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1. Fujino H, Fujita N, Hamamoto K, Oobu S, Kita M, Tanaka A, Matsubara H, Watanabe K, Heike T, Adachi S: Ring/marker chromosome derived from chromosome 7 in childhood acute megakaryoblastic leukemia with monosomy 7. Int J Hematol; 2010 Sep;92(2):386-90
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Ring/marker chromosome derived from chromosome 7 in childhood acute megakaryoblastic leukemia with monosomy 7.
  • In some cases of childhood acute megakaryoblastic leukemia (AMKL), G-band analysis reveals supernumerary ring/marker chromosomes along with monosomy 7.
  • We experienced three patients with AMKL, one of whom had Down's syndrome, whose blasts at the first visit exhibited both monosomy 7 and a ring/marker chromosome.
  • While it is not clear whether the ring/marker chromosome 7 affects the long-term prognosis of acute myeloid leukemia with monosomy 7, it may be of prognostic relevance to distinguish pure monosomy 7 from monosomy 7 with a ring/marker chromosome 7.
  • These methods may be useful for determining the optimal treatment and for elucidating the etiology of AMKL itself.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 7. Leukemia, Megakaryoblastic, Acute / genetics

  • Genetic Alliance. consumer health - Chromosome 7, Monosomy.
  • Genetic Alliance. consumer health - Acute Megakaryoblastic Leukemia.
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  • (PMID = 20809201.001).
  • [ISSN] 1865-3774
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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2. García-Fernández AJ, Rodríguez RA, Pérez-Pertejo Y, Balaña-Fouce R: Characterization of putrescine uptake in hamster amelanocytic melanoma AMEL-3 cells. Mol Cells; 2005 Aug 31;20(1):127-35
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  • [Title] Characterization of putrescine uptake in hamster amelanocytic melanoma AMEL-3 cells.
  • The uptake of putrescine, spermidine and spermine by Fortner's hamster amelanocytic melanoma AMEL-3 cells was observed in this study to be time-dependent, temperature-sensitive, pH-dependent and saturable.

  • Hazardous Substances Data Bank. Putrescine .
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  • (PMID = 16258251.001).
  • [ISSN] 1016-8478
  • [Journal-full-title] Molecules and cells
  • [ISO-abbreviation] Mol. Cells
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Amidines; 0 / Sulfhydryl Reagents; 2FZ7Y3VOQX / Spermine; O3C74ACM9V / Ethylmaleimide; U87FK77H25 / Spermidine; V10TVZ52E4 / Putrescine
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3. McCormack MP, Hall MA, Schoenwaelder SM, Zhao Q, Ellis S, Prentice JA, Clarke AJ, Slater NJ, Salmon JM, Jackson SP, Jane SM, Curtis DJ: A critical role for the transcription factor Scl in platelet production during stress thrombopoiesis. Blood; 2006 Oct 1;108(7):2248-56
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  • Quantitative real-time polymerase chain reaction showed that Scl-null platelets lacked NF-E2, and chromatin immunoprecipitation analysis demonstrated Scl binding to the NF-E2 promoter in the human megakaryoblastic-cell line Meg-01, along with its binding partners E47, Lmo2, and the cofactors Ldb1 and GATA-2.

  • Gene Ontology. gene/protein/disease-specific - Gene Ontology annotations from this paper .
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
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  • (PMID = 16763211.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / PHS HHS / / 237011; United States / PHS HHS / / 282400; United States / NHLBI NIH HHS / HL / P01 HL53749-03
  • [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 / Basic Helix-Loop-Helix Transcription Factors; 0 / NF-E2 Transcription Factor, p45 Subunit; 0 / Nfe2 protein, mouse; 0 / Proto-Oncogene Proteins; 0 / Tal1 protein, mouse; 9014-42-0 / Thrombopoietin
  • [Other-IDs] NLM/ PMC1895552
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4. Casali N, Riley LW: A phylogenomic analysis of the Actinomycetales mce operons. BMC Genomics; 2007 Feb 26;8:60
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  • Some of the Actinomycetales mce operons include an mkl gene, which encodes an ATPase resembling those of ABC uptake transporters.
  • The phylogenetic profile of Mkl orthologs exactly matched that of the Mce and YrbE proteins.
  • Through topology and motif analyses of YrbE homologs, we identified a region within the penultimate cytoplasmic loop that may serve as the site of interaction with the putative cognate Mkl ATPase.
  • Operons containing linked mkl, yrbE and mce genes, resembling the classic organization of an ABC importer, were found to be common in Gram-negative bacteria and appear to be associated with changes in properties of the cell surface.

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  • (PMID = 17324287.001).
  • [ISSN] 1471-2164
  • [Journal-full-title] BMC genomics
  • [ISO-abbreviation] BMC Genomics
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / R21 AI063350; United States / NIAID NIH HHS / AI / R21AI063350
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Bacterial Proteins
  • [Other-IDs] NLM/ PMC1810536
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5. Piccoli C, Ripoli M, Scrima R, Stanziale P, Di Ianni M, Moretti L, Biscottini B, Carella M, Boffoli D, Tabilio A, Capitanio N: MtDNA mutation associated with mitochondrial dysfunction in megakaryoblastic leukaemic cells. Leukemia; 2008 Oct;22(10):1938-41
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] MtDNA mutation associated with mitochondrial dysfunction in megakaryoblastic leukaemic cells.
  • [MeSH-major] DNA, Mitochondrial / genetics. Leukemia, Megakaryoblastic, Acute / genetics. Leukemia, Megakaryoblastic, Acute / metabolism. Mitochondria / metabolism. Mutation

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  • (PMID = 18368068.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA, Mitochondrial; 0 / Reactive Oxygen Species; EC 1.6.99.3 / NADH Dehydrogenase; EC 1.6.99.3 / NADH dehydrogenase subunit 1, human
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6. Barnard DR, Alonzo TA, Gerbing RB, Lange B, Woods WG, Children's Oncology Group: Comparison of childhood myelodysplastic syndrome, AML FAB M6 or M7, CCG 2891: report from the Children's Oncology Group. Pediatr Blood Cancer; 2007 Jul;49(1):17-22
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Comparison of childhood myelodysplastic syndrome, AML FAB M6 or M7, CCG 2891: report from the Children's Oncology Group.
  • BACKGROUND: Myelodysplastic syndromes (MDS), acute erythroleukemia (FAB M6), and acute megakaryocytic leukemia (FAB M7) have overlapping features.
  • PROCEDURE: Children without Down syndrome or acute promyelocytic leukemia who were newly diagnosed with primary myelodysplastic syndrome or acute myeloid leukemia (AML) M6 or M7 were compared to children with de novo AML M0-M5.
  • RESULTS: The presentation and outcomes of the 132 children diagnosed with MDS (60 children), AML FAB M6 (19 children), or AML FAB M7 (53 children) were similar.
  • Children with AML FAB M7 were diagnosed at a significantly younger age (P = 0.001).
  • Children with MDS, M6, or M7 had significantly lower white blood cell (WBC) counts (P = 0.001), lower peripheral blast counts (P < 0.001), and an increased frequency of -7/7q- (P = 0.003) at presentation.
  • All three groups had significantly inferior overall survival (OS) (P < 0.001) and event free survival (P < 0.001) compared with the 748 children diagnosed with AML FAB M0-M5 when assessed from entry on study.
  • However, when assessed from successful completion of induction therapy, the 5-year OS (P = 0.090)(49.1 vs. 56.9%) and disease-free survival (DFS) (P = 0.113)(38.0 vs. 46.3%) therapy were not significantly different from other children with AML.
  • CONCLUSIONS: Childhood AML FAB M6 and AML M7 resemble MDS in presentation, poor induction success rates, and outcomes.
  • [MeSH-major] Leukemia, Erythroblastic, Acute / diagnosis. Leukemia, Megakaryoblastic, Acute / diagnosis. Myelodysplastic Syndromes / diagnosis
  • [MeSH-minor] Acute Disease. Child. Child, Preschool. Diagnosis, Differential. Disease-Free Survival. Female. Humans. Male. Prognosis. Remission Induction. Survival Rate. Treatment Outcome


7. Kyttälä S, Habermann I, Minami T, Ehninger G, Kiani A: Regulation of Down Syndrome Critical Region 1 expression by Nuclear Factor of Activated T cells in megakaryocytes. Br J Haematol; 2009 Feb;144(3):395-408
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Megakaryocytic dysfunction can lead to neoplastic disorders, such as acute megakaryoblastic leukaemia, an entity with a 500-fold increased incidence in children with Down syndrome (DS).
  • Down Syndrome Critical Region 1 (DSCR1), a member of the calcipressin family of calcineurin inhibitors, is overexpressed in DS, and destabilization of the calcineurin/Nuclear Factor of Activated T cells (NFAT) pathway by overexpression of DSCR1 has been implicated in some of the pathophysiological features of the disease.
  • NFAT activation in megakaryocytes was induced by fibrillar collagen type I and was completely sensitive to the calcineurin inhibitor cyclosporin A.
  • These results suggest that DSCR1 acts as an endogenous feedback inhibitor of NFAT signalling in megakaryocytes, and may have implications for megakaryocytic gene expression in DS.

