blasts.
  • Unfortunately, optimal therapy is not known, although regimens designed for acute lymphoblastic leukemia may result in a better response rate.
  • [MeSH-major] Leukemia, Biphenotypic, Acute

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  • (PMID = 19209464.001).
  • [ISSN] 1330-0164
  • [Journal-full-title] Acta medica Croatica : c̆asopis Hravatske akademije medicinskih znanosti
  • [ISO-abbreviation] Acta Med Croatica
  • [Language] hrv
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Croatia
  • [Number-of-references] 30
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26. Takenokuchi M, Saigo K, Nakamachi Y, Kawano S, Hashimoto M, Fujioka T, Koizumi T, Tatsumi E, Kumagai S: Troglitazone inhibits cell growth and induces apoptosis of B-cell acute lymphoblastic leukemia cells with t(14;18). Acta Haematol; 2006;116(1):30-40
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  • [Title] Troglitazone inhibits cell growth and induces apoptosis of B-cell acute lymphoblastic leukemia cells with t(14;18).
  • Peroxisome proliferator-activated receptor-gamma (PPARgamma), a member of the nuclear receptor superfamily, has been detected in several human leukemia cells.
  • Recent studies reported that PPARgamma ligands inhibit cell proliferation and induce apoptosis in both normal and malignant B-lineage cells.
  • We investigated the expression of PPARgamma and the effects of PPARgamma ligands on UTree-O2, Bay91 and 380, three B-cell acute lymphoblastic leukemia (B-ALL) cell lines with t(14;18), which show a poor prognosis, accompanying c-myc abnormality.
  • Western blot analysis identified expression of PPARgamma protein and real-time PCR that of PPARgamma mRNA on the three cell lines.
  • Troglitazone (TGZ), a synthetic PPARgamma ligand, inhibited cell growth in these cell lines in a dose-dependent manner, which was associated with G(1) cell cycle arrest and apoptosis.
  • We assessed the expression of c-myc, an apoptosis-regulatory gene, since c-myc abnormality was detected in most B-ALL cells with t(14;18).
  • TGZ was found to dose-dependently downregulate the expression of c-myc mRNA and c-myc protein in the three cell lines.
  • These results suggest that TGZ inhibits cell growth via induction of G(1) cell cycle arrest and apoptosis in these cell lines and that TGZ-induced apoptosis, at least in part, may be related to the downregulation of c-myc expression.
  • Moreover, the downregulation of c-myc expression by TGZ may depend on a PPARgamma-independent mechanism.
  • [MeSH-minor] Adolescent. Adult. Aged. Apoptosis / drug effects. Blotting, Western. Cell Line, Tumor. Dose-Response Relationship, Drug. Down-Regulation / drug effects. Female. Gene Expression Regulation, Leukemic / drug effects. Humans. Ligands. Male. Prognosis. Proto-Oncogene Proteins c-myc / biosynthesis. Reverse Transcriptase Polymerase Chain Reaction


27. Han X, Bueso-Ramos CE: Precursor T-cell acute lymphoblastic leukemia/lymphoblastic lymphoma and acute biphenotypic leukemias. Am J Clin Pathol; 2007 Apr;127(4):528-44
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  • [Title] Precursor T-cell acute lymphoblastic leukemia/lymphoblastic lymphoma and acute biphenotypic leukemias.
  • Session 4 of the 2005 Society of Hematopathology/European Association for Haematopathology Workshop focused on case presentations of precursor T-cell acute lymphoblastic leukemia/lymphoblastic lymphoma (pre-T ALL/LBL) and acute biphenotypic leukemia.
  • Acute biphenotypic leukemias are characterized by a single population of blasts that express myeloid, T- or B-lineage antigens in various combinations and account for fewer than 4% of all acute leukemias.
  • An accurate diagnosis of pre-T ALL/LBL and acute biphenotypic leukemia requires a multiparametric approach, including examination of morphologic features, immunophenotype, clinical characteristics, and cytogenetic and molecular findings.
  • [MeSH-major] Biomarkers, Tumor / analysis. Leukemia, Lymphoid / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis


28. Mantadakis E, Danilatou V, Stiakaki E, Paterakis G, Papadhimitriou S, Kalmanti M: T-cell acute lymphoblastic leukemia relapsing as acute myelogenous leukemia. Pediatr Blood Cancer; 2007 Mar;48(3):354-7
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  • [Title] T-cell acute lymphoblastic leukemia relapsing as acute myelogenous leukemia.
  • We present the unusual case of a 16-year-old girl with T-cell acute lymphoblastic leukemia (ALL) with an early thymocyte immunophenotype without myeloid markers, who after 13 months of complete hematological remission relapsed as acute myelogenous leukemia (AML) with minimal differentiation and died of her disease.
  • Whether the AML represented a relapse with lineage switch of the original immature T-cell clone or a new secondary malignancy, could not be proven due to the absence of molecular or clonal markers.
  • This report suggests that a subset of CD7+ T-cell leukemias without mature T-cell antigens (CD4-, CD8-) are minimally differentiated and can relapse as AML.
  • [MeSH-major] Antigens, Differentiation, T-Lymphocyte / analysis. Antigens, Neoplasm / analysis. Leukemia, Myeloid / pathology. Leukemia-Lymphoma, Adult T-Cell / pathology. Neoplastic Stem Cells / pathology. T-Lymphocyte Subsets / pathology
  • [MeSH-minor] 6-Mercaptopurine / administration & dosage. Acute Disease. Adolescent. Antigens, CD7 / analysis. Antineoplastic Combined Chemotherapy Protocols / adverse effects. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Asparaginase / administration & dosage. Bone Marrow / pathology. Cell Differentiation. Cell Lineage. Core Binding Factor Alpha 2 Subunit / genetics. Cyclophosphamide / administration & dosage. Cytarabine / administration & dosage. Daunorubicin / administration & dosage. Dexamethasone / administration & dosage. Diagnosis, Differential. Doxorubicin / administration & dosage. Etoposide / administration & dosage. Etoposide / adverse effects. Fatal Outcome. Female. Gene Dosage. Histone-Lysine N-Methyltransferase. Humans. Immunophenotyping. Karyotyping. Methotrexate / administration & dosage. Myeloid-Lymphoid Leukemia Protein / genetics. Neoplasms, Second Primary / diagnosis. Proto-Oncogenes. Recurrence. Vincristine / administration & dosage

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  • Hazardous Substances Data Bank. CYTARABINE .
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  • [Copyright] (c) 2006 Wiley-Liss, Inc.
  • (PMID = 16206214.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD7; 0 / Antigens, Differentiation, T-Lymphocyte; 0 / Antigens, Neoplasm; 0 / Core Binding Factor Alpha 2 Subunit; 0 / MLL protein, human; 0 / RUNX1 protein, human; 04079A1RDZ / Cytarabine; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; 5J49Q6B70F / Vincristine; 6PLQ3CP4P3 / Etoposide; 7S5I7G3JQL / Dexamethasone; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; E7WED276I5 / 6-Mercaptopurine; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; EC 3.5.1.1 / Asparaginase; YL5FZ2Y5U1 / Methotrexate; ZS7284E0ZP / Daunorubicin
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29. 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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30. Rubnitz JE, Gibson B, Smith FO: Acute myeloid leukemia. Hematol Oncol Clin North Am; 2010 Feb;24(1):35-63
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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] Leukemia, Myeloid, Acute
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Central Nervous System Neoplasms. Child. Clone Cells / pathology. Hematopoietic Stem Cell Transplantation. Humans. Treatment Outcome

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  • [Copyright] Copyright (c) 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20113895.001).
  • [ISSN] 1558-1977
  • [Journal-full-title] Hematology/oncology clinics of North America
  • [ISO-abbreviation] Hematol. Oncol. 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 / Antineoplastic Agents
  • [Number-of-references] 229
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31. Sucić M, Batinić D, Zadro R, Mrsić S, Labar B: [Cytomorphology of acute mixed leukemia]. Acta Med Croatica; 2008 Oct;62(4):379-85
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  • [Title] [Cytomorphology of acute mixed leukemia].
  • [Transliterated title] Citomorfologija akutnih mjesovitih leukemija.
  • Biphenotypic acute leukemias (AL) with blasts expressing both myeloid and lymphoid antigens are grouped with undifferentiated AL and bilineal AL in the group of AL of ambiguous lineage.
  • RESULTS AND DISCUSSION: In the group of 169 adult AL patients, 116 were cytomorphologically classified as acute myeloblastic leukemias (AML), 35 as acute lymphoblastic leukemias (ALL) and 18 as acute undifferentiated leukemias (ANLM).
  • These observations are consistent with other studies and WHO determinations indicating that the majority of true biphenotypic leukemias are associated with immature monoblastic or myeloid cytomorphology or with lymphoid or undifferentiated characteristics, but may also express any AML cytomorphology type.
  • Thus, there is no direct correlation of leukemic cell cytomorphology and biphenotypic AL immunophenotype.
  • [MeSH-major] Leukemia, Biphenotypic, Acute / pathology
  • [MeSH-minor] Acute Disease. Humans. Immunophenotyping. Leukemia, Myeloid, Acute / classification. Leukemia, Myeloid, Acute / immunology. Leukemia, Myeloid, Acute / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / classification. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology

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  • (PMID = 19205415.001).
  • [ISSN] 1330-0164
  • [Journal-full-title] Acta medica Croatica : c̆asopis Hravatske akademije medicinskih znanosti
  • [ISO-abbreviation] Acta Med Croatica
  • [Language] hrv
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Croatia
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32. Chunsong H, Yuling H, Li W, Jie X, Gang Z, Qiuping Z, Qingping G, Kejian Z, Li Q, Chang AE, Youxin J, Jinquan T: CXC chemokine ligand 13 and CC chemokine ligand 19 cooperatively render resistance to apoptosis in B cell lineage acute and chronic lymphocytic leukemia CD23+CD5+ B cells. J Immunol; 2006 Nov 15;177(10):6713-22
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  • [Title] CXC chemokine ligand 13 and CC chemokine ligand 19 cooperatively render resistance to apoptosis in B cell lineage acute and chronic lymphocytic leukemia CD23+CD5+ B cells.
  • We have investigated expression and functions of CXCL13/CXCR5 and CCL19/CCR7 in CD23+CD5+ and CD23+CD5- B cells from cord blood (CB) and patients with B cell lineage acute or chronic lymphocytic leukemia (B-ALL or B-CLL).
  • Therefore, we suggest that normal lymphocytes, especially naive B and T cells, use CXCL13/CXCR5 and CCL19/CCR7 for migration, homing, maturation, and cell homeostasis as well as secondary lymphoid tissues organogenesis.
  • [MeSH-major] Apoptosis / immunology. B-Lymphocyte Subsets / immunology. B-Lymphocyte Subsets / metabolism. Burkitt Lymphoma / immunology. Chemokines, CC / physiology. Chemokines, CXC / physiology. Leukemia, Lymphocytic, Chronic, B-Cell / immunology
  • [MeSH-minor] Antigens, CD5 / biosynthesis. Cell Lineage / immunology. Chemokine CCL19. Chemokine CXCL13. Fetal Blood / cytology. Fetal Blood / immunology. Fetal Blood / metabolism. Humans. Lymphocyte Count. Proteins / metabolism. Proteins / physiology. Receptors, CCR7. Receptors, CXCR5. Receptors, Chemokine / biosynthesis. Receptors, IgE / biosynthesis

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  • (PMID = 17082584.001).
  • [ISSN] 0022-1767
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD5; 0 / CCL19 protein, human; 0 / CCR7 protein, human; 0 / CXCL13 protein, human; 0 / CXCR5 protein, human; 0 / Chemokine CCL19; 0 / Chemokine CXCL13; 0 / Chemokines, CC; 0 / Chemokines, CXC; 0 / PEG10 protein, human; 0 / Proteins; 0 / Receptors, CCR7; 0 / Receptors, CXCR5; 0 / Receptors, Chemokine; 0 / Receptors, IgE
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33. Vallera DA, Oh S, Chen H, Shu Y, Frankel AE: Bioengineering a unique deimmunized bispecific targeted toxin that simultaneously recognizes human CD22 and CD19 receptors in a mouse model of B-cell metastases. Mol Cancer Ther; 2010 Jun;9(6):1872-83
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  • [Title] Bioengineering a unique deimmunized bispecific targeted toxin that simultaneously recognizes human CD22 and CD19 receptors in a mouse model of B-cell metastases.
  • The aims were to reduce toxin immunogenicity using mutagenesis, measure the ability of mutated drug to elicit antitoxin antibody responses, and show that mutated drug was effective against systemic B-cell lymphoma in vivo.
  • Site-specific mutagenesis was used to mutate amino acids in seven key epitopic toxin regions that dictate B-cell generation of neutralizing antitoxin antibodies.
  • Finally, a powerful genetically altered luciferase xenograft model was used that could be imaged in real time to determine the effect on systemic malignant human B-cell lymphoma, Raji-luc.
  • Patient B-lineage acute lymphoblastic leukemia, B-cell chronic lymphocytic leukemia, and B lymphoma were high in CD22 and CD19 expression.

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  • (PMID = 20530709.001).
  • [ISSN] 1538-8514
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA108637; United States / NCI NIH HHS / CA / R01 CA082154; United States / NCI NIH HHS / CA / CA036725-25; United States / NCI NIH HHS / CA / CA108637-05; United States / NCI NIH HHS / CA / R01 CA036725; United States / NCI NIH HHS / CA / R01-CA36725; United States / NCI NIH HHS / CA / R01-CA082154; United States / NCI NIH HHS / CA / R01 CA108637-05; United States / NCI NIH HHS / CA / R01 CA036725-25
  • [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 / Antibodies, Bispecific; 0 / Antigens, CD19; 0 / Bacterial Toxins; 0 / Exotoxins; 0 / Sialic Acid Binding Ig-like Lectin 2; 0 / Virulence Factors; EC 2.4.2.- / ADP Ribose Transferases; EC 2.4.2.31 / toxA protein, Pseudomonas aeruginosa
  • [Other-IDs] NLM/ NIHMS198461; NLM/ PMC2884080
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34. Kazemi T, Asgarian-Omran H, Memarian A, Shabani M, Sharifian RA, Vossough P, Ansaripour B, Rabbani H, Shokri F: Low representation of Fc receptor-like 1-5 molecules in leukemic cells from Iranian patients with acute lymphoblastic leukemia. Cancer Immunol Immunother; 2009 Jun;58(6):989-96
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  • [Title] Low representation of Fc receptor-like 1-5 molecules in leukemic cells from Iranian patients with acute lymphoblastic leukemia.
  • Recent studies have demonstrated expression of Fc receptor-like (FCRL) molecules, a newly identified family with preferential B-cell lineage expression, in some chronic B-cell leukemias with possible implication for classification and/or targeted immunotherapy.
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Receptors, Cell Surface / genetics. Receptors, Fc / genetics. Receptors, Immunologic / genetics

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  • (PMID = 18802695.001).
  • [ISSN] 1432-0851
  • [Journal-full-title] Cancer immunology, immunotherapy : CII
  • [ISO-abbreviation] Cancer Immunol. Immunother.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / FCRL2 protein, human; 0 / FCRL4 protein, human; 0 / FCRL5 protein, human; 0 / FCRLA protein, human; 0 / Receptors, Cell Surface; 0 / Receptors, Fc; 0 / Receptors, Immunologic
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35. Zhang X, Wang M, Zhou C, Chen S, Wang J: The expression of iASPP in acute leukemias. Leuk Res; 2005 Feb;29(2):179-83
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  • [Title] The expression of iASPP in acute leukemias.
  • To examine the role of iASPP in acute leukemia (AL), we analyzed iASPP mRNA expression in AL by semi-quantitative reverse transcriptase polymerase chain reaction (RT-PCR).
  • There was no significant difference between acute lymphocytic leukemia (ALL) cells and acute myeloid leukemia (AML) cells (P = 0.593).
  • The expression level of iASPP gene and its overexpression in M3 and M4EO were significantly lower than in other subtypes of AML.
  • However, iASPP gene expression in AL cells was not associated with gender, age, initial white blood cell count or p53 type, but was associated with CD34 expression.
  • The results of the present study suggest that iASPP gene overexpression may play an important role in the leukemogenesis and/or disease progression of AL.
  • [MeSH-major] Gene Expression Regulation, Leukemic. Intracellular Signaling Peptides and Proteins / genetics. Leukemia, Myeloid, Acute / genetics. RNA, Messenger / genetics
  • [MeSH-minor] Adolescent. Adult. Cell Line, Tumor. Female. Humans. Male. Mutation. Repressor Proteins. Reverse Transcriptase Polymerase Chain Reaction / methods. Tumor Suppressor Protein p53 / antagonists & inhibitors. Tumor Suppressor Protein p53 / genetics. Tumor Suppressor Protein p53 / metabolism. Up-Regulation

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  • (PMID = 15607367.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Intracellular Signaling Peptides and Proteins; 0 / PPP1R13L protein, human; 0 / RNA, Messenger; 0 / Repressor Proteins; 0 / Tumor Suppressor Protein p53
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36. Haferlach T, Kern W, Schnittger S, Schoch C: Modern diagnostics in acute leukemias. Crit Rev Oncol Hematol; 2005 Nov;56(2):223-34
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Modern diagnostics in acute leukemias.
  • Acute leukemias are a heterogeneous group of diseases.
  • Improvements in patient's treatment resulting in better survival rates are closely linked to the biological understanding of the disease subtypes, which is assessed by specific diagnostic approaches.
  • Furthermore they are also needed for follow up studies focusing especially on minimal residual disease (MRD) to guide further treatment decisions based on the response of the disease to given treatment protocols.
  • Only by using a comprehensive diagnostic panel including cytomorphology, cytochemistry, multiparameter flow cytometry (MFC), cytogenetics, fluorescence in situ hybridization (FISH) and molecular genetic methods the correct diagnosis in acute leukemias can be established today.
  • [MeSH-major] Biomarkers, Tumor. Leukemia, Myeloid, Acute / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis

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  • (PMID = 16213152.001).
  • [ISSN] 1040-8428
  • [Journal-full-title] Critical reviews in oncology/hematology
  • [ISO-abbreviation] Crit. Rev. Oncol. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Number-of-references] 70
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37. Wu HJ, Chen Y: [Biological characteristics of hyperleukocytic acute leukemia]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2006 Jun;14(3):450-4
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  • [Title] [Biological characteristics of hyperleukocytic acute leukemia].
  • The study was to investigate the biological characteristics of hyperleucocyte acute leukemia (HAL) and its clinical significance.
  • In AML, monocytic leukemia is easier to become into HAL than other leukemias.
  • In ALL, T-lineage antigens of HAL group are more easily expressed than those of NHAL group; the leukemia cells of HAL group are naiver than those of NHAL group, meanwhile the prognosis of HAL is poor.

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  • (PMID = 16800918.001).
  • [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, CD14; 0 / Antigens, CD79; 0 / Antigens, CD8; 0 / Sialic Acid Binding Ig-like Lectin 2
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38. Bastida Vilá P, Palacio García C, Solsona Riera M, Ortega Aramburu JJ, Sánchez de Toledo Codina J: [Minimal residual disease in acute lymphoblastic leukemia: a new concept of complete remission]. An Pediatr (Barc); 2005 Nov;63(5):390-5
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  • [Title] [Minimal residual disease in acute lymphoblastic leukemia: a new concept of complete remission].
  • [Transliterated title] Leucemia mínima residual: nuevo concepto de remisión completa.
  • INTRODUCTION: Early response to induction treatment is one of the most important prognostic factors in children with acute lymphoblastic leukemia (ALL).
  • More sensitive techniques are required to measure residual leukemia and establish a new definition of complete remission.
  • OBJECTIVE: To identify minimal residual disease (MRD) by immunological techniques and define its prognostic impact in children with ALL.
  • All the children achieved complete cytological remission (< 5 %) with the induction treatment and had at least one useful phenotype for follow-up: 11 % were T phenotype, one was biphenotypic and the remainder were B cell leukemias.
  • Continued sequential monitoring may predict recurrence before the onset of clinical or hematologic manifestations.
  • [MeSH-major] Neoplasm, Residual / epidemiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / epidemiology

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  • (PMID = 16266612.001).
  • [ISSN] 1695-4033
  • [Journal-full-title] Anales de pediatría (Barcelona, Spain : 2003)
  • [ISO-abbreviation] An Pediatr (Barc)
  • [Language] spa
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Spain
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39. Scandura JM: Advances in the molecular genetics of acute leukemia. Curr Oncol Rep; 2005 Sep;7(5):323-32
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Advances in the molecular genetics of acute leukemia.
  • Acute leukemias are characterized by the unrestrained clonal proliferation of hematopoietic precursor cells coupled with aberrant or arrested differentiation.
  • The molecular basis of hematopoiesis and leukemogenesis is still being defined, yet it is increasingly evident that acute leukemias have recurrent molecular features that can be exploited for diagnostic, prognostic, and therapeutic purposes.
  • Modern molecular technologies already influence treatment strategies for these diseases, and it is likely that as such technology matures it will have an increasing impact on all aspects of acute leukemia management.
  • This article reviews recent developments in the molecular classification, prognostication, and treatment of the acute leukemias.
  • [MeSH-major] Gene Expression Regulation, Neoplastic. Leukemia / genetics
  • [MeSH-minor] Cell Line, Tumor. Epigenesis, Genetic. Humans. Immunophenotyping. Karyotyping. Medical Oncology / trends. Mutation. Nucleic Acid Hybridization. Oligonucleotide Array Sequence Analysis. Pharmacogenetics / methods. Phenotype. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Prognosis. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Translocation, Genetic

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  • (PMID = 16091192.001).
  • [ISSN] 1523-3790
  • [Journal-full-title] Current oncology reports
  • [ISO-abbreviation] Curr Oncol Rep
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Messenger
  • [Number-of-references] 50
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40. Suriya OM, Aleem A: Frank hematuria as the presentation feature of acute leukemia. Saudi J Kidney Dis Transpl; 2010 Sep;21(5):940-2
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  • [Title] Frank hematuria as the presentation feature of acute leukemia.
  • Muco-cutaneous bleeding is a common presenting feature of acute leukemias.
  • Hematuria as an isolated or main presenting feature of acute leukemia is rare.
  • We describe two cases of acute leukemia, a 19 year old male with acute lymphoblastic leukemia and a 52 year old male with acute myeloid leukemia, both presenting with gross hematuria.
  • Our cases highlight that hematuria should be remembered as a rare presenting feature of acute leukemia.
  • [MeSH-major] Hematuria / etiology. Leukemia, Myeloid, Acute / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis
  • [MeSH-minor] Blood Cell Count. Bone Marrow Examination. Fatal Outcome. Humans. Leukocyte Count. Male. Middle Aged. Thrombocytopenia / etiology. Treatment Outcome. Young Adult

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  • [CommentIn] Saudi J Kidney Dis Transpl. 2012 Sep;23(5):1088-9 [22982933.001]
  • (PMID = 20814137.001).
  • [ISSN] 1319-2442
  • [Journal-full-title] Saudi journal of kidney diseases and transplantation : an official publication of the Saudi Center for Organ Transplantation, Saudi Arabia
  • [ISO-abbreviation] Saudi J Kidney Dis Transpl
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Saudi Arabia
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41. Hu SY, Gu WY, Chen ZX, Wang XL, Cen JN, He HL, Chai YH, Chen CS: The significance of detecting WT1 expression in childhood acute leukemias. Pediatr Hematol Oncol; 2010 Nov;27(8):581-91
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The significance of detecting WT1 expression in childhood acute leukemias.
  • WT1 (Wilms' tumor gene 1) overexpression is implicated in the prognosis of acute leukemia.
  • The purpose of this study was to investigate WT1 expression and its clinical implication in childhood acute leukemia (AL) in Chinese population.
  • Bone marrow specimen from 200 children at different stages of acute leukemia and from 21 children without leukemia were studied.
  • The WT1 expression at diagnostic marrow specimen in both acute myeloid leukemia (AML) and acute lymphoid leukemia (ALL) was higher than control group, whereas WT1 expression in AML was higher than in ALL, and WT1 expression level in relapse in ALL increased more significantly than in AML.
  • The WT1 expression level showed positive correlation with the hypodiploidy and BCR-ABL fusion gene in acute leukemia.
  • A rapidly decrease of WT1 expression level predicted a good response to the induction therapy and low expression of WT1 correlates with remission status.
  • This study suggested that WT1 expression levels in acute leukemia can potentially be a marker for evaluating therapeutic efficacy, correlating with monitoring minimal residue disease, and predicting hematological relapse in children acute leukemia.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. WT1 Proteins / genetics

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  • (PMID = 20863155.001).
  • [ISSN] 1521-0669
  • [Journal-full-title] Pediatric hematology and oncology
  • [ISO-abbreviation] Pediatr Hematol Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / WT1 Proteins; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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42. Wang ZY, Chen QS: [Present status in studying immunotherapy for acute leukemia and its perspective--Editorial]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2005 Apr;13(2):169-73
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  • [Title] [Present status in studying immunotherapy for acute leukemia and its perspective--Editorial].
  • One of the important approaches for further prolonging remission duration and eradicating minimal residual disease in acute leukemia is immunotherapy.
  • Four kinds of immunotherapy for acute leukemia are under investigation:.
  • (1) monoclonal antibodies, among them, Mylotarg (cytotoxic antibiotic calicheamicin linked to CD33 Mab) is given for the treatment of refractory or relapsed acute myeloid leukemia and molecular relapse in acute promyelocytic leukemia with good results, Campath-1H (antiCD52 Mab) is administered in the treatment of prolymphocytic leukemia and Rituximab (anti-CD20 Mab) in B-PLL with high complete remission rates.
  • Other Mabs under preclinical and clinical trials include anti-IL-2 receptor Mab for the treatment of acute T lymphocytic leukemia, anti-220 kD Mab-6G7 for acute leukemias, recombinant immune toxin BL22 (anti-CD22) for hairy cell leukemia and Mabs labeled with radio-isotopes for different types of acute leukemias;.
  • (2) adoptive cellular immunotherapy using cytokine-induced killer cell, alloreactive NK cells, allogeneic or autologous leukemic-specific CD8(+) cytotoxic T lymphocytes, and other immune effector cells;.
  • (4) leukemia vaccines of several different formulations including antigen-specific, leukemia cell-based, leukemia antigen-pulsed dendritic cell (DC) and leukemia-derived DC vaccines, the latter two formulations are more attractive.
  • In conclusion, up to now, the most effective example of immunotherapy in acute leukemia is provided by the administration of Mabs, and the majority of other approaches in immunotherapy for acute leukemia although promising, need further studies.

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  • (PMID = 15854271.001).
  • [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] Editorial; English Abstract
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Cancer Vaccines
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43. 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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44. Bacher U, Schnittger S, Haferlach C, Haferlach T: Molecular diagnostics in acute leukemias. Clin Chem Lab Med; 2009;47(11):1333-41
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  • [Title] Molecular diagnostics in acute leukemias.
  • Acute myeloid leukemia (AML) and acute lymphoblastic leukemia (ALL) both represent highly heterogeneous entities on the basis of diverse cyto- and molecular genetic alterations with considerable influence on prognosis and therapeutic decisions.
  • Thus, molecular analysis based on various techniques, such as polymerase chain reaction (PCR) has become an essential part of the diagnostic panel for acute leukemia.
  • During the course of disease, the residual leukemic cell load can be monitored by highly sensitive quantitative PCR techniques ("real-time PCR").
  • This demonstrates that molecular diagnostics for acute leukemias are in continuous development.
  • This review summarizes the most important recurrent molecular markers seen in acute leukemias, their role in prognosis and therapy and provides an overview on the relevant PCR techniques.

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  • (PMID = 19817644.001).
  • [ISSN] 1437-4331
  • [Journal-full-title] Clinical chemistry and laboratory medicine
  • [ISO-abbreviation] Clin. Chem. Lab. Med.
  • [Language] ENG
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Number-of-references] 78
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45. Mi S, Lu J, Sun M, Li Z, Zhang H, Neilly MB, Wang Y, Qian Z, Jin J, Zhang Y, Bohlander SK, Le Beau MM, Larson RA, Golub TR, Rowley JD, Chen J: MicroRNA expression signatures accurately discriminate acute lymphoblastic leukemia from acute myeloid leukemia. Proc Natl Acad Sci U S A; 2007 Dec 11;104(50):19971-6
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  • [Title] MicroRNA expression signatures accurately discriminate acute lymphoblastic leukemia from acute myeloid leukemia.
  • Acute lymphoblastic leukemia (ALL) is the most common childhood cancer, whereas acute myeloid leukemia (AML) is the most common acute leukemia in adults.
  • Using the expression signatures of a minimum of two of these miRNAs resulted in an accuracy rate of >95% in the diagnosis of ALL and AML.
  • The differential expression patterns of these four miRNAs were validated further through large-scale real-time PCR on 98 acute leukemia samples covering most of the common cytogenetic subtypes, along with 10 normal control samples.
  • Taken together, we showed that expression signatures of as few as two miRNAs could accurately discriminate ALL from AML, and that epigenetic regulation might play an important role in the regulation of expression of miRNAs in acute leukemias.