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  • (PMID = 19036088.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Intracellular Signaling Peptides and Proteins; 0 / Muscle Proteins; 0 / NFATC Transcription Factors; 0 / RCAN1 protein, human; EC 3.1.3.16 / Calcineurin
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8. Fesenko DO, Mitiaeva ON, Nasedkina TV, Rubtsov PM, Lysov IuP, Zasedatelev AS: [HLA-DQA1, AB0 and AMEL genotyping of biological material by biochips]. Mol Biol (Mosk); 2010 May-Jun;44(3):456-62
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  • [Title] [HLA-DQA1, AB0 and AMEL genotyping of biological material by biochips].
  • A genotyping method of biological material for ABO, HLA-DQA1 and AMEL loci is described.

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  • (PMID = 20608169.001).
  • [ISSN] 0026-8984
  • [Journal-full-title] Molekuliarnaia biologiia
  • [ISO-abbreviation] Mol. Biol. (Mosk.)
  • [Language] rus
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Russia (Federation)
  • [Chemical-registry-number] 0 / ABO Blood-Group System; 0 / HLA-DQ Antigens; 0 / HLA-DQ alpha-Chains; 0 / HLA-DQA1 antigen
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9. Klusmann JH, Li Z, Böhmer K, Maroz A, Koch ML, Emmrich S, Godinho FJ, Orkin SH, Reinhardt D: miR-125b-2 is a potential oncomiR on human chromosome 21 in megakaryoblastic leukemia. Genes Dev; 2010 Mar 1;24(5):478-90
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  • [Title] miR-125b-2 is a potential oncomiR on human chromosome 21 in megakaryoblastic leukemia.
  • Children with trisomy 21/Down syndrome (DS) are at high risk to develop acute megakaryoblastic leukemia (DS-AMKL) and the related transient leukemia (DS-TL).
  • Here, we investigated the role of Hsa21-encoded miR-125b-2, a microRNA (miRNA) overexpressed in DS-AMKL/TL, in hematopoiesis and leukemogenesis.
  • We identified a function of miR-125b-2 in increasing proliferation and self-renewal of human and mouse megakaryocytic progenitors (MPs) and megakaryocytic/erythroid progenitors (MEPs).
  • miR-125b-2 overexpression did not affect megakaryocytic and erythroid differentiation, but severely perturbed myeloid differentiation.
  • The proproliferative effect of miR-125b-2 on MEPs accentuated the Gata1s mutation, whereas growth of DS-AMKL/TL cells was impaired upon miR-125b repression, suggesting synergism during leukemic transformation in GATA1s-mutated DS-AMKL/TL.
  • Gene Set Enrichment Analysis revealed that this target gene set is down-regulated in DS-AMKL patients highly expressing miR-125b.
  • Thus, we propose miR-125b-2 as a positive regulator of megakaryopoiesis and an oncomiR involved in the pathogenesis of trisomy 21-associated megakaryoblastic leukemia.
  • [MeSH-major] Chromosomes, Human, Pair 21 / genetics. Gene Expression Regulation, Leukemic. Leukemia, Megakaryoblastic, Acute / metabolism. MicroRNAs / metabolism

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  • (PMID = 20194440.001).
  • [ISSN] 1549-5477
  • [Journal-full-title] Genes & development
  • [ISO-abbreviation] Genes Dev.
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / R01 HL032259
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / GATA1 Transcription Factor; 0 / MIRN125 microRNA, human; 0 / MicroRNAs; 0 / Mirn125 microRNA, mouse; 0 / Repressor Proteins; 0 / ST18 protein, human; EC 3.1.26.3 / DICER1 protein, human; EC 3.1.26.3 / Ribonuclease III; EC 3.6.4.13 / DEAD-box RNA Helicases
  • [Other-IDs] NLM/ PMC2827843
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10. Miyauchi J, Ito Y, Tsukamoto K, Takahashi H, Ishikura K, Sugita K, Miyashita T: Blasts in transient leukaemia in neonates with Down syndrome differentiate into basophil/mast-cell and megakaryocyte lineages in vitro in association with down-regulation of truncated form of GATA1. Br J Haematol; 2010 Mar;148(6):898-909
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  • [Title] Blasts in transient leukaemia in neonates with Down syndrome differentiate into basophil/mast-cell and megakaryocyte lineages in vitro in association with down-regulation of truncated form of GATA1.
  • Mutations of GATA1, leading to aberrant expression of a truncated form of GATA1 (called GATA1s), are present in transient leukaemia (TL) in neonates with Down syndrome.
  • [MeSH-major] Down Syndrome / pathology. GATA1 Transcription Factor / metabolism. Leukemia, Megakaryoblastic, Acute / pathology. Neoplastic Stem Cells / ultrastructure


11. Tunstall-Pedoe O, Roy A, Karadimitris A, de la Fuente J, Fisk NM, Bennett P, Norton A, Vyas P, Roberts I: Abnormalities in the myeloid progenitor compartment in Down syndrome fetal liver precede acquisition of GATA1 mutations. Blood; 2008 Dec 1;112(12):4507-11
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  • [Title] Abnormalities in the myeloid progenitor compartment in Down syndrome fetal liver precede acquisition of GATA1 mutations.
  • Down syndrome (DS) children have a high frequency of acute megakaryoblastic leukemia (AMKL) in early childhood.
  • At least 2 in utero genetic events are required, although not sufficient, for DS-AMKL: trisomy 21 (T21) and N-terminal-truncating GATA1 mutations.
  • To investigate the role of T21 in DS-AMKL, we compared second trimester hemopoiesis in DS without GATA1 mutations to gestation-matched normal controls.
  • In all DS fetal livers (FLs), but not marrows, megakaryocyte-erythroid progenitor frequency was increased (55.9% +/- 4% vs 17.1% +/- 3%, CD34(+)CD38(+) cells; P < .001) with common myeloid progenitors (19.6% +/- 2% vs 44.0% +/- 7%) and granulocyte-monocyte (GM) progenitors (15.8% +/- 4% vs 34.5% +/- 9%) commensurately reduced.
  • These data indicate that T21 itself profoundly disturbs FL hemopoiesis and they provide a testable hypothesis to explain the increased susceptibility to GATA1 mutations in DS-AMKL and DS-associated transient myeloproliferative disorder.
  • [MeSH-major] Congenital Abnormalities / genetics. Down Syndrome / complications. Down Syndrome / genetics. GATA1 Transcription Factor / genetics. Genetic Predisposition to Disease / etiology. Liver Diseases / genetics. Myeloid Progenitor Cells / pathology
  • [MeSH-minor] Antigens, CD34 / metabolism. Cell Count. Female. Humans. Leukemia, Megakaryoblastic, Acute / complications. Leukemia, Megakaryoblastic, Acute / embryology. Leukemia, Megakaryoblastic, Acute / genetics. Mutation / physiology. Pregnancy. Pregnancy Trimester, Second. Time Factors


12. Durmaz R, Zozio T, Gunal S, Yaman A, Cavusoglu C, Guney C, Sola C, Rastogi N: Genetic diversity and major spoligotype families of drug-resistant Mycobacterium tuberculosis clinical isolates from different regions of Turkey. Infect Genet Evol; 2007 Jul;7(4):513-9
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  • The major spoligotyping-defined shared-types (STs) and corresponding lineages were, ST 41 (22.5%, LAM7-TUR), ST53 (19.5%, ill-defined T super-family), ST 50 (6.5%, Haarlem 3), ST 1261 (4.5%, LAM7-TUR), ST 47 (3.5%, Haarlem 1), as well as two STs that belonged to undefined clades (ST 284, 3%, and ST 2067, 2.5%).
  • Our results underline the highly diverse nature of drug-resistant tuberculosis in our study population, as well as its ongoing transmission with lineages that are specific to these regions, the most predominant being the LAM7-TUR lineage which shows an enhanced phylogeographical specificity for Turkey.