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  • (PMID = 18056805.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA040046; United States / NCI NIH HHS / CA / CA40046
  • [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 / MicroRNAs; 9007-49-2 / DNA
  • [Other-IDs] NLM/ PMC2148407
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46. Pogorelov VM, Diagileva OA, Lugovskaia SA, Kozinets GI: [Principles and potentialities of the standardization of morphocytochemical diagnosis of acute leukemias]. Klin Lab Diagn; 2006 Jul;(7):20-2, 35-8
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  • [Title] [Principles and potentialities of the standardization of morphocytochemical diagnosis of acute leukemias].
  • Under the present conditions, the competitive capacity of a health care facility is provided by the high level and timeliness of diagnosis of disease.
  • The diagnosis of the types of acute leukemia (AL) may be accomplished immunologically, by using a 33-marker panel and without consideration of the morphocytochemical parameters of blast cells.
  • Moreover, morphocytochemical data more exactly define the stages of blast cell differentiation than does the immunological phenotype.
  • Only M0, M6, and M7 forms of leukemia require compulsory blast cell phenotyping, particularly in the differential diagnosis of acute myeloid leukemia and acute lymphoblastic leukemia.
  • Search for new markers of leukemia cells, including lesions at the chromosomal or molecular levels, is under way.
  • Some of them are only of theoretical value while other markers have been already used by hematologists to diagnose leukemia.
  • Standardization in this essence is the self-assessment of a facility and reference comparison, which are based on the principles of its orientation to the patient, the adjusted system for controlling the quality of health care that is up to the world standards rather than the compliance with the state-regulated standard.
  • The present paper discusses the ways of establishing the uniform rates and requirements for the morphocytochemical diagnosis of acute leukemias.
  • [MeSH-major] Biomarkers, Tumor / analysis. Blast Crisis / diagnosis. Leukemia / diagnosis
  • [MeSH-minor] Acute Disease. Diagnosis, Differential. Humans. Immunohistochemistry / methods. Immunohistochemistry / standards. Immunophenotyping / methods. Immunophenotyping / standards

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  • (PMID = 16925061.001).
  • [ISSN] 0869-2084
  • [Journal-full-title] Klinicheskaia laboratornaia diagnostika
  • [ISO-abbreviation] Klin. Lab. Diagn.
  • [Language] rus
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Russia (Federation)
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Number-of-references] 8
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47. Zhao Y, Wang QS, Dou LP, Bo J, Li HH, Jing Y, Yu L: [Methylation of Id4 gene promoter in acute leukemia]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2007 Dec;15(6):1156-60
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  • [Title] [Methylation of Id4 gene promoter in acute leukemia].
  • This study was purpose to investigate the difference of Id4 gene promoter methylation between healthy individuals and acute leukemia patients.
  • MS-PCR methods were used to detect the status of Id4 gene methylation in healthy individuals and acute leukemia patients.
  • Id4 gene methylation was found in all 8 cases of relapsed acute leukemias.
  • It is concluded that as compared with healthy individuals, Id4 gene in acute leukemia patients was methylated in different degrees.
  • The change of Id4 gene methylation is thought to be associated with occurrence of acute leukemia.

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  • (PMID = 18088456.001).
  • [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; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / ID4 protein, human; 0 / Inhibitor of Differentiation Proteins
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48. 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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49. 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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50. Wananukul S, Nuchprayoon I, Siripanich H: Mucocutaneous findings in febrile neutropenic children with acute leukemias. J Med Assoc Thai; 2005 Jun;88(6):817-23
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  • [Title] Mucocutaneous findings in febrile neutropenic children with acute leukemias.
  • Febrile neutropenia is common in children with leukemia.
  • The authors prospectively examined children with fever with neutropenia in acute leukemia, aged 1-15 years, who were admitted to the Department of Pediatrics, King Chulalongkorn Memorial Hospital, between September 2000 and August 2001.
  • The prevalence of infection was found in severe neutropenia (absolute neutrophil count, ANC less than 500 cell/cu mm), moderate neutropenia (ANC, 500-1000 cell/cu mm) and mild neutropenia (ANC, 1001-1500 cell/cu mm) was 72%, 9% and 5%, respectively.
  • Daily physical examination of skin and mucous membrane are suggested for proper and prompt diagnosis and treatment of febrile neutropenic children with acute leukemia to reduce mortality and morbidity in these patients.
  • A Guideline for the use of antimicrobial agents in neutropenic patients with acute leukemia is proposed In conclusion, infection was commonly found in severe neutropenia.
  • Mucocutaneous infection was the most common site of infection infebrile neutropenia in children with leukemia.
  • [MeSH-major] Fever. Neutropenia / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Skin Diseases / etiology

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  • (PMID = 16083222.001).
  • [ISSN] 0125-2208
  • [Journal-full-title] Journal of the Medical Association of Thailand = Chotmaihet thangphaet
  • [ISO-abbreviation] J Med Assoc Thai
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Thailand
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51. Pawińska K, Balwierz W, Baran J: [Minimal residual disease in childhood acute leukemias]. Przegl Lek; 2006;63(1):41-3
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  • [Title] [Minimal residual disease in childhood acute leukemias].
  • Monitoring of residual leukemic cells, so called minimal residual disease (MRD) in acute leukemias is of great importance in clinical practice.
  • Especially evaluation of early response to treatment has a important prognostic value, and modifies the therapy schedule in a nowadays used treatment protocols.
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis

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  • (PMID = 16892899.001).
  • [ISSN] 0033-2240
  • [Journal-full-title] Przegla̧d lekarski
  • [ISO-abbreviation] Prz. Lek.
  • [Language] pol
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Number-of-references] 20
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52. Wojcik I, Szybka M, Golanska E, Rieske P, Blonski JZ, Robak T, Bartkowiak J: Abnormalities of the P53, MDM2, BCL2 and BAX genes in acute leukemias. Neoplasma; 2005;52(4):318-24
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  • [Title] Abnormalities of the P53, MDM2, BCL2 and BAX genes in acute leukemias.
  • Abnormalities of the P53 network have been implicated in the pathogenesis of acute lymphoblastic leukemia (ALL) and acute myeloblastic leukemia (AML).
  • To gain further insight into the role of P53 network in the evolution of acute leukemias, the P53, MDM2, BCL2 and BAX mRNAexpressions in portion samples from patients with ALL and AML were analyzed using multiplex RT-PCR.
  • Although a low frequency of molecular disturbances of the P53 and the MDM2 genes was detected in this study, there was a high percentage of cases with increased mRNA level of P53 and MDM2.
  • A high frequency of BCL2 mRNA overexpression and a relatively low frequency of BAX mRNA overexpression detected in both analyzed leukemias in this study, indicate that altered transcription of these genes may be involved in leukemogenesis.
  • [MeSH-major] Gene Amplification. Gene Expression Profiling. Leukemia, Myeloid, Acute / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 16059649.001).
  • [ISSN] 0028-2685
  • [Journal-full-title] Neoplasma
  • [ISO-abbreviation] Neoplasma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Slovakia
  • [Chemical-registry-number] 0 / BAX protein, human; 0 / Nuclear Proteins; 0 / Proto-Oncogene Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / RNA, Messenger; 0 / bcl-2-Associated X Protein; EC 6.3.2.19 / MDM2 protein, human; EC 6.3.2.19 / Proto-Oncogene Proteins c-mdm2
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53. Blum W, Klisovic RB, Becker H, Yang X, Rozewski DM, Phelps MA, Garzon R, Walker A, Chandler JC, Whitman SP, Curfman J, Liu S, Schaaf L, Mickle J, Kefauver C, Devine SM, Grever MR, Marcucci G, Byrd JC: Dose escalation of lenalidomide in relapsed or refractory acute leukemias. J Clin Oncol; 2010 Nov 20;28(33):4919-25
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  • [Title] Dose escalation of lenalidomide in relapsed or refractory acute leukemias.
  • We report results of a phase I dose-escalation trial of lenalidomide in relapsed or refractory acute leukemia.
  • PATIENTS AND METHODS: Thirty-one adults with acute myeloid leukemia (AML) and four adults with acute lymphoblastic leukemia (ALL) were enrolled.
  • Two of four patients who received lenalidomide as initial therapy for AML relapse after allogeneic transplantation achieved durable CR after development of cutaneous graft-versus-host disease, without donor leukocyte infusion.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Thalidomide / analogs & derivatives

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  • (PMID = 20956622.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P50 CA140158; United States / NCI NIH HHS / CA / K23 CA120708; United States / NCI NIH HHS / CA / P50-CA140158; United States / NCI NIH HHS / CA / K23CA120708; United States / NCRR NIH HHS / RR / UL1 RR025755; United States / NCI NIH HHS / CA / P30 CA016058
  • [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 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / Antineoplastic Agents; 0 / CD33 protein, human; 0 / Sialic Acid Binding Ig-like Lectin 3; 4Z8R6ORS6L / Thalidomide; F0P408N6V4 / lenalidomide
  • [Other-IDs] NLM/ PMC3020696
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54. Zwaan CM, Reinhardt D, Hitzler J, Vyas P: Acute leukemias in children with Down syndrome. Hematol Oncol Clin North Am; 2010 Feb;24(1):19-34
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  • [Title] Acute leukemias in children with Down syndrome.
  • Children with Down syndrome have an increased risk for developing both acute myeloid as well as lymphoblastic leukemia.
  • These leukemias differ in presenting characteristics and underlying biology when compared with leukemias occurring in non-Down syndrome children.
  • Myeloid leukemia in children with Down syndrome is preceded by a preleukemic clone (transient leukemia or transient myeloproliferative disorder), which may disappear spontaneously, but may also need treatment in case of severe symptoms.
  • Twenty percent of children with transient leukemia subsequently develop myeloid leukemia.
  • This transition offers a unique model to study the stepwise development of leukemia and of gene dosage effects mediated by aneuploidy.
  • [MeSH-major] Down Syndrome / complications. Leukemia, Myeloid, Acute / etiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / etiology
  • [MeSH-minor] Child. Clone Cells / pathology. Humans. Leukemia

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  • [Copyright] Copyright (c) 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20113894.001).
  • [ISSN] 1558-1977
  • [Journal-full-title] Hematology/oncology clinics of North America
  • [ISO-abbreviation] Hematol. Oncol. Clin. North Am.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 83
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55. Zwaan MC, Reinhardt D, Hitzler J, Vyas P: Acute leukemias in children with Down syndrome. Pediatr Clin North Am; 2008 Feb;55(1):53-70, x
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  • [Title] Acute leukemias in children with Down syndrome.
  • Children with Down syndrome have an increased risk for developing both acute myeloid as well as lymphoblastic leukemia.
  • These leukemias differ in presenting characteristics and underlying biology when compared with leukemias occurring in non-Down syndrome children.
  • Myeloid leukemia in children with Down syndrome is preceded by a preleukemic clone (transient leukemia or transient myeloproliferative disorder), which may disappear spontaneously, but may also need treatment in case of severe symptoms.
  • Twenty percent of children with transient leukemia subsequently develop myeloid leukemia.
  • This transition offers a unique model to study the stepwise development of leukemia, and of gene dosage effects mediated by aneuploidy.
  • [MeSH-major] Down Syndrome / complications. Leukemia, Myeloid / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child. Child, Preschool. Clinical Trials as Topic. Disease Progression. Humans. Infant. Infant, Newborn. Mutation

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  • (PMID = 18242315.001).
  • [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
  • [Number-of-references] 83
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56. Van Vlierberghe P, Palomero T, Khiabanian H, Van der Meulen J, Castillo M, Van Roy N, De Moerloose B, Philippé J, González-García S, Toribio ML, Taghon T, Zuurbier L, Cauwelier B, Harrison CJ, Schwab C, Pisecker M, Strehl S, Langerak AW, Gecz J, Sonneveld E, Pieters R, Paietta E, Rowe JM, Wiernik PH, Benoit Y, Soulier J, Poppe B, Yao X, Cordon-Cardo C, Meijerink J, Rabadan R, Speleman F, Ferrando A: PHF6 mutations in T-cell acute lymphoblastic leukemia. Nat Genet; 2010 Apr;42(4):338-42
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  • [Title] PHF6 mutations in T-cell acute lymphoblastic leukemia.
  • T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive hematological malignancy with an increased incidence in males.
  • Mutational loss of PHF6 is importantly associated with leukemias driven by aberrant expression of the homeobox transcription factor oncogenes TLX1 and TLX3.
  • Overall, these results identify PHF6 as a new X-linked tumor suppressor in T-ALL and point to a strong genetic interaction between PHF6 loss and aberrant expression of TLX transcription factors in the pathogenesis of this disease.

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  • (PMID = 20228800.001).
  • [ISSN] 1546-1718
  • [Journal-full-title] Nature genetics
  • [ISO-abbreviation] Nat. Genet.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA120196-03; United States / NIAID NIH HHS / AI / U54-AI057158; United States / NCI NIH HHS / CA / R01 CA129382; United States / NCI NIH HHS / CA / R01 CA129382-03; United States / NCI NIH HHS / CA / CA129382-03; United States / NCI NIH HHS / CA / CA120196-03; United States / NCI NIH HHS / CA / R01CA120196; United States / NIAID NIH HHS / AI / U54 AI057158; United States / NCI NIH HHS / CA / R01CA129382; United States / NCI NIH HHS / CA / R01 CA120196; United States / NLM NIH HHS / LM / 1R01LM010140-01; United States / NCI NIH HHS / CA / U24 CA114737; United States / NLM NIH HHS / LM / R01 LM010140; United States / NCI NIH HHS / CA / R01 CA155743
  • [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 / Carrier Proteins; 0 / Homeodomain Proteins; 0 / PHF6 protein, human; 0 / Proto-Oncogene Proteins; 0 / TLX3 protein, human; 143275-75-6 / TLX1 protein, human
  • [Other-IDs] NLM/ NIHMS176587; NLM/ PMC2847364
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57. Morgan MA, Reuter CW: Molecularly targeted therapies in myelodysplastic syndromes and acute myeloid leukemias. Ann Hematol; 2006 Mar;85(3):139-63
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  • [Title] Molecularly targeted therapies in myelodysplastic syndromes and acute myeloid leukemias.
  • Although there has been significant progress in acute myeloid leukemia (AML) treatment in younger adults during the last decade, standard induction therapy still fails to induce remission in up to 40% of AML patients.
  • Additionally, relapses are common in 50-70% of patients who achieve a complete remission, and only 20-30% of patients enjoy long-term disease-free survival.
  • The advanced age of the majority of MDS patients limits the therapeutic strategies often to supportive care.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Enzyme Inhibitors / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Myelodysplastic Syndromes / drug therapy
  • [MeSH-minor] Age Factors. Animals. Cell Proliferation / drug effects. DNA Methylation / drug effects. Disease-Free Survival. Histone Acetyltransferases / antagonists & inhibitors. Humans. Neovascularization, Pathologic / drug therapy. Neovascularization, Pathologic / metabolism. Protein Processing, Post-Translational / drug effects. Receptor, Macrophage Colony-Stimulating Factor / antagonists & inhibitors. Receptor, Macrophage Colony-Stimulating Factor / metabolism. Remission Induction / methods


58. Parovichnikova EN, Savchenko VG, Verniuk MA, Vinogradova OA, Misiurin AV, Vorob'ev IA, Domracheva EV, Tikhonova LIu, Rukavitsyn OA, Rossiev VA, Kliasova GA, Turkina AG, Liubimova LS, Mendeleeva LP, Isaev VG: [Acute lymphoblastic leukemias with aberrations of BCR-ABL genes]. Ter Arkh; 2005;77(7):11-6
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  • [Title] [Acute lymphoblastic leukemias with aberrations of BCR-ABL genes].
  • AIM: To develop an original therapeutic strategy in Ph-positive acute lymphoblastic leukemia (ALL).
  • [MeSH-major] Fusion Proteins, bcr-abl / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 16116902.001).
  • [ISSN] 0040-3660
  • [Journal-full-title] Terapevticheskiĭ arkhiv
  • [ISO-abbreviation] Ter. Arkh.
  • [Language] rus
  • [Publication-type] Comparative Study; English Abstract; Journal Article
  • [Publication-country] Russia (Federation)
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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59. Nervi C, Fazi F, Rosa A, Fatica A, Bozzoni I: Emerging role for microRNAs in acute promyelocytic leukemia. Curr Top Microbiol Immunol; 2007;313:73-84
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  • [Title] Emerging role for microRNAs in acute promyelocytic leukemia.
  • These transcription factors have been found mutated or altered by chromosomal translocations associated with leukemias, indicating their role in the pathogenesis of these malignancies.
  • Epigenetic mechanisms such as DNA methylation, posttranslational modifications of histones, remodeling of nucleosomes, and expression of small regulatory RNAs all contribute to the regulation of gene expression and determination of cell and tissue specificity.
  • Their expression appears to be tissue-specific and highly regulated according to the cell's developmental lineage and stage.
  • Interestingly, miRNAs expressed in hematopoietic cells have been found mutated or altered by chromosomal translocations associated with leukemias.
  • The expression levels of a specific miR-223 correlate with the differentiation fate of myeloid precursors.
  • The activation of both pathways of transcriptional regulation by the myeloid lineage-specific transcription factor C/EBPalpha (CCAAT/enhancer-binding protein-alpha), and posttranscriptional regulation by miR-223 appears essential for granulocytic differentiation and clinical response of acute promyelocytic leukemia (APL) blasts to all-trans retinoic acid (ATRA).
  • Together, this evidence underlies transcription factors, chromatin remodeling, and miRNAs as ultimate determinants for the correct organization of cell type-specific gene arrays and hematopoietic differentiation, therefore providing new targets for the diagnosis and treatment of leukemias.
  • [MeSH-major] Leukemia, Promyelocytic, Acute / physiopathology. MicroRNAs / metabolism

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  • (PMID = 17217039.001).
  • [ISSN] 0070-217X
  • [Journal-full-title] Current topics in microbiology and immunology
  • [ISO-abbreviation] Curr. Top. Microbiol. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / CCAAT-Enhancer-Binding Protein-alpha; 0 / MicroRNAs; 0 / NFI Transcription Factors
  • [Number-of-references] 40
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60. Xu XQ, Wang JM, Lü SQ, Chen L, Yang JM, Zhang WP, Song XM, Hou J, Ni X, Qiu HY: Clinical and biological characteristics of adult biphenotypic acute leukemia in comparison with that of acute myeloid leukemia and acute lymphoblastic leukemia: a case series of a Chinese population. Haematologica; 2009 Jul;94(7):919-27
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  • [Title] Clinical and biological characteristics of adult biphenotypic acute leukemia in comparison with that of acute myeloid leukemia and acute lymphoblastic leukemia: a case series of a Chinese population.
  • BACKGROUND: Biphenotypic acute leukemia is a rare disorder that is difficult to diagnose.
  • There is still a lack of studies in biphenotypic acute leukemia in a Chinese population.
  • We present here a comprehensive investigation of the clinical and biological characteristics, and outcome of biphenotypic acute leukemia in our hospital in over a seven year period.
  • DESIGN AND METHODS: We retrospectively analyzed 452 adult acute leukemia patients diagnosed according to French-American-British (FAB) classification and biphenotypic acute leukemia diagnosed according to European Group for the Immunological Characterization of Leukemias (EGIL) classification, respectively.
  • Biological characteristics, response to treatment, and outcome were examined in biphenotypic acute leukemia patients and compared with that in acute myeloid leukemia and acute lymphoblastic leukemia patients with complete follow-up profiles diagnosed in the same period.
  • RESULTS: Of 452 acute leukemia patients, 21 cases (4.6%) were diagnosed as biphenotypic acute leukemia.
  • When compared with acute myeloid leukemia and acute lymphoblastic leukemia, patients with biphenotypic acute leukemia showed significantly higher incidence of CD34 antigen expression, unfavorable karyotypes, and extramedullary infiltration (p<0.05).
  • In this cohort of patients with biphenotypic acute leukemia, t(9;22) was the most common abnormality in chromosome structure.
  • The median disease-free survival and overall survival in biphenotypic acute leukemia patients was five months and ten months, respectively, significantly shorter than those in acute myeloid leukemia and acute lymphoblastic leukemia patients (p<0.05).
  • CONCLUSIONS: The prognosis of biphenotypic acute leukemia patients is poor when compared with de novo acute myeloid leukemia or acute lymphoblastic leukemia.
  • Biphenotypic acute leukemia patients showed a much higher incidence of CD34 antigen expression, complex abnormal karyotype, extramedullary infiltration, relapse, and resistance to therapy after relapse.
  • [MeSH-major] Leukemia, Biphenotypic, Acute / diagnosis. Leukemia, Myeloid, Acute / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis


61. Brusa G, Zuffa E, Hattinger CM, Serra M, Remondini D, Castellani G, Righi S, Campidelli C, Pileri S, Zinzani PL, Gabriele A, Mancini M, Corrado P, Barbieri E, Santucci MA: Genomic imbalances associated with secondary acute leukemias in Hodgkin lymphoma. Oncol Rep; 2007 Dec;18(6):1427-34
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  • [Title] Genomic imbalances associated with secondary acute leukemias in Hodgkin lymphoma.
  • Secondary tumors and leukemias are major complications in Hodgkin lymphoma (HL).
  • To distinguish genomic imbalances associated with the development of acute myeloid leukemia (AML) in HL we used an array-based comparative genomic hybridization (aCGH) strategy on whole lymph node biopsies of HL patient.
  • They involved AFM137XA11, a 9p11.2 pericentric region; FGFR1, the FGF receptor most frequently translocated in AML; PPARBP, a co-activator of nuclear receptors RARalpha, RXR and TRbeta1; AFM217YD10, a 17q25 telomeric region; FGR, an SRC2 kinase involved in cytokine production by NK and CD4+ NKT cells; GATA3, a Th2-specific transcription factor; TOP1, involved in DNA recombination and repair; WT1, a transcription factor involved in CD8+ T cell response against leukaemic blasts.
  • [MeSH-major] Chromosome Aberrations. Hodgkin Disease / genetics. Leukemia, Myeloid, Acute / genetics. Neoplasms, Second Primary / genetics


62. Abdallah E, Hajji Z, Mellal Z, Belmekki M, Bencherifa F, Berraho A: [Macular serous detachment revealing acute lymphoblastic leukemia]. J Fr Ophtalmol; 2005 Jan;28(1):39-44
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  • [Title] [Macular serous detachment revealing acute lymphoblastic leukemia].
  • BACKGROUND: Leukemias are a group of malignant diseases caused by immature hematopoietic cells proliferating in the blood marrow.
  • OBSERVATION: We report a case of a 42-year-old women presenting with loss of vision caused by serous macular detachment.
  • The investigations showed the diagnosis of acute lymphoblastic leukemia.
  • DISCUSSION: Ocular involvement is seen in 28%-80% of leukemia cases.
  • Serous detachment of the neuroepithelium is seldom reported, and can be the first symptom of the disease.
  • CONCLUSION: Ocular manifestations of leukemia are frequent but rarely reveal the disease.
  • However, the diagnosis of leukemia should be considered in case of pigmentary epithelium involvement.
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Retinal Detachment / etiology

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  • (PMID = 15767897.001).
  • [ISSN] 0181-5512
  • [Journal-full-title] Journal français d'ophtalmologie
  • [ISO-abbreviation] J Fr Ophtalmol
  • [Language] fre
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] France
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63. Dorantes-Acosta E, Arreguin-Gonzalez F, Rodriguez-Osorio CA, Sadowinski S, Pelayo R, Medina-Sanson A: Acute myelogenous leukemia switch lineage upon relapse to acute lymphoblastic leukemia: a case report. Cases J; 2009;2:154
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  • [Title] Acute myelogenous leukemia switch lineage upon relapse to acute lymphoblastic leukemia: a case report.
  • Acute leukemia, the most common form of cancer in children, accounts for approximately 30% of all childhood malignancies, with acute lymphoblastic leukemia being five times more frequent than acute myeloid leukemia.
  • Lineage switch is the term that has been used to describe the phenomenon of acute leukemias that meet the standard French-American-British system criteria for a particular lineage (either lymphoid or myeloid) upon initial diagnosis, but meet the criteria for the opposite lineage at relapse.
  • Many reports have documented conversions of acute lymphoblastic leukemia to acute myeloid leukemia.
  • Here, we report the case of a 4-year-old child with acute myeloid leukemia, which upon relapse switched to acute lymphoblastic leukemia.
  • The morphologic, phenotypic, and molecular features suggest the origin of a new leukemic clone.

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  • [Cites] Ther Clin Risk Manag. 2008 Apr;4(2):327-36 [18728851.001]
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  • (PMID = 19946525.001).
  • [ISSN] 1757-1626
  • [Journal-full-title] Cases journal
  • [ISO-abbreviation] Cases J
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2783110
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64. Ji Y, Zhang W, Wang J, Gu L: mRNA expression of the XAGE-1 gene in human acute leukemia. Int J Hematol; 2010 Mar;91(2):209-12
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  • [Title] mRNA expression of the XAGE-1 gene in human acute leukemia.
  • We analyzed the expression of 4 XAGE-1 transcript variant gene in human acute leukemias by reverse-transcription polymerase chain reaction.
  • Among the 114 acute leukemias, 14/63 (22.22%) of the acute myeloid leukemia samples were positive for XAGE-1b genes.
  • XAGE-1b mRNA expression was detected in 10/51 (19.61%) of the acute lymphocyte leukemia samples.
  • However, we did not find any important correlation between XAGE-1b mRNA expression and clinical characteristics, such as sex, leukemia type, response to therapy and the percentage of blast in the first diagnosed bone marrow.
  • We concluded that the XAGE-1b gene was expressed at the mRNA level in a proportion of human acute leukemia.
  • [MeSH-major] Antigens, Neoplasm / genetics. Gene Expression Regulation, Leukemic. Leukemia, Myeloid, Acute / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 20178013.001).
  • [ISSN] 1865-3774
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / RNA, Messenger; 0 / XAGE1A protein, human
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65. Kiss F, Buslig J, Szegedi I, Scholtz B, Kappelmayer J, Kiss C: Early relapse after rituximab chemoimmunotherapy. Pediatr Blood Cancer; 2008 Feb;50(2):372-5
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  • In relapsed/refractory childhood acute lymphoblastic leukemia (ALL) of the B-cell lineage rituximab, a monoclonal anti-CD20 antibody was used successfully in some cases.
  • We report on a 15-year-old female with relapsed CD20-positive B-cell progenitor ALL treated with rituximab because of positive minimal residual disease signals after chemotherapy, as checked by flow cytometry and real time quantitative-PCR.
  • The patient died with fulminant aspergillosis before hematopoietic stem cell transplantation could be performed.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy
  • [MeSH-minor] Adolescent. Antibodies, Monoclonal, Murine-Derived. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Combined Modality Therapy. Female. Flow Cytometry. Gene Rearrangement, delta-Chain T-Cell Antigen Receptor. Humans. Neoplasm, Residual / pathology. Recurrence. Rituximab

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  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • (PMID = 17973316.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 4F4X42SYQ6 / Rituximab
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66. Poros A, Lovas N: [The role of imatinib in the treatment of acute lymphoid leukemias]. Orv Hetil; 2005 May 1;146(18 Suppl 1):905-10
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  • [Title] [The role of imatinib in the treatment of acute lymphoid leukemias].
  • The paper reviews current data on the use of imatinib in acute lymphoid leukemia.
  • A brief description of classification of acute lymphoid leukemia and the therapeutic developments of the last 30 years are presented with particular emphasis on the clinical and biological features of Philadelphia positive acute lymphoid leukemia.
  • The main therapeutic principles of acute lymphoid leukemia and the role of minimal residual disease in therapeutic indications are summarized.
  • In Philadelphia positive acute lymphoid leukemia, in addition to chemotherapy and bone marrow transplantation, the tyrosine kinase inhibitor imatinib mesylate has been increasingly administered.
  • Based on the above considerations the current indications of imatinib treatment in Philadelphia positive acute lymphoid leukemia can be summarized as follows: a) during the induction phase along with chemotherapy;.
  • c) before stem cell transplantation to eradicate minimal residual disease;.
  • e) after stem cell transplantation for the treatment of minimal residual disease and/or relapse, alone or in combination with donor lymphocyte immunotherapy.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Bone Marrow Transplantation. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Piperazines / therapeutic use. Protein Kinase Inhibitors / therapeutic use. Pyrimidines / therapeutic use
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Benzamides. Chemotherapy, Adjuvant. Humans. Imatinib Mesylate. Immunotherapy. Lymphocytes. Neoplasm, Residual / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy. Protein-Tyrosine Kinases / antagonists & inhibitors. Remission Induction. Treatment Outcome