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  • [ErratumIn] Infect Genet Evol. 2008 Mar;8(2):227
  • (PMID = 17462962.001).
  • [ISSN] 1567-1348
  • [Journal-full-title] Infection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases
  • [ISO-abbreviation] Infect. Genet. Evol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
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13. Lee AB, Harker-Murray P, Ferrieri P, Schleiss MR, Tolar J: Bacterial meningitis from Rothia mucilaginosa in patients with malignancy or undergoing hematopoietic stem cell transplantation. Pediatr Blood Cancer; 2008 Mar;50(3):673-6
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  • [MeSH-major] Actinomycetales Infections / microbiology. Cord Blood Stem Cell Transplantation. Leukemia, Megakaryoblastic, Acute / surgery. Meningitis, Bacterial / microbiology. Micrococcaceae / isolation & purification. Opportunistic Infections / microbiology. Postoperative Complications / microbiology

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  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • (PMID = 17588235.001).
  • [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 / Anti-Bacterial Agents; 0 / Thienamycins; 6Q205EH1VU / Vancomycin; 9M416Z9QNR / Ceftazidime; FV9J3JU8B1 / meropenem; VJT6J7R4TR / Rifampin
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14. Hiramatsu H, Morishima T, Nakanishi H, Mizushima Y, Miyazaki M, Matsubara H, Kobayashi M, Nakahata T, Adachi S: Successful treatment of a patient with Klinefelter's syndrome complicated by mediastinal germ cell tumor and AML(M7). Bone Marrow Transplant; 2008 May;41(10):907-8
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  • [Title] Successful treatment of a patient with Klinefelter's syndrome complicated by mediastinal germ cell tumor and AML(M7).
  • [MeSH-major] Klinefelter Syndrome / complications. Klinefelter Syndrome / therapy. Leukemia, Megakaryoblastic, Acute / drug therapy. Leukemia, Megakaryoblastic, Acute / etiology. Mediastinal Neoplasms / etiology. Mediastinal Neoplasms / surgery. Teratoma / etiology. Teratoma / surgery

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  • (PMID = 18223696.001).
  • [ISSN] 0268-3369
  • [Journal-full-title] Bone marrow transplantation
  • [ISO-abbreviation] Bone Marrow Transplant.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] England
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15. Sire JY, Delgado SC, Girondot M: Hen's teeth with enamel cap: from dream to impossibility. BMC Evol Biol; 2008;8:246
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  • RESULTS: Using bioinformatics, we assessed the fate of the four dental proteins thought to be specific to enamel (amelogenin, AMEL; ameloblastin, AMBN; enamelin, ENAM) and to dentin (dentin sialophosphoprotein, DSPP) in the chicken genome.
  • We found the full-length chicken AMEL and the only N-terminal region of DSPP, and both are invalidated genes.

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  • (PMID = 18775069.001).
  • [ISSN] 1471-2148
  • [Journal-full-title] BMC evolutionary biology
  • [ISO-abbreviation] BMC Evol. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Dental Enamel Proteins
  • [Other-IDs] NLM/ PMC2542379
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16. Pine SR, Guo Q, Yin C, Jayabose S, Levendoglu-Tugal O, Ozkaynak MF, Sandoval C: GATA1 as a new target to detect minimal residual disease in both transient leukemia and megakaryoblastic leukemia of Down syndrome. Leuk Res; 2005 Nov;29(11):1353-6
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  • [Title] GATA1 as a new target to detect minimal residual disease in both transient leukemia and megakaryoblastic leukemia of Down syndrome.
  • Acquired mutations in exon 2 of the GATA1 gene are detected in most Down syndrome (DS) patients with transient leukemia (TL) and acute megakaryoblastic leukemia (AMKL).
  • We sought to determine if GATA1 mutations can be utilized as markers for minimal residual disease (MRD).
  • We show that molecular monitoring of GATA1 mutations is possible in Down syndrome patients with TL and AMKL, and GATA1 could be a stable marker for MRD monitoring.
  • [MeSH-major] Down Syndrome / genetics. GATA1 Transcription Factor / genetics. Leukemia / diagnosis. Leukemia / genetics. Leukemia, Megakaryoblastic, Acute / diagnosis. Leukemia, Megakaryoblastic, Acute / genetics

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  • [CommentIn] Leuk Res. 2005 Nov;29(11):1239-40 [15925405.001]
  • (PMID = 15916804.001).
  • [ISSN] 0145-2126
  • [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
  • [Chemical-registry-number] 0 / GATA1 Transcription Factor
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17. Gonzalez Garcia JR, Meza-Espinoza JP: Use of the International System for Human Cytogenetic Nomenclature (ISCN). Blood; 2006 Dec 1;108(12):3952-3; author reply 3953
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [MeSH-major] Blast Crisis / genetics. Cytogenetics. Down Syndrome / genetics. Leukemia, Megakaryoblastic, Acute / genetics. Terminology as Topic

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  • [CommentOn] Blood. 2006 Jun 15;107(12):4606-13 [16469874.001]
  • (PMID = 17114573.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Comment; Letter
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Enzymes; RFM9X3LJ49 / Bilirubin
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18. Rainis L, Toki T, Pimanda JE, Rosenthal E, Machol K, Strehl S, Göttgens B, Ito E, Izraeli S: The proto-oncogene ERG in megakaryoblastic leukemias. Cancer Res; 2005 Sep 1;65(17):7596-602
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The proto-oncogene ERG in megakaryoblastic leukemias.
  • Acquired additions of chromosome 21 are a common finding in leukemias, suggesting a contributory role to leukemogenesis.
  • About 10% of patients with a germ line trisomy 21 (Down syndrome) are born with transient megakaryoblastic leukemia.
  • The gene or genes on chromosome 21 whose overexpression promote the megakaryoblastic phenotype are presently unknown.
  • We show that ERG is expressed in hematopoietic stem cells, megakaryoblastic cell lines, and in primary leukemic cells from Down syndrome patients.
  • ERG expression is induced upon megakaryocytic differentiation of the erythroleukemia cell lines K562 and UT-7, and forced expression of ERG in K562 cells induces erythroid to megakaryoblastic phenotypic switch.
  • We also show that ERG activates the gpIb megakaryocytic promoter and binds the gpIIb promoter in vivo.
  • Furthermore, both ERG and ETS2 bind in vivo the hematopoietic enhancer of SCL/TAL1, a key regulator of hematopoietic stem cell and megakaryocytic development.
  • We propose that trisomy 21 facilitates the occurrence of megakaryoblastic leukemias through a shift toward the megakaryoblastic lineage caused by the excess expression of ERG, and possibly by other chromosome 21 genes, such as RUNX1 and ETS2, in hematopoietic progenitor cells, coupled with a differentiation arrest caused by the acquisition of mutations in GATA1.
  • [MeSH-major] DNA-Binding Proteins / genetics. Leukemia, Megakaryoblastic, Acute / genetics. Oncogene Proteins / genetics. Trans-Activators / genetics
  • [MeSH-minor] Base Sequence. Basic Helix-Loop-Helix Transcription Factors. Cell Lineage. Chromosomes, Human, Pair 21 / genetics. Erythroid-Specific DNA-Binding Factors. GATA1 Transcription Factor. HeLa Cells. Hematopoietic Stem Cells / metabolism. Humans. K562 Cells. Leukemia, Erythroblastic, Acute / genetics. Leukemia, Erythroblastic, Acute / pathology. Molecular Sequence Data. Promoter Regions, Genetic. Proto-Oncogene Proteins / metabolism. Transcription Factors / genetics. Transcription Factors / metabolism