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  • (PMID = 15921303.001).
  • [ISSN] 0030-6002
  • [Journal-full-title] Orvosi hetilap
  • [ISO-abbreviation] Orv Hetil
  • [Language] hun
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Hungary
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases
  • [Number-of-references] 45
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67. Abdool A, Yeh CH, Kantarjian H, O'Brien S, Bruey J, Giles F, Albitar M: Circulating CD33 and its clinical value in acute leukemia. Exp Hematol; 2010 Jun;38(6):462-71
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  • [Title] Circulating CD33 and its clinical value in acute leukemia.
  • OBJECTIVE: CD33 is a cell surface antigen for committed myelomonocytic lineage.
  • We explored the potential of detecting CD33 as cell-free circulating protein in patients with leukemia.
  • MATERIALS AND METHODS: We developed a quantitative bead-based immunoflow cytometry assay to measure cell-free circulating CD33 (cCD33) levels in the plasma of patients with acute leukemia, and correlated these results with corresponding clinical behavior.
  • We measured cCD33 levels in the plasma of 48 healthy subjects and in patients with acute myelogenous leukemia (n = 98), acute lymphoblastic leukemia (n = 46), myelodysplastic syndrome (MDS) (n = 50), and myeloproliferative disorder (n = 49).
  • RESULTS: Patients with acute myeloid leukemia and myeloproliferative disorders had significantly higher concentrations of cCD33 than the other patient groups and normal individuals (p = 0.0001), and among these groups, MDS patients displayed the lowest cCD33 levels (p = 0.02).
  • Circulating CD33 values correlated positively with the CD33(+) blast cell counts in these patients.
  • While there was no correlation between cCD33 levels and survival in acute myelogenous leukemia and MDS, higher cCD33 plasma concentrations did correlate with shorter survival in acute lymphoblastic leukemia (p = 0.03), and with shorter complete remission duration in acute myelogenous leukemia (p = 0.04) and MDS (p = 0.03).
  • CONCLUSION: Circulating CD33 can be detected in the plasma from patients with leukemias, and cCD33 levels may have clinical implication, e.g., predictive and prognostic value, in these patients.
  • [MeSH-major] Antigens, CD / blood. Antigens, Differentiation, Myelomonocytic / blood. Leukemia, Myeloid, Acute / blood
  • [MeSH-minor] Acute Disease. Case-Control Studies. Cell Line, Tumor. Cell-Free System. Flow Cytometry. Humans. Sialic Acid Binding Ig-like Lectin 3

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  • [Copyright] Copyright 2010 ISEH - Society for Hematology and Stem Cells. Published by Elsevier Inc. All rights reserved.
  • (PMID = 20362641.001).
  • [ISSN] 1873-2399
  • [Journal-full-title] Experimental hematology
  • [ISO-abbreviation] Exp. Hematol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD33 protein, human; 0 / Sialic Acid Binding Ig-like Lectin 3
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68. Fu JF, Liang DC, Shih LY: Analysis of acute leukemias with MLL/ENL fusion transcripts: identification of two novel breakpoints in ENL. Am J Clin Pathol; 2007 Jan;127(1):24-30
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  • [Title] Analysis of acute leukemias with MLL/ENL fusion transcripts: identification of two novel breakpoints in ENL.
  • t(11;19)(q23;p13.3); is one of the common chromosomal translocations in acute leukemias involving MLL rearrangements.
  • In a study of acute leukemias, 148 patients were identified to have MLL rearrangements by Southern blot analysis.
  • Of 15 patients with MLL/ENL, 7 had precursor B-cell acute lymphoblastic leukemia, 4 had T-cell acute lymphoblastic leukemia, and 4 had acute myeloid leukemia.
  • [MeSH-major] Leukemia, Myeloid / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Neoplasm Proteins / genetics. Nuclear Proteins / genetics. Oncogene Fusion / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Transcription Factors / genetics. Translocation, Genetic / genetics
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Child. Child, Preschool. Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 19 / genetics. Female. Gene Rearrangement. Histone-Lysine N-Methyltransferase. Humans. Infant. Infant, Newborn. Male. Reverse Transcriptase Polymerase Chain Reaction. Treatment Outcome

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  • (PMID = 17145626.001).
  • [ISSN] 0002-9173
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MLL protein, human; 0 / MLLT1 protein, human; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / Transcription Factors; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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69. Sachdeva MU, Ahluwalia J, Das R, Varma N, Garewal G: Role of FAB classification of acute leukemias in era of immunophenotyping. Indian J Pathol Microbiol; 2006 Oct;49(4):524-7
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  • [Title] Role of FAB classification of acute leukemias in era of immunophenotyping.
  • French-American-British classification for leukemias had been widely accepted due to its objectiveness and good reproducibility.
  • WHO classification of leukemias was formulated in 1997 with a purpose of further enhancing the objectivity.
  • A retrospective analysis of all acute leukemias over a period of 2 years was done.
  • Out of total of 469 cases of acute leukemias, 193 were diagnosed as Acute Lymphoblastic Leukemia (ALL), 200 as Acute Myeloid Leukemia (AML), and 76 cases diagnosed as Acute Leukemia, cytochemically undifferentiated.
  • Hence, only 16% of all leukemias remained unclassifiable.
  • [MeSH-major] Histocytochemistry / methods. Leukemia / classification. Leukemia, Myeloid / classification. Leukemia, Myeloid / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / classification. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis
  • [MeSH-minor] Acute Disease. Adult. Child. Child, Preschool. Cytogenetics / methods. Humans. Immunophenotyping / methods

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  • (PMID = 17183842.001).
  • [ISSN] 0377-4929
  • [Journal-full-title] Indian journal of pathology & microbiology
  • [ISO-abbreviation] Indian J Pathol Microbiol
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] India
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70. Wadleigh M, Stone RM: The role of myeloid growth factors in acute leukemia. J Natl Compr Canc Netw; 2009 Jan;7(1):84-91
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  • [Title] The role of myeloid growth factors in acute leukemia.
  • Myeloid growth factors granulocyte-colony stimulating and granulocyte macrophage colony-stimulating factors have been extensively studied in acute leukemias.
  • Whether administered before, during, or after chemotherapy for acute myeloid leukemia and acute lymphoblastic leukemia, these agents reduce the duration of neutropenia and seem to be safe and well tolerated.
  • Despite consistently showing a shorter duration of neutropenia, multiple, prospective, randomized trials have documented only modest benefits in terms of reduction in the incidence and severity of infections, without substantial gains or impact in complete remission, overall survival, and disease-free survival rates.
  • Growth factors have also been used to recruit quiescent leukemia cells into the S-phase of the cell cycle to increase their susceptibility to chemotherapy with the goal to reduce relapse and resistance.
  • Randomized trials evaluating this priming strategy have consistently shown improvement in disease- or event-free survival in the intermediate-risk group of patients with acute myeloid leukemia, but no overall survival benefit.
  • This article focuses on the clinical experience with these agents as adjuncts to the treatment of acute leukemias.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Granulocyte Colony-Stimulating Factor / therapeutic use. Granulocyte-Macrophage Colony-Stimulating Factor / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Neutropenia / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • (PMID = 19176208.001).
  • [ISSN] 1540-1405
  • [Journal-full-title] Journal of the National Comprehensive Cancer Network : JNCCN
  • [ISO-abbreviation] J Natl Compr Canc Netw
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Recombinant Proteins; 143011-72-7 / Granulocyte Colony-Stimulating Factor; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor
  • [Number-of-references] 45
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71. Salerni BL, Bates DJ, Albershardt TC, Lowrey CH, Eastman A: Vinblastine induces acute, cell cycle phase-independent apoptosis in some leukemias and lymphomas and can induce acute apoptosis in others when Mcl-1 is suppressed. Mol Cancer Ther; 2010 Apr;9(4):791-802
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  • [Title] Vinblastine induces acute, cell cycle phase-independent apoptosis in some leukemias and lymphomas and can induce acute apoptosis in others when Mcl-1 is suppressed.
  • Inhibition of the extracellular signal-regulated kinase by PD98059 dramatically accelerates vinblastine-mediated apoptosis in ML-1 leukemia with cells dying in 4 hours from all phases of the cell cycle.
  • Inhibition of protein synthesis by cycloheximide also markedly accelerated vinblastine-induced apoptosis, showing that the proteins required for this acute apoptosis are constitutively expressed.
  • We also investigated the response of 13 other leukemia and lymphoma cell lines and cells from seven chronic lymphocytic leukemia patients.
  • Four cell lines and all chronic lymphocytic leukemia cells were killed in 6 hours by vinblastine alone.
  • Two additional cell lines were sensitized to vinblastine by PD98059, which suppressed Mcl-1.
  • This acute apoptosis either alone or in combination with PD98059 required vinblastine-mediated activation of c-Jun-NH(2)-terminal kinase.
  • PD98059 did not suppress Mcl-1 in other cell lines whereas sorafenib did, but this did not sensitize the cells to vinblastine, suggesting that the acute apoptosis varies depending on which Bcl-2 protein mediates protection.
  • Most of the cell lines were sensitized to vinblastine by cycloheximide, suggesting that inhibition of a short-lived protein in addition to Mcl-1 can acutely sensitize cells.

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  • (PMID = 20371726.001).
  • [ISSN] 1538-8514
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / T32 CA009658-17; United States / NCI NIH HHS / CA / CA23108; United States / NCI NIH HHS / CA / CA009658-17; United States / NCI NIH HHS / CA / T32 CA009658; United States / NCI NIH HHS / CA / R01 CA050224; United States / NCI NIH HHS / CA / P30 CA023108-315657; United States / NCI NIH HHS / CA / P30 CA023108; United States / NCI NIH HHS / CA / CA023108-315657; United States / NCI NIH HHS / CA / CA050224-14; United States / NCI NIH HHS / CA / R01 CA050224-14; United States / NCI NIH HHS / CA / CA50224
  • [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 / 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one; 0 / Flavonoids; 0 / Myeloid Cell Leukemia Sequence 1 Protein; 0 / Proto-Oncogene Proteins c-bcl-2; 5V9KLZ54CY / Vinblastine; 98600C0908 / Cycloheximide; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases
  • [Other-IDs] NLM/ NIHMS184304; NLM/ PMC2852489
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72. Cruse JM, Lewis RE, Pierce S, Lam J, Tadros Y: Aberrant expression of CD7, CD56, and CD79a antigens in acute myeloid leukemias. Exp Mol Pathol; 2005 Aug;79(1):39-41
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  • [Title] Aberrant expression of CD7, CD56, and CD79a antigens in acute myeloid leukemias.
  • CD7 and CD56 expression at diagnosis has been associated with low remission rates and biological aggressiveness in a significant proportion of acute leukemias.
  • Among 46 patients with acute myeloid leukemia, we found CD7 expression in 15 cases (32.6%) and CD56 positivity in 10 patients (21.7%).
  • Six of these myeloid leukemia cases (13%) showed expression of both CD7 and CD56.
  • Among the 10 that were acute myeloblastic leukemia, 8 expressed CD7, 4 expressed CD56, and 4 were positive for CD79a.
  • Thus, these markers were expressed early in hemopoietic ontogeny in the lesser-differentiated acute myeloid leukemia subtypes, including FAB M0, M1, and M2.
  • Whereas CD7 and CD56 were each positive in 4 cases of acute myelomonocytic leukemia (FAB M4 subtype), there was no CD79a expression in the M4 cases.
  • CD7 is expressed by mature T cells, NK cells, and an immature myeloid cell subset.
  • NK cells and a T cell subset express CD56.
  • By contrast, CD79a is a B cell marker that is assigned a high score of 2.0 in the differentiation of acute leukemias of ambiguous lineage in the WHO classification.
  • The aberrant expression of CD7, CD56, and CD79a, representing the capacity of these leukemias for trilineal expression of leukocyte differentiation antigens, portends a poor prognosis.
  • [MeSH-major] Antigens, CD / biosynthesis. Antigens, CD56 / biosynthesis. Antigens, CD7 / biosynthesis. Biomarkers, Tumor / analysis. Leukemia, Myeloid, Acute / metabolism. Receptors, Antigen, B-Cell / biosynthesis

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  • (PMID = 16005710.001).
  • [ISSN] 0014-4800
  • [Journal-full-title] Experimental and molecular pathology
  • [ISO-abbreviation] Exp. Mol. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD56; 0 / Antigens, CD7; 0 / Antigens, CD79; 0 / Biomarkers, Tumor; 0 / CD79A protein, human; 0 / Receptors, Antigen, B-Cell
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73. Al-Seraihy AS, Owaidah TM, Ayas M, El-Solh H, Al-Mahr M, Al-Ahmari A, Belgaumi AF: Clinical characteristics and outcome of children with biphenotypic acute leukemia. Haematologica; 2009 Dec;94(12):1682-90
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  • [Title] Clinical characteristics and outcome of children with biphenotypic acute leukemia.
  • BACKGROUND: Knowledge concerning the clinical and biological presentation, as well as the outcome of treatment, of biphenotypic acute leukemia in children is limited.
  • DESIGN AND METHODS: This retrospective review analyzes the clinical features and outcome of children with biphenotypic acute leukemia diagnosed and treated over an 8-year period.
  • According to the EGIL scoring system 24 (3.7%) of 633 patients with acute leukemia were classified as having biphenotypic acute leukemia.
  • The diagnostic work-up and results were reviewed specifically for this study in the light of the newly published WHO criteria for the diagnosis of leukemia of ambiguous lineage.
  • Based on these criteria, 11 (1.7%) patients were categorized according to the new nomenclature as having mixed phenotype acute leukemia.
  • Patients received therapy based on a treatment regimen for acute lymphocytic leukemia regimen, which included myeloid-effective agents.
  • The survival of those patients who underwent hematopoietic stem cell transplantation in first complete remission was not different from that of the patients who were treated with chemotherapy alone (overall survival: 70.1% versus 81.1%, respectively, p=0.39; event-free survival: 70.1% versus 76.2%, respectively, p=0.75).
  • The outcome of the 11 patients who were retrospectively classified as having mixed phenotype acute leukemia according to the new WHO criteria was excellent, with no relapses or deaths occurring among these patients.
  • CONCLUSIONS: An acute lymphocytic leukemia type of induction therapy, using agents that are active against lymphoid and myeloid leukemias, appears to be more effective in achieving and maintaining complete remissions regardless of whether the patients are classified according to EGIL criteria or the new WHO criteria.
  • Hematopoietic stem cell transplantation may not be necessary for all patients in first complete remission.
  • [MeSH-major] Leukemia, Biphenotypic, Acute / diagnosis. Leukemia, Biphenotypic, Acute / therapy
  • [MeSH-minor] Antigens, CD / analysis. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child. Child, Preschool. Female. Flow Cytometry. Follow-Up Studies. Hematopoietic Stem Cell Transplantation. Humans. Immunophenotyping. In Situ Hybridization, Fluorescence. Infant. Kaplan-Meier Estimate. Karyotyping. Male. Outcome Assessment (Health Care) / methods. Remission Induction. Retrospective Studies