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  • (PMID = 16140924.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / DNA-Binding Proteins; 0 / ERG protein, human; 0 / Erythroid-Specific DNA-Binding Factors; 0 / GATA1 Transcription Factor; 0 / GATA1 protein, human; 0 / Oncogene Proteins; 0 / Proto-Oncogene Proteins; 0 / Trans-Activators; 0 / Transcription Factors; 135471-20-4 / TAL1 protein, human
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19. Bacher U, Kohlmann A, Haferlach C, Haferlach T: Gene expression profiling in acute myeloid leukaemia (AML). Best Pract Res Clin Haematol; 2009 Jun;22(2):169-80
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  • [Title] Gene expression profiling in acute myeloid leukaemia (AML).
  • In view of the genetic heterogeneity of acute myeloid leukaemia (AML), gene expression profiling (GEP) with the possibility of investigating the expression of tens of thousands of genes in parallel represents a promising approach to facilitate and improve the diagnostic process in this complex disorder.
  • In the last decade, following the introduction of this methodology in leukaemia research, various studies have demonstrated that classification of the majority of known genetic subclasses in AML can be performed with high accuracy by GEP.
  • International multicentre studies such as the MILE study (Microarray Innovations in LEukemia) pave the way to a standardised workflow of GEP in routine diagnostics in AML.
  • [MeSH-major] Gene Expression Profiling. Leukemia, Myeloid, Acute / genetics
  • [MeSH-minor] Humans. Leukemia, Megakaryoblastic, Acute / genetics. Leukemia, Promyelocytic, Acute / genetics. Microarray Analysis. Nuclear Proteins / genetics. fms-Like Tyrosine Kinase 3 / genetics

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  • (PMID = 19698926.001).
  • [ISSN] 1532-1924
  • [Journal-full-title] Best practice & research. Clinical haematology
  • [ISO-abbreviation] Best Pract Res Clin Haematol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Nuclear Proteins; 117896-08-9 / nucleophosmin; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
  • [Number-of-references] 62
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20. Kuhl C, Atzberger A, Iborra F, Nieswandt B, Porcher C, Vyas P: GATA1-mediated megakaryocyte differentiation and growth control can be uncoupled and mapped to different domains in GATA1. Mol Cell Biol; 2005 Oct;25(19):8592-606
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  • Moreover, acquired mutations deleting the N-terminal 84 amino acids are specifically detected in megakaryocytic leukemia in human Down syndrome patients.

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  • (PMID = 16166640.001).
  • [ISSN] 0270-7306
  • [Journal-full-title] Molecular and cellular biology
  • [ISO-abbreviation] Mol. Cell. Biol.
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / MC/ U137973816
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD9; 0 / CD9 protein, human; 0 / Cd9 protein, mouse; 0 / GATA1 Transcription Factor; 0 / Gata1 protein, mouse; 0 / Membrane Glycoproteins; 0 / Platelet Membrane Glycoprotein IIb; 147336-22-9 / Green Fluorescent Proteins; 9007-49-2 / DNA
  • [Other-IDs] NLM/ PMC1265752
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21. Stepensky P, Brooks R, Waldman E, Revel-Vilk S, Izraeli S, Resnick I, Weintraub M: A rare case of GATA1 negative chemoresistant acute megakaryocytic leukemia in an 8-month-old infant with trisomy 21. Pediatr Blood Cancer; 2010 Jul 1;54(7):1048-9
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  • [Title] A rare case of GATA1 negative chemoresistant acute megakaryocytic leukemia in an 8-month-old infant with trisomy 21.
  • Children with Down syndrome (DS) have a unique form of acute megakaryocytic leukemia (AMKL) characterized by the presence of mutations in the GATA1 gene leading to increased chemosensitivity and a favorable outcome.
  • We describe an 8-month-old male with DS who was diagnosed with AMKL without a mutation in the GATA1 gene.
  • The patient was treated according to the DS-AML-regimen but his disease progressed and he succumbed 9 months later.
  • This rare case of DS AMKL without a GATA1 mutation with an unfavorable outcome suggests that GATA1 testing may play a useful role in initial stratification.
  • [MeSH-major] Down Syndrome / complications. GATA1 Transcription Factor / genetics. Leukemia, Megakaryoblastic, Acute / complications

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  • [Copyright] Copyright 2010 Wiley-Liss, Inc.
  • (PMID = 20108342.001).
  • [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 / Antineoplastic Agents; 0 / GATA1 Transcription Factor; 0 / GATA1 protein, human
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22. Alioglu B, Avci Z, Canan O, Ozcay F, Demirhan B, Ozbek N: Invasive esophageal aspergillosis associated with acute myelogenous leukemia: successful therapy with combination caspofungin and liposomal amphotericin B. Pediatr Hematol Oncol; 2007 Jan-Feb;24(1):63-8
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  • [Title] Invasive esophageal aspergillosis associated with acute myelogenous leukemia: successful therapy with combination caspofungin and liposomal amphotericin B.
  • Aspergillosis is one of the most common invasive fungal infections in patients with leukemia.
  • The lungs are most often affected, but the esophagus can also be involved.The authors report the case of a child with leukemia who developed invasive esophageal aspergillosis.
  • The patient was already receiving empirical liposomal amphotericin B when the diagnosis was made, so a second antifungal (caspofungin) was added to the regimen.
  • [MeSH-major] Amphotericin B / therapeutic use. Antifungal Agents / therapeutic use. Aspergillosis / drug therapy. Esophageal Diseases / drug therapy. Leukemia, Megakaryoblastic, Acute / complications. Peptides, Cyclic / therapeutic use


23. Niu C, Zhang J, Breslin P, Onciu M, Ma Z, Morris SW: c-Myc is a target of RNA-binding motif protein 15 in the regulation of adult hematopoietic stem cell and megakaryocyte development. Blood; 2009 Sep 3;114(10):2087-96
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  • RNA-binding motif protein 15 (RBM15) is involved in the RBM15-megakaryoblastic leukemia 1 fusion in acute megakaryoblastic leukemia.
  • Although Rbm15 has been reported to be required for B-cell differentiation and to inhibit myeloid and megakaryocytic expansion, it is not clear what the normal functions of Rbm15 are in the regulation of hematopoietic stem cell (HSC) and megakaryocyte development.


24. 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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  • [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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25. Majewski IJ, Metcalf D, Mielke LA, Krebs DL, Ellis S, Carpinelli MR, Mifsud S, Di Rago L, Corbin J, Nicola NA, Hilton DJ, Alexander WS: A mutation in the translation initiation codon of Gata-1 disrupts megakaryocyte maturation and causes thrombocytopenia. Proc Natl Acad Sci U S A; 2006 Sep 19;103(38):14146-51
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  • We have generated mice from a N-ethyl-N-nitrosourea mutagenesis screen that carry a mutation in the translation initiation codon of Gata-1, termed Plt13, which is equivalent to mutations found in patients with acute megakaryoblastic leukemia and Down syndrome.

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  • (PMID = 16966598.001).
  • [ISSN] 0027-8424
  • [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
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Alkylating Agents; 0 / Codon; 0 / GATA1 Transcription Factor; 0 / Gata1 protein, mouse; 0 / Protein Isoforms; P8M1T4190R / Ethylnitrosourea
  • [Other-IDs] NLM/ PMC1599926
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26. Hu M, Chen Y, Kwok JT: Building sparse multiple-kernel SVM classifiers. IEEE Trans Neural Netw; 2009 May;20(5):827-39
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  • In this paper, we further extend this idea by integrating with techniques from multiple-kernel learning (MKL).