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  • (PMID = 19713227.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antigens, CD
  • [Other-IDs] NLM/ PMC2791935
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74. Berköz M, Yalin S: Association of CYP2B6 G15631T polymorphism with acute leukemia susceptibility. Leuk Res; 2009 Jul;33(7):919-23
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  • [Title] Association of CYP2B6 G15631T polymorphism with acute leukemia susceptibility.
  • In this study, we aimed to determine whether any association exists between genetic polymorphism in CYP2B6G15631T and individual susceptibility to acute leukemia.
  • Our study group consisted of 80 acute leukemia patients and 100 unrelated healthy volunteers as a control group.
  • 44 of the acute leukemia patients were diagnosed with acute lymphoblastic leukemia (ALL) and 36 patients with acute myeloid leukemia (AML).
  • The TT genotype (homozygous variant) was not observed in either control or leukemia cases.
  • Logistic regression analyses showed a significant correlation between the CYP2B6 G15631T polymorphism (GT) and acute leukemia patients (OR=2.481, 95% CI=1.353-4.551, p=0.003).
  • Our findings indicate that GT genotype may be an important genetic determinant for acute leukemias.
  • According to our knowledge, this is the first report of an association between acute leukemia cases and the CYP2B6 G15631T polymorphism.
  • [MeSH-major] Aryl Hydrocarbon Hydroxylases / genetics. Leukemia, Myeloid, Acute / genetics. Oxidoreductases, N-Demethylating / genetics. Polymorphism, Genetic / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Case-Control Studies. Child. Child, Preschool. Cytochrome P-450 CYP2B6. DNA, Neoplasm / genetics. Disease Susceptibility. Genotype. Humans. Middle Aged. Polymerase Chain Reaction. Young Adult

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  • (PMID = 19144407.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA, Neoplasm; EC 1.14.14.1 / Aryl Hydrocarbon Hydroxylases; EC 1.14.14.1 / CYP2B6 protein, human; EC 1.14.14.1 / Cytochrome P-450 CYP2B6; EC 1.5.- / Oxidoreductases, N-Demethylating
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75. Passweg JR, Chalandon Y, Matthes T, Beris P, Aapro MS, Plan PA: [Acute leukemias]. Rev Med Suisse; 2008 May 21;4(158):1272-4, 1276-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Acute leukemias].
  • [MeSH-major] Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy

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  • (PMID = 18616210.001).
  • [ISSN] 1660-9379
  • [Journal-full-title] Revue médicale suisse
  • [ISO-abbreviation] Rev Med Suisse
  • [Language] fre
  • [Publication-type] Journal Article; Review
  • [Publication-country] Switzerland
  • [Number-of-references] 22
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76. Goel R, Kumar R, Bakhshi S: Transformation of childhood MDS-refractory anemia to acute lymphoblastic leukemia. J Pediatr Hematol Oncol; 2007 Oct;29(10):725-7
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  • [Title] Transformation of childhood MDS-refractory anemia to acute lymphoblastic leukemia.
  • Myelodysplastic syndromes (MDS) are clonal disorders of hematopoietic stem cell.
  • Patients have a deteriorating course with about 30% evolving into acute leukemias usually of the myeloid phenotype.
  • Evolution into acute lymphoblastic leukemia is a rare and intriguing phenomenon seen in far less than 1% of adult cases, and extremely rare in pediatric population.
  • We report a case of childhood MDS-refractory anemia transforming into acute lymphoblastic leukemia after an interval of 21 months since presentation and being on cyclosporine therapy for 9.5 months.
  • [MeSH-major] Anemia, Refractory / complications. Myelodysplastic Syndromes / complications. Precursor Cell Lymphoblastic Leukemia-Lymphoma / etiology


77. Zhao Y, Yu L, Wang QS, Li HH, Bo J, Wang SH, Jin HJ, Lou FD: [Id4 gene methylation for detection of minimal residual disease in acute leukemia]. Zhonghua Xue Ye Xue Za Zhi; 2006 May;27(5):298-301
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  • [Title] [Id4 gene methylation for detection of minimal residual disease in acute leukemia].
  • OBJECTIVE: To evaluate the possibility of Id4 gene promoter methylation as a biomarker for minimal residual disease (MRD) detection in acute leukemia.
  • METHODS: Methylation specific-PCR technique was used to detect Id4 gene methylation in samples with different percentages of leukemia cells from leukemia cell line and bone marrows from leukemia patients in complete remission (CR).
  • RESULTS: Id4 gene methylation could be detected in samples containing 1% or lower leukemia cells.
  • Frequency of Id4 gene methylation in acute lymphoblastic leukemia (ALL) patients in CR was 64.3% being higher than that in acute myeloid leukemia (AML) patients in CR.
  • CONCLUSION: Id4 gene promoter methylation is a candidate of biomarker for MRD detection in acute leukemias.
  • [MeSH-major] DNA Methylation. Inhibitor of Differentiation Proteins / genetics. Leukemia / diagnosis. Neoplasm, Residual / diagnosis
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Cell Line. Female. Humans. Male. Middle Aged. Polymerase Chain Reaction / methods. Promoter Regions, Genetic / genetics. Young Adult

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  • (PMID = 16875575.001).
  • [ISSN] 0253-2727
  • [Journal-full-title] Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi
  • [ISO-abbreviation] Zhonghua Xue Ye Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / ID4 protein, human; 0 / Inhibitor of Differentiation Proteins
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78. Berman JN, Look AT: Targeting transcription factors in acute leukemia in children. Curr Drug Targets; 2007 Jun;8(6):727-37
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  • [Title] Targeting transcription factors in acute leukemia in children.
  • Transcription factors play essential roles in controlling normal blood development and their alteration leads to abnormalities in cell proliferation, differentiation and survival.
  • In many childhood acute leukemias, transcription factors are altered through chromosomal translocations that change their functional properties resulting in repressed activity or inappropriate activation.
  • The development of therapies that specifically target these molecular abnormalities holds promise for improving the outcome in diseases that remain challenging to treat, such as childhood T-cell acute lymphoblastic leukemia and acute myeloid leukemia, with improved toxicity profiles.
  • All trans-retinoic acid and arsenic trioxide have already demonstrated efficacy in acute promyelocytic leukemia in both adults and children.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Drug Delivery Systems. Leukemia / drug therapy. Transcription Factors / drug effects
  • [MeSH-minor] Acute Disease. Arsenicals / pharmacology. Arsenicals / therapeutic use. Child. DNA Methylation / drug effects. Histone Deacetylase Inhibitors. Humans. Oxides / pharmacology. Oxides / therapeutic use. Tretinoin / pharmacology. Tretinoin / therapeutic use

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  • (PMID = 17584028.001).
  • [ISSN] 1873-5592
  • [Journal-full-title] Current drug targets
  • [ISO-abbreviation] Curr Drug Targets
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Arsenicals; 0 / Histone Deacetylase Inhibitors; 0 / Oxides; 0 / Transcription Factors; 5688UTC01R / Tretinoin; S7V92P67HO / arsenic trioxide
  • [Number-of-references] 113
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79. Shen Q, Chen Z, Liu XP, Xing HY, Wang M, Wang JX: [Expression of PTEN mRNA in acute leukemia and its clinical significance]. Zhonghua Xue Ye Xue Za Zhi; 2005 Aug;26(8):493-6
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  • [Title] [Expression of PTEN mRNA in acute leukemia and its clinical significance].
  • OBJECTIVE: To explore PTEN gene expression and its clinical significance in acute leukemia.
  • METHODS: The expression levels of PTEN mRNA in 5 leukemia cell lines, 87 patients with acute leukemias (AL), including 59 acute myeloid leukemia (AML), 26 acute lymphoblastic leukemia (ALL), and 2 acute hybrid leukemia, 21 AL in complete remission (AL-CR), 31 chronic myelogenous leukemia (CML) and 14 normal controls were assayed by RT-PCR.
  • RESULTS: PTEN mRNA was detected in K562 cell line, but not in Kasumi-1, HL-60, U937, Nalm-6 cell lines.
  • The decreased level of PTEN mRNA had a positive correlation with poor-prognostic factors (high white blood cell count of > or = 20 x 10(9)/L and chromosome abnormality).
  • [MeSH-major] Leukemia / metabolism. PTEN Phosphohydrolase / metabolism
  • [MeSH-minor] Cell Line, Tumor. Humans. RNA, Messenger / genetics. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 16383243.001).
  • [ISSN] 0253-2727
  • [Journal-full-title] Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi
  • [ISO-abbreviation] Zhonghua Xue Ye Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / RNA, Messenger; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase
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80. Kojima K, Burks JK, Arts J, Andreeff M: The novel tryptamine derivative JNJ-26854165 induces wild-type p53- and E2F1-mediated apoptosis in acute myeloid and lymphoid leukemias. Mol Cancer Ther; 2010 Sep;9(9):2545-57
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  • [Title] The novel tryptamine derivative JNJ-26854165 induces wild-type p53- and E2F1-mediated apoptosis in acute myeloid and lymphoid leukemias.
  • The development of small-molecule activators of p53 is currently focused on malignancies containing a wild-type p53 genotype, which is present in most leukemias.
  • Here, we report the effects of JNJ-26854165 in acute leukemias.
  • JNJ-26854165 treatment induced p53-mediated apoptosis in acute leukemia cells with wild-type p53, in which p53 rapidly drives transcription-independent apoptosis followed by activation of a transcription-dependent pathway.
  • Apoptotic activity of JNJ-26854165 against primary acute leukemia cells was maintained in leukemia/stroma cocultures, unlike doxorubicin, which has reduced cytrotoxicity in coculture systems.
  • Our data suggest that JNJ-26854165 may provide a novel therapeutic approach for the treatment of acute leukemias.
  • [MeSH-major] Apoptosis / drug effects. E2F1 Transcription Factor / metabolism. Genes, p53. Leukemia, Myeloid, Acute / drug therapy. Tryptamines / pharmacology
  • [MeSH-minor] Cell Line, Tumor. Humans. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology. Transfection

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  • (PMID = 20736344.001).
  • [ISSN] 1538-8514
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA89346; United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / R01 CA089346-03; United States / NCI NIH HHS / CA / CA49639; United States / NCI NIH HHS / CA / P01 CA049639-09A19007; United States / NCI NIH HHS / CA / CA16672; United States / NCI NIH HHS / CA / P01 CA055164-09; United States / NCI NIH HHS / CA / R01 CA089346; United States / NCI NIH HHS / CA / P30 CA016672-22S29015; United States / NCI NIH HHS / CA / P01 CA055164-08; United States / NCI NIH HHS / CA / CA55164; United States / NCI NIH HHS / CA / P01 CA049639; United States / NCI NIH HHS / CA / P01 CA055164
  • [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 / E2F1 Transcription Factor; 0 / Tryptamines
  • [Other-IDs] NLM/ NIHMS231527; NLM/ PMC2949269
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81. Styczynski J, Czyzewski K, Wysocki M: Ex vivo activity of thalidomide in childhood acute leukemia. Leuk Lymphoma; 2006 Jun;47(6):1123-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Ex vivo activity of thalidomide in childhood acute leukemia.
  • Thalidomide is a drug with anti-angiogenic, anti-inflammatory, immunomodulatory and anti-cancer properties that were found to inhibit the production of TNF-alpha in vitro, stimulate reactive oxygen species production, and inhibit VEGFR in acute leukemias.
  • Ex vivo activity of thalidomide as a single agent and in combination with prednisolone or cytarabine in childhood acute leukemias was analyzed.
  • Forty samples of childhood acute lymphoblastic leukemia (ALL) and 13 acute myeloid leukemia (AML) were tested for cytotoxicity by the MTT assay and cell cycle phases by flow cytometry.
  • Control studies were performed on 9 samples of normal lymphocytes and 4 cell lines.
  • Thalidomide increased apoptosis in lymphoblasts, and modulated cell cycle arrest caused by prednisolone but not cytarabine in childhood acute lymphoblastic leukemia samples.
  • [MeSH-major] Angiogenesis Inhibitors / pharmacology. Leukemia, Myeloid, Acute / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Thalidomide / pharmacology
  • [MeSH-minor] Cell Cycle. Child. Child, Preschool. Cytarabine / pharmacology. Female. Humans. Immunophenotyping. Infant. Male. Prednisolone / pharmacology. Tetrazolium Salts / pharmacology. Thiazoles / pharmacology

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  • Hazardous Substances Data Bank. CYTARABINE .
  • Hazardous Substances Data Bank. METHYLTHIAZOLETETRAZOLIUM .
  • Hazardous Substances Data Bank. PREDNISOLONE .
  • Hazardous Substances Data Bank. THALIDOMIDE .
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  • (PMID = 16840205.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Tetrazolium Salts; 0 / Thiazoles; 04079A1RDZ / Cytarabine; 298-93-1 / thiazolyl blue; 4Z8R6ORS6L / Thalidomide; 9PHQ9Y1OLM / Prednisolone
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82. Hiddemann W: Acute leukemias. Crit Rev Oncol Hematol; 2005 Nov;56(2):193
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  • [Title] Acute leukemias.
  • [MeSH-major] Leukemia, Myeloid, Acute / therapy
  • [MeSH-minor] Acute Disease. Cell Differentiation. Cell Proliferation. Clinical Trials, Phase I as Topic. Clinical Trials, Phase II as Topic. Combined Modality Therapy / methods. History, 19th Century. Humans

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  • (PMID = 16203157.001).
  • [ISSN] 1040-8428
  • [Journal-full-title] Critical reviews in oncology/hematology
  • [ISO-abbreviation] Crit. Rev. Oncol. Hematol.
  • [Language] eng
  • [Publication-type] Editorial; Historical Article
  • [Publication-country] Ireland
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83. Ning BT, Tang YM, Chen YH, Shen HQ, Qian BQ: Comparison between CD19 and CD20 expression patterns on acute leukemic cells. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2005 Dec;13(6):943-7
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  • [Title] Comparison between CD19 and CD20 expression patterns on acute leukemic cells.
  • In order to provide the evidences for CD19 as a better antibody targeting molecule for B lineage acute leukemias than CD20 through the multi-parameter flow-cytometry analysis of leukemia cells, the samples from 321 patients with acute leukemia (AL) were immunophenotyped by multi-color flow cytometry and CD45/SSC gating strategy followed by the analysis of CD19 and CD20 expression.
  • The results showed that the positive rate of CD19 (115/116, 99.1%) in 116 cases with B lineage acute lymphoblastic leukemia (B lineage ALL) was significantly higher than that of CD20 (33/116, 28.4%) (P < 0.01); in 17 patients with B lineage/Myeloid (B/My) acute mixed lineage leukemia (AMLL), the former positive rate (17/17, 100%) was also higher than the latter (5/17, 29.4%) (P < 0.01).
  • Both of the two antigens were negative in 29 patients with acute T lymphoblastic leukemia and 7 patients with T/My AMLL.
  • The positive rates of CD19 and CD20 in 152 patients with acute myeloid leukemia (AML) were 7.2% and 2.0%, respectively.
  • The specificity of CD19 and CD20 in B lymphocytic lineage was 92.3% (132/143) and 92.7% (38/41), respectively, while the sensitivity was 99.2% (132/133) and 28.6% (38/133), respectively, the former sensitivity was significantly higher than the latter (chi(2) = 144.018, P = 0.001).
  • It is concluded that CD19 continuously and steadily express on almost all subtypes of B lineage leukemic cells with homogeneous pattern while only a small number of leukemias express CD20.
  • These indicate that CD19 may be a better antibody targeting molecule than CD20 for patients with B-lineage acute leukemia.