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  • (PMID = 19342346.001).
  • [ISSN] 1941-0093
  • [Journal-full-title] IEEE transactions on neural networks
  • [ISO-abbreviation] IEEE Trans Neural Netw
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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27. Akdag A, Tunç B, Oğuz S, Dilli D, Dilmen U: A newborn with Down syndrome-transient myeloproliferative disorder. J Perinat Med; 2010 Jul;38(4):445-7
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  • [Title] A newborn with Down syndrome-transient myeloproliferative disorder.
  • [MeSH-minor] Age Factors. Ascites / etiology. Female. Humans. Hydrops Fetalis / etiology. Infant. Infant, Newborn. Leukemia, Megakaryoblastic, Acute / etiology

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  • (PMID = 20443668.001).
  • [ISSN] 1619-3997
  • [Journal-full-title] Journal of perinatal medicine
  • [ISO-abbreviation] J Perinat Med
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] Germany
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28. Elagib KE, Mihaylov IS, Delehanty LL, Bullock GC, Ouma KD, Caronia JF, Gonias SL, Goldfarb AN: Cross-talk of GATA-1 and P-TEFb in megakaryocyte differentiation. Blood; 2008 Dec 15;112(13):4884-94
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  • In megakaryopoiesis, loss of GATA-1 function produces complex developmental abnormalities and underlies the pathogenesis of megakaryocytic leukemia in Down syndrome.
  • Megakaryocytic induction was associated with dynamic changes in endogenous P-TEFb composition, including recruitment of GATA-1 and dissociation of HEXIM1, a Cdk9 inhibitor. shRNA knockdowns and pharmacologic inhibition both confirmed contribution of Cdk9 activity to megakaryocytic differentiation.
  • In mice with megakaryocytic GATA-1 deficiency, Cdk9 inhibition produced a fulminant but reversible megakaryoblastic disorder reminiscent of the transient myeloproliferative disorder of Down syndrome.
  • Our results offer evidence for P-TEFb cross-talk with GATA-1 in megakaryocytic differentiation, a program with parallels to cardiomyocyte hypertrophy.

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  • [CommentIn] Blood. 2008 Dec 15;112(13):4786-7 [19064734.001]
  • (PMID = 18780834.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA093735; United States / NCI NIH HHS / CA / CA100057; United States / NCI NIH HHS / CA / R56 CA100057; United States / NCI NIH HHS / CA / R01 CA100057; United States / NHLBI NIH HHS / HL / F32 HL0860046; United States / NCI NIH HHS / CA / CA93735; United States / NCI NIH HHS / CA / T32 CA009109
  • [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 / GATA1 Transcription Factor; 0 / GATA1 protein, human; 0 / Gata1 protein, mouse; EC 2.7.11.- / Positive Transcriptional Elongation Factor B; EC 2.7.11.22 / Cyclin-Dependent Kinase 9
  • [Other-IDs] NLM/ PMC2597596
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29. Sandoval C, Pine SR, Guo Q, Sastry S, Stewart J, Kronn D, Jayabose S: Tetrasomy 21 transient leukemia with a GATA1 mutation in a phenotypically normal trisomy 21 mosaic infant: case report and review of the literature. Pediatr Blood Cancer; 2005 Jan;44(1):85-91
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Tetrasomy 21 transient leukemia with a GATA1 mutation in a phenotypically normal trisomy 21 mosaic infant: case report and review of the literature.
  • Infants with constitutional trisomy 21 are at increased risk of developing transient and acute megakaryoblastic leukemia (AMKL).
  • Mutations in GATA1 have been identified in trisomy 21 patients with AMKL, and this lesion is thought to be an initial event by virtue of its presence during transient leukemia.
  • Transient leukemia is also observed in phenotypically normal infants albeit much less commonly so.
  • Almost all these infants are mosaic for trisomy 21, and the clinical course of transient leukemia recapitulates that observed in constitutional trisomy 21.
  • We report a phenotypically normal infant with tetrasomy 21 transient leukemia, GATA1 mutation within exon 2, and trisomy 21 mosaicism restricted to the hematopoietic tissue.
  • Two years after diagnosis, low levels of trisomy 21 persisted in the peripheral blood, which resolved 2.5 years after diagnosis.
  • The literature review identified 32 phenotypically normal infants with transient leukemia.
  • Ninety-one percent (29 of 32) were observed and three received chemotherapy at diagnosis of transient leukemia.
  • Nineteen percent (6 of 32) developed acute leukemia, and four continued in remission (two died).
  • Transient leukemia in trisomy 21 mosaicism recapitulates the condition observed in constitutional trisomy 21 at the biological and clinical levels.
  • Infants should be followed for the development of acute leukemia.
  • [MeSH-major] DNA-Binding Proteins / genetics. Down Syndrome / genetics. Leukemia, Megakaryoblastic, Acute / genetics. Transcription Factors / genetics

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  • [Copyright] (c) 2004 Wiley-Liss, Inc.
  • (PMID = 15390279.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / Erythroid-Specific DNA-Binding Factors; 0 / GATA1 Transcription Factor; 0 / GATA1 protein, human; 0 / Transcription Factors
  • [Number-of-references] 46
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30. Osato M, Ito Y: Increased dosage of the RUNX1/AML1 gene: a third mode of RUNX leukemia? Crit Rev Eukaryot Gene Expr; 2005;15(3):217-28
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  • [Title] Increased dosage of the RUNX1/AML1 gene: a third mode of RUNX leukemia?
  • RUNX1/AML1, located on chromosome 21, is a key factor in the generation and maintenance of hematopoietic stem cells and the gene most frequently implicated in human leukemias.
  • Chromosome translocations and point mutations are well-documented genetic alterations in RUNX leukemia (also known as CBF leukemia).
  • The possibility that this mode might underlie Down syndrome-related leukemias caused by trisomy of chromosome 21 is discussed.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / metabolism. Down Syndrome / genetics. Gene Dosage. Leukemia / genetics
  • [MeSH-minor] Animals. B-Lymphocytes / metabolism. Basic-Leucine Zipper Transcription Factors / metabolism. Core Binding Factor Alpha 1 Subunit / genetics. Core Binding Factor Alpha 1 Subunit / metabolism. DNA-Binding Proteins / metabolism. Fanconi Anemia Complementation Group Proteins / metabolism. GATA1 Transcription Factor / genetics. Gene Expression Regulation, Leukemic. Humans. Leukemia, Megakaryoblastic, Acute / genetics. Lymphoma / genetics. Mice. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Proto-Oncogene Protein c-ets-2 / metabolism. Retroviridae / genetics. Thrombopoiesis / genetics. Trans-Activators / metabolism

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  • (PMID = 16390318.001).
  • [ISSN] 1045-4403
  • [Journal-full-title] Critical reviews in eukaryotic gene expression
  • [ISO-abbreviation] Crit. Rev. Eukaryot. Gene Expr.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / BACH1 protein, human; 0 / Basic-Leucine Zipper Transcription Factors; 0 / Core Binding Factor Alpha 1 Subunit; 0 / Core Binding Factor Alpha 2 Subunit; 0 / DNA-Binding Proteins; 0 / ERG protein, human; 0 / ETS2 protein, human; 0 / Fanconi Anemia Complementation Group Proteins; 0 / GATA1 Transcription Factor; 0 / Proto-Oncogene Protein c-ets-2; 0 / RUNX1 protein, human; 0 / Trans-Activators
  • [Number-of-references] 66
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31. Greiner O, Bornhauser BC, Delabesse E, Ballerini P, Landman-Parker J, Bourquin JP: The CALM-AF10 fusion is a rare event in acute megakaryoblastic leukemia. Leukemia; 2007 Dec;21(12):2568-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The CALM-AF10 fusion is a rare event in acute megakaryoblastic leukemia.
  • [MeSH-major] Chromosomes, Human, Pair 10 / genetics. Chromosomes, Human, Pair 11 / genetics. Leukemia, Megakaryoblastic, Acute / genetics. Oncogene Fusion. Oncogene Proteins, Fusion / genetics. Translocation, Genetic

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  • [CommentOn] Leukemia. 2007 Feb;21(2):352-3 [17170719.001]
  • (PMID = 17611559.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Comment; Letter
  • [Publication-country] England
  • [Chemical-registry-number] 0 / AF10-CALM fusion protein, human; 0 / MLLT10 protein, human; 0 / Monomeric Clathrin Assembly Proteins; 0 / Oncogene Proteins, Fusion; 0 / PICALM protein, human; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / Transcription Factors
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32. Maki K, Yamagata T, Yamazaki I, Oda H, Mitani K: Development of megakaryoblastic leukaemia in Runx1-Evi1 knock-in chimaeric mouse. Leukemia; 2006 Aug;20(8):1458-60
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Development of megakaryoblastic leukaemia in Runx1-Evi1 knock-in chimaeric mouse.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / physiology. DNA-Binding Proteins / physiology. Leukemia, Megakaryoblastic, Acute / etiology. Proto-Oncogenes / physiology. Transcription Factors / physiology

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  • (PMID = 16761014.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / DNA-Binding Proteins; 0 / Evi1 protein, mouse; 0 / Runx1 protein, mouse; 0 / Transcription Factors
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33. Galimberti S, Canestraro M, Maffei R, Marasca R, Guerrini F, Piaggi S, Ciabatti E, Petrini M: Vorinostat interferes with Wnt and NF-kappaB pathways in the M-07e cell line. Leukemia; 2009 Oct;23(10):1935-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Hydroxamic Acids / pharmacology. Leukemia, Megakaryoblastic, Acute / drug therapy. Leukemia, Megakaryoblastic, Acute / metabolism. NF-kappa B / metabolism. Wnt Proteins / metabolism

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  • (PMID = 19626048.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Letter
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Biomarkers, Tumor; 0 / Histone Deacetylase Inhibitors; 0 / Hydroxamic Acids; 0 / NF-kappa B; 0 / Wnt Proteins; 58IFB293JI / vorinostat
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34. Taub JW, Ge Y: Down syndrome, drug metabolism and chromosome 21. Pediatr Blood Cancer; 2005 Jan;44(1):33-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • It has been recognized that chromosomal abnormalities in childhood leukemia, are linked to both leukemogenesis and segregate patients into prognostic treatment groups.
  • This is best exemplified in cases of children with Down syndrome (DS), who have significantly higher risks of developing leukemia compared to non-DS children and distinctive treatment outcomes, particularly in cases of acute myeloid leukemia (AML).
  • The high event-free survival (EFS) rates of DS AML patients and in particular, patients with megakaryocytic leukemia (AMkL), at least in part reflects an increased sensitivity to cytosine arabinoside (ara-C) secondary to increased expression of the chromosome 21-localized gene, cystathionine-beta-synthase, and potentially global mechanisms which increase the susceptibility of cells to undergo apoptosis.
  • Somatic mutations of the X-linked transcription factor gene, GATA1, have been detected uniformly and exclusively in DS AMkL cases, which may lead to altered expression of GATA1 target genes and alter the metabolism of drugs including ara-C.
  • Hyperdiploid acute lymphoblastic leukemia (ALL) cells with extra copies of chromosome 21, generate higher levels of the active methotrexate (MTX) metabolite, MTX polyglutamates.
  • Microarray technology should lead to the identification of additional gene targets linked to the treatment response of specific cytogenetic leukemia subgroups.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / metabolism. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Chromosomes, Human, Pair 21. Down Syndrome / complications. Leukemia, Megakaryoblastic, Acute / drug therapy. Leukemia, Myeloid / drug therapy
  • [MeSH-minor] Acute Disease. Antineoplastic Agents, Alkylating / adverse effects. Antineoplastic Agents, Alkylating / metabolism. Antineoplastic Agents, Alkylating / therapeutic use. Child. Disease-Free Survival. Humans. Methotrexate / adverse effects. Methotrexate / metabolism. Methotrexate / therapeutic use. Prognosis

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  • [Copyright] (c) 2004 Wiley-Liss, Inc.
  • (PMID = 15390307.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA92308
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; YL5FZ2Y5U1 / Methotrexate
  • [Number-of-references] 45
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35. Ho K, Valdez F, Garcia R, Tirado CA: JAK2 Translocations in hematological malignancies: Review of the literature. J Assoc Genet Technol; 2010;36(3):107-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • It is involved in the regulation of different cytokines and growth factors and plays an important role in the diagnosis and treatment of myeloproliferative neoplasms (Smith et al., 2008).
  • Chromosome 9p24 abnormalities have been described in myeloid and lymphoid neoplasms including chronic myelogenous leukemia (CML), acute megakaryoblastic leukemia, CD10+ B-cell acute lymphoblastic leukemia, T-cell ALL and chronic myeloproliferative disorders (CMD) (Smith et al., 2008; Lacronique et al., 1997).

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  • (PMID = 20978341.001).
  • [ISSN] 1523-7834
  • [Journal-full-title] Journal of the Association of Genetic Technologists
  • [ISO-abbreviation] J Assoc Genet Technol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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36. Kurkjian C, Patel S, Kamble R, Dunn ST, Kern W, Kharfan-Dabaja MA: Acute promyelocytic leukemia and constitutional trisomy 21. Cancer Genet Cytogenet; 2006 Mar;165(2):176-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acute promyelocytic leukemia and constitutional trisomy 21.
  • The incidence of acute myelogenous leukemia (AML) in patients with constitutional trisomy 21 is estimated to be 1 in 300; it is usually seen before age four.
  • Clinical and epidemiological data confirm the improved life expectancy of patients with Down syndrome and their increased susceptibility to the development of leukemia, among other cancers.
  • The most frequent subtype of AML associated with Down syndrome is acute megakaryoblastic leukemia (FAB: M7).
  • The description of acute promyelocytic leukemia (APL) in adult patients with Down syndrome is exceedingly rare.
  • [MeSH-major] Down Syndrome. Leukemia, Promyelocytic, Acute / genetics

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  • (PMID = 16527614.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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37. Muntean AG, Crispino JD: Differential requirements for the activation domain and FOG-interaction surface of GATA-1 in megakaryocyte gene expression and development. Blood; 2005 Aug 15;106(4):1223-31
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  • Second, children with Down syndrome who develop acute megakaryoblastic leukemia harbor mutations in GATA1 that lead to the exclusive expression of a shorter isoform named GATA-1s.
  • To determine the effect of these patient-specific mutations on GATA-1 function, we first compared the gene expression profile between wild-type and GATA-1-deficient megakaryocytes.

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  • (PMID = 15860665.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA101774-03; United States / NCI NIH HHS / CA / R01 CA101774; United States / NCI NIH HHS / CA / R01 CA-101774; United States / NCI NIH HHS / CA / R01 CA101774-03
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / DNA-Binding Proteins; 0 / Erythroid-Specific DNA-Binding Factors; 0 / GATA1 Transcription Factor; 0 / Gata1 protein, mouse; 0 / Nuclear Proteins; 0 / Transcription Factors; 0 / Zfpm1 protein, mouse
  • [Other-IDs] NLM/ PMC1895209
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38. Daniëls L, Guerti K, Vermeulen K, De Raeve H, Van Assche E, Van de Velde AL, Berneman ZN, Van Der Planken M: Acute myeloid leukaemia of mixed megakaryocytic and erythroid origin: a case report and review of the literature. Acta Clin Belg; 2007 Sep-Oct;62(5):308-14
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  • [Title] Acute myeloid leukaemia of mixed megakaryocytic and erythroid origin: a case report and review of the literature.
  • We report the case of a 78-year-old man who presented with acute myeloid leukaemia showing subpopulations of cells expressing platelet-associated markers and the presence of a pan-myeloid component, besides glycophorin A-positive cells.
  • Most of the immature cells had a proerythroblast-like morphology and we classified this case as an FAB-M6 variant, as suggested by Bain (1).
  • According to the WHO classification, this leukaemia fulfilled the criteria of'AML with multilineage dysplasia' (2).
  • Immunophenotyping characteristics showed two distinct aberrant subpopulations, a young pan-myeloid (CD45+ with low density, CD34+, CD117+, CD13+, CD33+, partial cytoplasmic myeloperoxidase (MPO)+) population with platelet-associated markers (CD41+, CD42+, CD61+) and a CD45+, CD117+, CD34- population with partial CD235a positivity indicative for erythroid maturation.
  • This case belongs to the group of 'early' erythroblastic leukaemias where a subset of progenitor cells present with erythroid-megakaryocyte bipotentiality or are blocked at an early BFU-E (burst-forming unit erythrocyte)-like stage of erythroid differentiation (11, 12, 13).
  • [MeSH-major] Bone Marrow Cells / pathology. Leukemia, Erythroblastic, Acute / diagnosis. Leukemia, Megakaryoblastic, Acute / diagnosis
  • [MeSH-minor] Aged. Biopsy, Needle. Diagnosis, Differential. Fatal Outcome. Humans. Immunophenotyping. Male