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  • (PMID = 16403255.001).
  • [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] ENG
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, CD19; 0 / Antigens, CD20
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84. Forestier E, Schmiegelow K, Nordic Society of Paediatric Haematology and Oncology NOPHO: The incidence peaks of the childhood acute leukemias reflect specific cytogenetic aberrations. J Pediatr Hematol Oncol; 2006 Aug;28(8):486-95
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  • [Title] The incidence peaks of the childhood acute leukemias reflect specific cytogenetic aberrations.
  • The correlation between age and karyotype was studied in 1425, 0 to 14.9 years old children who were diagnosed with acute lymphoblastic leukemia (ALL) or acute myeloblastic leukemia.
  • Almost 80% of the non-Down B-cell precursor ALL cases in the 2 to 7 years frequency peak group who had aberrant cytogenetic results had either a high-hyperdiploid clone (51 to 61 chromosomes) or a translocation t(12;21)(p13;q22).
  • Among B-cell precursor ALL cases, high white blood cell counts correlated with earlier age at diagnosis (rS=-0.23; P<0.001) being most evident for 11q23/MLL-aberrations, translocation t(12;21)(p13;q22), and high-hyperdiploidy.
  • Among acute myeloblastic leukemia patients, frequency peaks were found for those with MLL/11q23 rearrangements (peak: first year), Down syndrome (peak: second to third year), or cytogenetic abnormalities other than translocations t(8;21), t(15;17), and inv(16)/t(16;16) (peak: first to third year).
  • The epidemiology of the cytogenetic subsets of acute leukemias questions whether age as a disease-related prognostic parameter has any relevance in childhood leukemia clinical research beyond being a surrogate marker for more important, truly biologic features such as cytogenetic aberrations and white cell count at diagnosis.
  • Further research is needed to explore whether the 2 to 7 years age incidence peak in childhood ALL harbor yet unidentified cytogenetic subsets with the same natural history as the high-hyperdiploid and t(12;21)-positive leukemias.
  • [MeSH-major] Chromosome Aberrations. Leukemia, Myeloid, Acute / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 16912588.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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85. Zangrando A, Dell'orto MC, Te Kronnie G, Basso G: MLL rearrangements in pediatric acute lymphoblastic and myeloblastic leukemias: MLL specific and lineage specific signatures. BMC Med Genomics; 2009;2:36
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  • [Title] MLL rearrangements in pediatric acute lymphoblastic and myeloblastic leukemias: MLL specific and lineage specific signatures.
  • BACKGROUND: The presence of MLL rearrangements in acute leukemia results in a complex number of biological modifications that still remain largely unexplained.
  • Armstrong et al. proposed MLL rearrangement positive ALL as a distinct subgroup, separated from acute lymphoblastic (ALL) and myeloblastic leukemia (AML), with a specific gene expression profile.
  • Here we show that MLL, from both ALL and AML origin, share a signature identified by a small set of genes suggesting a common genetic disregulation that could be at the basis of mixed lineage leukemia in both phenotypes.
  • A final subset of 14 genes grants the characterization of acute leukemia patients with and without MLL rearrangements.
  • CONCLUSION: Our study demonstrated that a small subset of genes identifies MLL-specific rearrangements and clearly separates acute leukemia samples according to lineage origin.

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  • (PMID = 19549311.001).
  • [ISSN] 1755-8794
  • [Journal-full-title] BMC medical genomics
  • [ISO-abbreviation] BMC Med Genomics
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2709660
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86. Sholl LM, Longtine J: Molecular analysis of gene rearrangements and mutations in acute leukemias and myeloproliferative neoplasms. Curr Protoc Hum Genet; 2010 Oct;Chapter 10:Unit 10.4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Molecular analysis of gene rearrangements and mutations in acute leukemias and myeloproliferative neoplasms.
  • A large subset of acute leukemias and other myeloproliferative neoplasms contain specific genetic alterations, many of which are associated with unique clinical and pathologic features.
  • These alterations include chromosomal translocations leading to oncogenic fusion genes, as well as mutations leading to aberrant activation of a variety of proteins critical to hematopoietic progenitor cell proliferation and differentiation.
  • Molecular analysis is central to diagnosis and clinical management of leukemias, permitting genetic confirmation of a clinical and histologic impression, providing prognostic and predictive information, and facilitating detection of minimal residual disease.
  • This unit will outline approaches to the molecular diagnosis of the most frequent and clinically relevant genetic alterations in acute leukemias and myeloproliferative neoplasms.

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  • (PMID = 20891029.001).
  • [ISSN] 1934-8258
  • [Journal-full-title] Current protocols in human genetics
  • [ISO-abbreviation] Curr Protoc Hum Genet
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] United States
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87. Forman SJ: Allogeneic hematopoietic cell transplantation for acute lymphoblastic leukemia in adults. Hematol Oncol Clin North Am; 2009 Oct;23(5):1011-31, vi
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  • [Title] Allogeneic hematopoietic cell transplantation for acute lymphoblastic leukemia in adults.
  • Acute lymphoblastic leukemia (ALL) is a hematologic malignancy of the bone marrow characterized by the rapid proliferation and subsequent accumulation of immature lymphocytes.
  • ALL accounts for 20% of all acute leukemias that are seen in adults over the age of 20 years.
  • In the past 2 decades, there has been substantial improvement in the understanding of the molecular biology of the disease and in the management of adult patients who have this disorder, including allogeneic transplantation This article reviews the biology of adult ALL, the relationship of specific disease characteristics to the natural history of the disease and the role of allogeneic hematopoietic cell transplantation in the management of adult patients with this disease.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy


88. Nishiuchi T, Ohnishi H, Kamada R, Kikuchi F, Shintani T, Waki F, Kitanaka A, Kubota Y, Tanaka T, Ishida T: Acute leukemia of ambiguous lineage, biphenotype, without CD34, TdT or TCR-rearrangement. Intern Med; 2009;48(16):1437-41
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  • [Title] Acute leukemia of ambiguous lineage, biphenotype, without CD34, TdT or TCR-rearrangement.
  • Biphenotypic acute leukemia (BAL) is a rare entity that comprises 0.5-3% of all acute leukemias and probably arises from multipotent progenitor cells.
  • We report the case of a 41-year-old man with BAL having myeloid and T-lymphoid lineage phenotypes.
  • [MeSH-major] Antigens, CD34 / genetics. Cell Lineage / genetics. DNA Nucleotidylexotransferase / genetics. Gene Rearrangement / genetics. Leukemia, Biphenotypic, Acute / genetics. Receptors, Antigen, T-Cell. Receptors, Antigen, T-Cell, alpha-beta / genetics. Receptors, Antigen, T-Cell, gamma-delta / genetics

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  • (PMID = 19687594.001).
  • [ISSN] 1349-7235
  • [Journal-full-title] Internal medicine (Tokyo, Japan)
  • [ISO-abbreviation] Intern. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Receptors, Antigen, T-Cell; 0 / Receptors, Antigen, T-Cell, alpha-beta; 0 / Receptors, Antigen, T-Cell, gamma-delta; EC 2.7.7.31 / DNA Nucleotidylexotransferase
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89. Teuffel O, Stanulla M, Cario G, Ludwig WD, Rottgers S, Schafer BW, Zimmermann M, Schrappe M, Niggli FK: Anemia and survival in childhood acute lymphoblastic leukemia. Haematologica; 2008 Nov;93(11):1652-7
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  • [Title] Anemia and survival in childhood acute lymphoblastic leukemia.
  • BACKGROUND: Several studies have demonstrated that patients with childhood acute lymphoblastic leukemia presenting with mild anemia at diagnosis have an increased risk of poor outcome compared to patients with more severe anemia.
  • However, it has not been reported whether there is any correlation between degree of anemia and leukemia subtype.
  • DESIGN AND METHODS: In a cohort of 1162 patients with childhood acute lymphoblastic leukemia we analyzed whether there was a correlation between degree of anemia and leukemia subtype.
  • The degree of anemia was significantly different for three distinct groups of patients compared to the remaining patients (mean hemoglobin; T-cell leukemia: 106 g/L versus 76 g/L (precursor B-cell acute lymphoblastic leukemia); within precursor B-cell ALL: TEL-AML1 positive: 68 g/L versus 79 g/L; BCR-ABL positive: 93 g/L versus 76 g/L; each p<0.05).
  • Furthermore, in contrast to the entire study group, patients with T-cell leukemia, TEL-AML1(+), and BCR-ABL(+) precursor B-cell leukemia had a more favorable prognosis if presenting with a higher hemoglobin level (>/=80 g/L).
  • CONCLUSIONS: These observations indicate that the formerly reported direct correlation between severity of anemia and survival in childhood acute lymphoblastic leukemia mainly reflects differences in the degree of anemia between distinct biological subgroups with different treatment outcomes.
  • On the other hand, the inverse relationship between severity of anemia and survival found within specific subgroups suggests that very low hemoglobin levels at diagnosis are associated with more advanced disease in these subgroups.
  • [MeSH-major] Anemia / epidemiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications. Precursor Cell Lymphoblastic Leukemia-Lymphoma / mortality
  • [MeSH-minor] Burkitt Lymphoma / complications. Burkitt Lymphoma / genetics. Burkitt Lymphoma / mortality. Child. Cohort Studies. Core Binding Factor Alpha 2 Subunit / genetics. Disease-Free Survival. Fusion Proteins, bcr-abl / genetics. Hemoglobins / metabolism. Homeodomain Proteins / genetics. Humans. Leukemia, T-Cell / complications. Leukemia, T-Cell / genetics. Leukemia, T-Cell / mortality. Leukocyte Count. Mutation. Oncogene Proteins, Fusion / genetics. Risk Factors. Survival Analysis. Treatment Outcome

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  • (PMID = 18815194.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / Hemoglobins; 0 / Homeodomain Proteins; 0 / Oncogene Proteins, Fusion; 0 / RUNX1 protein, human; 146150-85-8 / E2A-Pbx1 fusion protein; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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90. Forester CM, Braunreiter CL, Yaish H, Hedlund GL, Afify Z: Tumefactive intracranial presentation of precursor B-cell acute lymphoblastic leukemia. Pediatr Radiol; 2009 Nov;39(11):1230-3
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  • [Title] Tumefactive intracranial presentation of precursor B-cell acute lymphoblastic leukemia.
  • In children, leukemia is the most common malignancy, and approximately 75% of leukemias are acute lymphoblastic leukemia (ALL).
  • Central nervous system leukemia is found at diagnosis in fewer than 5% of children with ALL.
  • Leukemic intracranial masses have been described with acute myeloid leukemia, but ALL presenting as a mass lesion is rare.
  • We describe a unique case of an intracranial confirmed precursor B cell (pre-B) ALL mass in a 13-year-old girl that was diagnosed by brain CT, MRI and cerebral angiography, and confirmed by biopsy.
  • [MeSH-major] Brain Neoplasms / diagnosis. Cerebral Angiography / methods. Magnetic Resonance Imaging / methods. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Tomography, X-Ray Computed / methods


91. Williams RT, Sherr CJ: The ARF tumor suppressor in acute leukemias: insights from mouse models of Bcr-Abl-induced acute lymphoblastic leukemia. Adv Exp Med Biol; 2007;604:107-14
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  • [Title] The ARF tumor suppressor in acute leukemias: insights from mouse models of Bcr-Abl-induced acute lymphoblastic leukemia.
  • The prototypical Bcr-Abl chimeric oncoprotein is central to the pathogenesis of chronic myelogenous leukemias (CMLs) and a subset of acute lymphoblastic leukemias (Ph+ ALLs).
  • In murine bone marrow transplant models and after transfer of syngeneic Bcr-Abl-transformed pre-B cells into immunocompetent recipient animals, Arf gene inactivation dramatically decreases the latency and enhances the aggressiveness of Bcr-Abl-induced lymphoblastic leukemia.
  • Despite exquisite in vitro sensitivity of Arf-null, BCR-ABL+ pre-B cells to imatinib, these cells efficiently establish lethal leukemias when introduced into immunocompetent mice that receive continuous, maximal imatinib therapy.
  • [MeSH-major] Fusion Proteins, bcr-abl / metabolism. Gene Expression Regulation, Neoplastic. Genes, Tumor Suppressor. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology. Tumor Suppressor Protein p14ARF / physiology
  • [MeSH-minor] Animals. Antineoplastic Agents / pharmacology. Benzamides. Disease Models, Animal. Drug Resistance, Neoplasm. Humans. Imatinib Mesylate. Interleukin-7 / metabolism. Mice. Piperazines / pharmacology. Pyrimidines / pharmacology

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  • (PMID = 17695724.001).
  • [ISSN] 0065-2598
  • [Journal-full-title] Advances in experimental medicine and biology
  • [ISO-abbreviation] Adv. Exp. Med. Biol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / T32-CA70089
  • [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 / Antineoplastic Agents; 0 / Benzamides; 0 / Interleukin-7; 0 / Piperazines; 0 / Pyrimidines; 0 / Tumor Suppressor Protein p14ARF; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Fusion Proteins, bcr-abl
  • [Number-of-references] 20
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92. Röhrs S, Dirks WG, Meyer C, Marschalek R, Scherr M, Slany R, Wallace A, Drexler HG, Quentmeier H: Hypomethylation and expression of BEX2, IGSF4 and TIMP3 indicative of MLL translocations in acute myeloid leukemia. Mol Cancer; 2009;8:86
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  • [Title] Hypomethylation and expression of BEX2, IGSF4 and TIMP3 indicative of MLL translocations in acute myeloid leukemia.
  • BACKGROUND: Translocations of the Mixed Lineage Leukemia (MLL) gene occur in a subset (5%) of acute myeloid leukemias (AML), and in mixed phenotype acute leukemias in infancy - a disease with extremely poor prognosis.
  • Wild-type (wt) MLL possesses histone methyltransferase activity and functions at the level of chromatin organization by affecting the expression of specific target genes.
  • Hence, acute lymphoblastic leukemias (ALL) with MLL mutations (MLLmu) exhibit characteristic gene expression profiles including high-level expression of HOXA cluster genes.
  • Here, we aimed to relate MLL mutational status and tumor suppressor gene (TSG) methylation/expression in acute leukemia cell lines.
  • RESULTS: Using MS-MLPA (methylation-specific multiplex ligation-dependent probe amplification assay), methylation of 24 different TSG was analyzed in 28 MLLmu and MLLwt acute leukemia cell lines.
  • Hypomethylation and expression of the TSG BEX2, IGSF4 and TIMP3 turned out to be characteristic of MLLmu AML cell lines.
  • MLLwt AML cell lines displayed hypermethylated TSG promoters resulting in transcriptional silencing.
  • This concept was supported by our observation that Bex2 mRNA levels in MLL-ENL transgenic mouse cell lines required expression of the MLL fusion gene.
  • CONCLUSION: These results suggest that the conspicuous expression of the TSG BEX2, IGSF4 and TIMP3 in MLLmu AML cell lines is the consequence of altered epigenetic properties of MLL fusion proteins.
  • [MeSH-major] Immunoglobulins / metabolism. Leukemia, Myeloid, Acute / genetics. Membrane Proteins / metabolism. Myeloid-Lymphoid Leukemia Protein / metabolism. Nerve Tissue Proteins / metabolism. Tissue Inhibitor of Metalloproteinase-3 / metabolism. Translocation, Genetic. Tumor Suppressor Proteins / metabolism
  • [MeSH-minor] Azacitidine / pharmacology. Cell Adhesion Molecules. Cell Line, Tumor. DNA Methylation / drug effects. Gene Expression Regulation, Leukemic / drug effects. Histones / metabolism. Humans. Hydroxamic Acids / pharmacology. Mutation / genetics. Oncogene Proteins, Fusion / metabolism. Promoter Regions, Genetic. Receptors, Retinoic Acid / metabolism. Sequence Analysis, DNA. Transcription, Genetic / drug effects