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  • (PMID = 18229464.001).
  • [ISSN] 1784-3286
  • [Journal-full-title] Acta clinica Belgica
  • [ISO-abbreviation] Acta Clin Belg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Belgium
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39. Sandoval C, Pine SR: Down syndrome and GATA1-related transient leukemia. J Pediatr; 2007 Mar;150(3):e34
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Down syndrome and GATA1-related transient leukemia.
  • [MeSH-major] Down Syndrome / diagnosis. GATA1 Transcription Factor / genetics. Leukemia, Megakaryoblastic, Acute / genetics
  • [MeSH-minor] Humans. In Situ Hybridization, Fluorescence. Infant. Leukemia / etiology. Leukemia / genetics. Mutation. Prognosis. Risk Assessment

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  • [CommentOn] J Pediatr. 2006 May;148(5):687-9 [16737888.001]
  • (PMID = 17307526.001).
  • [ISSN] 1097-6833
  • [Journal-full-title] The Journal of pediatrics
  • [ISO-abbreviation] J. Pediatr.
  • [Language] eng
  • [Publication-type] Case Reports; Comment; Letter
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / GATA1 Transcription Factor; 0 / GATA1 protein, human
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40. Papageorgiou SG, Pappa V, Economopoulou C, Tsirigotis P, Konsioti F, Ionnidou ED, Chondropoulos S, Vasilatou D, Papageorgiou E, Economopoulos T, Dervenoulas J: Dasatinib induces long-term remission in imatinib-resistant Philadelphia chromosome-positive acute megakaryoblastic leukemia but fails to prevent development of central nervous system progression. Leuk Res; 2010 Sep;34(9):e254-6
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  • [Title] Dasatinib induces long-term remission in imatinib-resistant Philadelphia chromosome-positive acute megakaryoblastic leukemia but fails to prevent development of central nervous system progression.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Central Nervous System Neoplasms / secondary. Leukemia, Megakaryoblastic, Acute / drug therapy. Philadelphia Chromosome. Piperazines / therapeutic use. Pyrimidines / therapeutic use. Thiazoles / therapeutic use

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  • (PMID = 20392492.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 0 / Thiazoles; 8A1O1M485B / Imatinib Mesylate; RBZ1571X5H / Dasatinib
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41. Yazaki A, Tamaru S, Sasaki Y, Komatsu N, Wada H, Shiku H, Nishikawa M: Inhibition by Rho-kinase and protein kinase C of myosin phosphatase is involved in thrombin-induced shape change of megakaryocytic leukemia cell line UT-7/TPO. Cell Signal; 2005 Mar;17(3):321-30
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  • [Title] Inhibition by Rho-kinase and protein kinase C of myosin phosphatase is involved in thrombin-induced shape change of megakaryocytic leukemia cell line UT-7/TPO.
  • Thrombin induced a shape change of UT-7/TPO, a thrombopoietin-dependent human megakaryocytic cell line.
  • [MeSH-minor] Cell Line, Tumor. Humans. Intracellular Signaling Peptides and Proteins. Leukemia. Microscopy, Confocal. Myosin Light Chains / metabolism. Myosin-Light-Chain Kinase / biosynthesis. Phosphorylation. Protein Subunits / metabolism. Pseudopodia / drug effects. Pseudopodia / metabolism. Signal Transduction. rho-Associated Kinases

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  • (PMID = 15567063.001).
  • [ISSN] 0898-6568
  • [Journal-full-title] Cellular signalling
  • [ISO-abbreviation] Cell. Signal.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Intracellular Signaling Peptides and Proteins; 0 / Myosin Light Chains; 0 / Protein Subunits; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / rho-Associated Kinases; EC 2.7.11.13 / Protein Kinase C; EC 2.7.11.18 / Myosin-Light-Chain Kinase; EC 3.1.3.53 / Myosin-Light-Chain Phosphatase; EC 3.4.21.5 / Thrombin
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42. Higashihara M, Watanabe M, Usuda S, Miyazaki K: Smooth muscle type isoform of 20 kDa myosin light chain is expressed in monocyte/macrophage cell lineage. J Smooth Muscle Res; 2008 Feb;44(1):29-40
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  • [Title] Smooth muscle type isoform of 20 kDa myosin light chain is expressed in monocyte/macrophage cell lineage.
  • We previously reported the cloning of the full-length cDNAs of 20 kDa regulatory myosin light chain (MLC-2), named as MLC-2A, from Meg-01, a human megakaryoblastic leukemia cell line (J.
  • We now cloned another MLC-2 isoforms from human platelets and U937, a human monocytic leukemia cell line, named as MLC-2B and MLC-2C, respectively.
  • These results indicate that smooth muscle type isoform, MLC-2C is the inducible isoform, and might play a crucial role in monocyte/macrophage cell lineage.

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  • (PMID = 18480596.001).
  • [ISSN] 0916-8737
  • [Journal-full-title] Journal of smooth muscle research = Nihon Heikatsukin Gakkai kikanshi
  • [ISO-abbreviation] J Smooth Muscle Res
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Myosin Light Chains; 0 / Protein Isoforms; 0 / RNA, Messenger; 0 / myosin light chain 2; EC 3.6.1.- / Cardiac Myosins
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43. Delgado-Lamas JL, Garcés-Ruiz OM, Aguilar-López LB, Borjas-Gutiérrez C, Flores-Márquez MR, Luna-Zaizar H, Delgado-Chávez R: [A clinical and therapeutic analysis in acute megakaryoblastic leukemia]. Rev Med Inst Mex Seguro Soc; 2009 Mar-Apr;47(2):193-8
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  • [Title] [A clinical and therapeutic analysis in acute megakaryoblastic leukemia].
  • [Transliterated title] Análisis clínico-terapéutico de leucemia aguda megacarioblástica.
  • OBJECTIVE: to show clinical and therapeutic findings in patients with diagnosis of acute megakaryoblastic leukemia (AML).
  • METHODS: twenty four patients with diagnosis AML was carried out.
  • The diagnosis was established by a highly clinical suspicious, with immunophenotype cytometry flow or/and bone biopsy with immunohistochemistry study which proves definitely AML.
  • [MeSH-major] Leukemia, Megakaryoblastic, Acute / diagnosis. Leukemia, Megakaryoblastic, Acute / therapy

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  • (PMID = 19744390.001).
  • [ISSN] 0443-5117
  • [Journal-full-title] Revista médica del Instituto Mexicano del Seguro Social
  • [ISO-abbreviation] Rev Med Inst Mex Seguro Soc
  • [Language] spa
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Mexico
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44. Nakagawa K, Kuzumaki N: Transcriptional activity of megakaryoblastic leukemia 1 (MKL1) is repressed by SUMO modification. Genes Cells; 2005 Aug;10(8):835-50
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  • [Title] Transcriptional activity of megakaryoblastic leukemia 1 (MKL1) is repressed by SUMO modification.
  • Megakaryoblastic leukemia 1 (MKL1) was originally identified as a gene translocated in megakaryoblastic leukemia.
  • [MeSH-major] DNA-Binding Proteins / metabolism. Leukemia, Megakaryoblastic, Acute / metabolism. SUMO-1 Protein / metabolism. Transcription, Genetic