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  • (PMID = 19835597.001).
  • [ISSN] 1476-4598
  • [Journal-full-title] Molecular cancer
  • [ISO-abbreviation] Mol. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / BEX2 protein, human; 0 / CADM1 protein, human; 0 / Cell Adhesion Molecules; 0 / Histones; 0 / Hydroxamic Acids; 0 / Immunoglobulins; 0 / MLL-ENL oncoprotein, human; 0 / Membrane Proteins; 0 / Nerve Tissue Proteins; 0 / Oncogene Proteins, Fusion; 0 / Receptors, Retinoic Acid; 0 / TIMP3 protein, human; 0 / Tissue Inhibitor of Metalloproteinase-3; 0 / Tumor Suppressor Proteins; 0 / retinoic acid receptor beta; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; 3X2S926L3Z / trichostatin A; M801H13NRU / Azacitidine
  • [Other-IDs] NLM/ PMC2770485
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93. Weerkamp F, van Dongen JJ, Staal FJ: Notch and Wnt signaling in T-lymphocyte development and acute lymphoblastic leukemia. Leukemia; 2006 Jul;20(7):1197-205
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  • [Title] Notch and Wnt signaling in T-lymphocyte development and acute lymphoblastic leukemia.
  • Many acute lymphoblastic leukemias can be considered as malignant counterparts of cells in the various stages of normal lymphoid development in bone marrow and thymus.
  • T-cell development in the thymus is an ordered and tightly controlled process.
  • Two evolutionary conserved signaling pathways, which were first discovered in Drosophila, control the earliest steps of T-cell development.
  • These are the Notch and Wnt-signaling routes, which both are deregulated in several types of leukemias.
  • In this review we discuss both pathways, with respect to their signaling mechanisms, functions during T-cell development and their roles in development of leukemias, especially T-cell acute lymphoblastic leukemia.
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Receptors, Notch / metabolism. Signal Transduction / physiology. T-Lymphocytes / metabolism. Wnt Proteins / metabolism

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  • (PMID = 16688226.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Receptors, Notch; 0 / Wnt Proteins
  • [Number-of-references] 123
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94. Altucci L, Clarke N, Nebbioso A, Scognamiglio A, Gronemeyer H: Acute myeloid leukemia: therapeutic impact of epigenetic drugs. Int J Biochem Cell Biol; 2005 Sep;37(9):1752-62
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  • [Title] Acute myeloid leukemia: therapeutic impact of epigenetic drugs.
  • Acute myeloid leukemia (AML) is not a single disease but a group of malignancies in which the clonal expansion of various types of hematopoietic precursor cells in the bone marrow leads to perturbation of the delicate balance between self-renewal and differentiation that is characteristic of normal hematopoiesis.
  • An increasing number of genetic aberrations, such as chromosomal translocations that alter the function of transcription regulatory factors, has been identified as the cause of AML and shown to act by deregulating gene programming at both the genetic and epigenetic level.
  • While the genetic aberrations occurring in acute myeloid leukemia are fairly well understood, we have only recently become aware of the epigenetic deregulation associated with leukemia, in particular with myeloid leukemias.
  • In this review we focus on the epigenetic mechanisms associated with acute myeloid leukemogenesis and discuss the therapeutic potential of epigenetic modulators such as histone deacetylase and DNA methyltransferase inhibitors.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Epigenesis, Genetic. Leukemia, Myeloid / drug therapy. Leukemia, Myeloid / genetics. Mutation / genetics
  • [MeSH-minor] Acetylation. Acute Disease. Amino Acid Sequence. Animals. DNA Methylation. Gene Expression Regulation, Neoplastic. Gene Silencing. Histone Deacetylase Inhibitors. Humans. Molecular Sequence Data

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  • (PMID = 15964234.001).
  • [ISSN] 1357-2725
  • [Journal-full-title] The international journal of biochemistry & cell biology
  • [ISO-abbreviation] Int. J. Biochem. Cell Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Histone Deacetylase Inhibitors
  • [Number-of-references] 54
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95. Murati A, Gervais C, Carbuccia N, Finetti P, Cervera N, Adélaïde J, Struski S, Lippert E, Mugneret F, Tigaud I, Penther D, Bastard C, Poppe B, Speleman F, Baranger L, Luquet I, Cornillet-Lefebvre P, Nadal N, Nguyen-Khac F, Pérot C, Olschwang S, Bertucci F, Chaffanet M, Lessard M, Mozziconacci MJ, Birnbaum D, Groupe Francophone de Cytogénétique Hématologique: Genome profiling of acute myelomonocytic leukemia: alteration of the MYB locus in MYST3-linked cases. Leukemia; 2009 Jan;23(1):85-94
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  • [Title] Genome profiling of acute myelomonocytic leukemia: alteration of the MYB locus in MYST3-linked cases.
  • The t(8;16)(p11;p13) is a rare translocation involved in de novo and therapy-related myelomonocytic and monocytic acute leukemia.
  • MYST3-linked acute myeloid leukemias (AMLs) share specific clinical and biological features and a poor prognosis.
  • We have established the genome and gene expression profiles of a multicentric series of 61 M4/M5 AMLs including 18 MYST3-linked AMLs by using array comparative genome hybridization (aCGH) (n=52) and DNA microarrays (n=44), respectively.
  • These features, reminiscent of T-cell acute lymphoid leukemia (ALL), suggest the targeting of a common T-myeloid progenitor.
  • [MeSH-major] Gene Expression Profiling / methods. Genes, myb / genetics. Histone Acetyltransferases / genetics. Leukemia, Myelomonocytic, Acute / genetics

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  • (PMID = 18818702.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD4; 0 / Homeodomain Proteins; 0 / Proto-Oncogene Proteins c-myb; 157907-48-7 / HoxA protein; EC 2.3.1.48 / Histone Acetyltransferases; EC 2.3.1.48 / KAT6A protein, human
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96. Abd El-Ghaffar HA, Aladle DA, Farahat SE, Abd El-Hady N: P-glycoprotein (P-170) expression in acute leukemias. Hematology; 2006 Feb;11(1):35-41
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] P-glycoprotein (P-170) expression in acute leukemias.
  • Multidrug resistance (MDR) is still a major obstacle to chemotherapy success in acute myeloid leukemia (AML) and to a less extent acute lymphoblastic leukemia (ALL).
  • This study was planned to study the expression of P-glycoprotein/170 in patients with acute leukemia and the effect of Cyclosporin A (CSA) as a modulator of P-glycoprotein functional activity.
  • The study was carried out on 20 patients with acute leukemia (14 AML cases and 6 ALL cases).
  • Flow cytometric analysis of P-gp/170 surface expression was performed using UIC-2 MoAb together with the functional assay using Rhodamine 123 (Rh 123) and Cyclosporin A as a modulator.P-gp/170 was expressed on the leukemic cells of 37.5% of relapsed patients (40.0% of AML and 33.3% of ALL cases), whereas 27.2% of de novo patients expressed P-gp/170 (33.3% of AML cases and 0% of ALL cases).
  • The functional activity of MDR-1 gp was 71.4% in AML and 33.3% in ALL patients compared with16.6% in normal lymphocytes.
  • From this study, it is clear that P-gp/170 is expressed to a higher degree in leukemic cells and this is greater in relapsed compared to de novo cases and more in AML than ALL blasts.
  • [MeSH-major] Drug Resistance, Multiple. Drug Resistance, Neoplasm. Gene Expression Regulation, Leukemic. Leukemia, Myeloid, Acute / metabolism. P-Glycoprotein / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism

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  • (PMID = 16522547.001).
  • [ISSN] 1024-5332
  • [Journal-full-title] Hematology (Amsterdam, Netherlands)
  • [ISO-abbreviation] Hematology
  • [Language] eng
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / P-Glycoprotein
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97. Subramaniam P, Babu KL, Nagarathna J: Oral manifestations in acute lymphoblastic leukemic children under chemotherapy. J Clin Pediatr Dent; 2008;32(4):319-24
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  • [Title] Oral manifestations in acute lymphoblastic leukemic children under chemotherapy.
  • Leukemia is a common malignancy seen in young children and acute lymphoblastic leukemia (ALL) accounts for 75% of all leukemias.
  • Immune suppression caused due to disease and therapy makes these children more prone to bacterial, fungal infections and at times reactivation of viral diseases.
  • [MeSH-major] Oral Ulcer / etiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Stomatitis / etiology

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  • (PMID = 18767465.001).
  • [ISSN] 1053-4628
  • [Journal-full-title] The Journal of clinical pediatric dentistry
  • [ISO-abbreviation] J Clin Pediatr Dent
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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98. Chim CS, Wong AS, Kwong YL: Epigenetic inactivation of the CIP/KIP cell-cycle control pathway in acute leukemias. Am J Hematol; 2005 Dec;80(4):282-7
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  • [Title] Epigenetic inactivation of the CIP/KIP cell-cycle control pathway in acute leukemias.
  • Dysregulation of the cell cycle is important in oncogenesis.
  • We analyzed the potential inactivation of the CIP/KIP family of the cyclin E/CDK/RB pathway by gene promoter hypermethylation in leukemias.
  • The methylation-specific polymerase chain reaction (MSP) with primers for methylated (M-MSP) and unmethylated (U-MSP) alleles of the p21, p27, and p57 genes was used to study five leukemic cell lines, 50 acute myeloid leukemia (AML) samples, and 25 acute lymphoblastic leukemia (ALL) samples. p21 was hemizygously methylated in Raji and Jurkat but remained unmethylated in U937, HL60, and NB4. p27 was hemizygously methylated in Raji but unmethylated in the other cell lines. p57 was completely methylated in Raji and NB4, hemizygously methylated in U937, and unmethylated in HL60 and Jurkat.
  • Therefore, methylation inactivation of the INK4/CDK/RB pathway in leukemia is infrequent.
  • [MeSH-major] Calcium-Binding Proteins / metabolism. Cell Cycle. Cyclin-Dependent Kinase Inhibitor Proteins / metabolism. DNA Methylation. Epigenesis, Genetic. Gene Expression Regulation, Leukemic. Leukemia, Myeloid, Acute / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism
  • [MeSH-minor] Alleles. Cell Line, Tumor. Humans. Polymerase Chain Reaction. Signal Transduction / genetics

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  • [Copyright] (c) 2005 Wiley-Liss, Inc.
  • (PMID = 16315255.001).
  • [ISSN] 0361-8609
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CIB1 protein, human; 0 / Calcium-Binding Proteins; 0 / Cyclin-Dependent Kinase Inhibitor Proteins
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99. Aydin-Sayitoglu M, Hatirnaz O, Erensoy N, Ozbek U: Role of CYP2D6, CYP1A1, CYP2E1, GSTT1, and GSTM1 genes in the susceptibility to acute leukemias. Am J Hematol; 2006 Mar;81(3):162-70
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  • [Title] Role of CYP2D6, CYP1A1, CYP2E1, GSTT1, and GSTM1 genes in the susceptibility to acute leukemias.
  • Acute leukemias (ALs) are heterogeneous diseases.
  • Functional polymorphisms in the genes encoding detoxification enzymes cause inter-individual differences, which contribute to leukemia susceptibility.
  • The CYP2D6*3 variant allele frequency was lower in the overall acute leukemia patients (0.6%) compared to controls (P = 0.03).
  • No association was found for the studied CYP2D6*4, CYP1A1*2A, and GSTT1"null" variants and the risk of acute leuke-mia (ALL or AML).
  • This case-control study suggests a contribution of CYP2E1, CYP2D6, and GSTM1 "null" variants to the development of acute leukemias.
  • [MeSH-major] Cytochrome P-450 CYP1A1 / genetics. Cytochrome P-450 CYP2D6 / genetics. Cytochrome P-450 CYP2E1 / genetics. Genetic Predisposition to Disease. Glutathione Transferase / genetics. Leukemia, Myeloid, Acute / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 16493615.001).
  • [ISSN] 0361-8609
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 1.14.13.- / Cytochrome P-450 CYP2E1; EC 1.14.14.1 / Cytochrome P-450 CYP1A1; EC 1.14.14.1 / Cytochrome P-450 CYP2D6; EC 2.5.1.- / glutathione S-transferase T1; EC 2.5.1.18 / Glutathione Transferase; EC 2.5.1.18 / glutathione S-transferase M1
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100. Caligiuri MA, Briesewitz R, Yu J, Wang L, Wei M, Arnoczky KJ, Marburger TB, Wen J, Perrotti D, Bloomfield CD, Whitman SP: Novel c-CBL and CBL-b ubiquitin ligase mutations in human acute myeloid leukemia. Blood; 2007 Aug 1;110(3):1022-4
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  • [Title] Novel c-CBL and CBL-b ubiquitin ligase mutations in human acute myeloid leukemia.
  • Many TKs are mutationally or autocrine activated and/or often overexpressed at the mRNA and protein levels in acute leukemias.
  • We hypothesized that CBL is mutated in patients with acute myeloid leukemia (AML).
  • Four of 12 patients and the MOLM-13 cell line harbored c-CBL mutations, either RNA splicing mutations, missense mutations, or a nucleotide insertion.

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  • (PMID = 17475912.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA 89341; United States / NCI NIH HHS / CA / R01 CA089341; United States / NCI NIH HHS / CA / P30 CA 16058; United States / NCI NIH HHS / CA / K01 CA096887; United States / NCI NIH HHS / CA / P30 CA016058; United States / NCI NIH HHS / CA / K01 CA 96887
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / RNA, Small Interfering; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 6.3.2.- / CBL protein, human; EC 6.3.2.- / Proto-Oncogene Proteins c-cbl; EC 6.3.2.19 / CBLB protein, human
  • [Other-IDs] NLM/ PMC1924768
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