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  • (PMID = 16098147.001).
  • [ISSN] 1356-9597
  • [Journal-full-title] Genes to cells : devoted to molecular & cellular mechanisms
  • [ISO-abbreviation] Genes Cells
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / Oncogene Proteins, Fusion; 0 / SUMO-1 Protein; 0 / Serum Response Factor; 98600C0908 / Cycloheximide; EC 3.6.5.2 / rhoA GTP-Binding Protein; EC 6.3.2.19 / Ubiquitin-Conjugating Enzymes; EC 6.3.2.19 / ubiquitin-conjugating enzyme UBC9
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45. Scharenberg MA, Chiquet-Ehrismann R, Asparuhova MB: Megakaryoblastic leukemia protein-1 (MKL1): Increasing evidence for an involvement in cancer progression and metastasis. Int J Biochem Cell Biol; 2010 Dec;42(12):1911-4
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  • [Title] Megakaryoblastic leukemia protein-1 (MKL1): Increasing evidence for an involvement in cancer progression and metastasis.
  • Megakaryoblastic leukemia protein-1 (MKL1), also termed MAL, MRTF-A, and BSAC, belongs to the MRTF family of transcription factors that share evolutionary conserved domains required for actin-binding, homo- and heterodimerization, high-order chromatin organization and transcriptional activation.
  • MKL1 regulates many processes, including muscle cell differentiation, cardiovascular development, remodeling of neuronal networks in the developing and adult brain, megakaryocytic differentiation and migration, modulation of cellular motile functions and epithelial-mesenchymal transition.
  • Moreover, deregulation by genetic alterations and/or altered expression of MKL1 can contribute to a number of pathological processes such as coronary artery disease, sarcopenia, acute megakaryoblastic leukemia, and cancer.
  • [MeSH-minor] Animals. Disease Progression. Humans. Neoplasm Metastasis

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  • [Copyright] Copyright © 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 20816842.001).
  • [ISSN] 1878-5875
  • [Journal-full-title] The international journal of biochemistry & cell biology
  • [ISO-abbreviation] Int. J. Biochem. Cell Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / MKL1 protein, human; 0 / MKL1 protein, mouse; 0 / Oncogene Proteins, Fusion; 0 / Trans-Activators
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46. Gurgul A, Radko A, Słota E: Characteristics of X- and Y-chromosome specific regions of the amelogenin gene and a PCR-based method for sex identification in red deer (Cervus elaphus). Mol Biol Rep; 2010 Jul;37(6):2915-8
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  • The present study attempts to analyse sequences of the X- and Y-chromosome specific regions of the amelogenin (AMEL) gene in red deer.

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  • (PMID = 19809889.001).
  • [ISSN] 1573-4978
  • [Journal-full-title] Molecular biology reports
  • [ISO-abbreviation] Mol. Biol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article
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47. Tefferi A: JAK and MPL mutations in myeloid malignancies. Leuk Lymphoma; 2008 Mar;49(3):388-97
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  • [Title] JAK and MPL mutations in myeloid malignancies.
  • The Janus family of non-receptor tyrosine kinases (JAK1, JAK2, JAK3 and tyrosine kinase 2) transduces signals downstream of type I and II cytokine receptors via signal transducers and activators of transcription (STATs).
  • JAK3 is important in lymphoid and JAK2 in myeloid cell proliferation and differentiation.
  • ETV6-JAK2, PCM1-JAK2, BCR-JAK2) mutations have respectively been described in acute megakaryocytic leukemia and acute leukemia/chronic myeloid malignancies.

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  • (PMID = 18297515.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Receptors, Thrombopoietin; 0 / STAT Transcription Factors; 143641-95-6 / MPL protein, human; EC 2.7.10.2 / Janus Kinase 2; EC 2.7.10.2 / Janus Kinase 3
  • [Number-of-references] 167
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48. Sire JY, Delgado S, Girondot M: The amelogenin story: origin and evolution. Eur J Oral Sci; 2006 May;114 Suppl 1:64-77; discussion 93-5, 379-80
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  • Genome sequencing and gene mapping have permitted the identification of HEVIN (SPARC-Like1) as the probable ancestor of the enamel matrix proteins (EMPs), amelogenin (AMEL), ameloblastin (AMBN) and enamelin (ENAM).
  • AMEL genes available in databases, and new sequences obtained in blast searching genomes or expressed sequence tags, were compiled (22 full-length sequences), aligned, and the ancestral sequence calculated and used to search for similarities using psi-blast.
  • AMEL and AMBN are sister genes, which diverged after duplication of a common ancestor issued from ENAM.
  • Comparisons of gene organization, amino acid sequences and location of ENAM and AMBN, adjacent on the same chromosome, suggest that AMBN is closer to ENAM than AMEL.
  • This supports AMEL as being derived from AMBN duplication.
  • The story of AMEL origin is completed as follows: SPARC-->HEVIN-->ENAM-->AMBN-->AMEL.

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  • (PMID = 16674665.001).
  • [ISSN] 0909-8836
  • [Journal-full-title] European journal of oral sciences
  • [ISO-abbreviation] Eur. J. Oral Sci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / AMBN protein, human; 0 / Amelogenin; 0 / Calcium-Binding Proteins; 0 / Dental Enamel Proteins; 0 / Extracellular Matrix Proteins; 0 / SPARCL1 protein, human; 0 / tuftelin
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49. Ariffin H, Garcia JC, Daud SS, Ibrahim K, Aizah N, Ong GB, Chong LA, Mohamad Z: GATA1 mutations in patients with down syndrome and acute megakaryoblastic leukaemia do not always confer a good prognosis. Pediatr Blood Cancer; 2009 Jul;53(1):108-11
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  • [Title] GATA1 mutations in patients with down syndrome and acute megakaryoblastic leukaemia do not always confer a good prognosis.
  • Children with Down syndrome and acute megakaryoblastic leukemia (DS-AMKL) have been shown to have increased sensitivity to cytarabine based chemotherapy.
  • The excellent prognosis in patients with DS-AMKL may be due to mutations in the GATA1 gene leading to reduced expression of the enzyme cytidine deaminase.
  • We report two cases of DS-AMKL with GATA1 mutations who had poor outcome.
  • We speculate that other factors can affect overall outcome in patients with DS-AMKL irrespective of the presence of GATA1 mutations.
  • [MeSH-major] Cytidine Deaminase / metabolism. Down Syndrome / genetics. GATA1 Transcription Factor / genetics. Leukemia, Megakaryoblastic, Acute / genetics. Mutation

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  • [Copyright] Copyright 2009 Wiley-Liss, Inc.
  • (PMID = 19260099.001).
  • [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 / GATA1 Transcription Factor; 0 / GATA1 protein, human; EC 3.5.4.5 / Cytidine Deaminase
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50. Descot A, Rex-Haffner M, Courtois G, Bluteau D, Menssen A, Mercher T, Bernard OA, Treisman R, Posern G: OTT-MAL is a deregulated activator of serum response factor-dependent gene expression. Mol Cell Biol; 2008 Oct;28(20):6171-81
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  • The OTT-MAL/RBM15-MKL1 fusion protein is the result of the recurrent translocation t(1;22) in acute megakaryocytic leukemia in infants.

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  • (PMID = 18710951.001).
  • [ISSN] 1098-5549
  • [Journal-full-title] Molecular and cellular biology
  • [ISO-abbreviation] Mol. Cell. Biol.
  • [Language] ENG
  • [Grant] United Kingdom / Cancer Research UK / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Actins; 0 / Early Growth Response Protein 1; 0 / OTT-MAL fusion protein, human; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins c-fos; 0 / Serum Response Factor; 0 / Ternary Complex Factors; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 3.6.5.2 / rhoA GTP-Binding Protein
  • [Other-IDs] NLM/ PMC2577437
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51. Foss B, Bruserud O: Platelet functions and clinical effects in acute myelogenous leukemia. Thromb Haemost; 2008 Jan;99(1):27-37
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  • [Title] Platelet functions and clinical effects in acute myelogenous leukemia.
  • Interactions may also be involved between platelets and circulating malignant cells, which is suggested by the effects platelets seem to have on metastasis and the various platelet abnormalities observed in various malignant disorders, including acute myelogenous leukemia (AML) and other leukemias.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Blood Platelets / metabolism. Leukemia, Myeloid, Acute / blood. Leukemia, Myeloid, Acute / therapy. Leukocytes / metabolism. Platelet Activation. Platelet Transfusion. Stem Cell Transplantation
  • [MeSH-minor] Animals. Apoptosis. Cell Communication. Cell Proliferation. Cytokines / blood. Hematopoietic Stem Cells / metabolism. Hemorrhage / blood. Hemorrhage / etiology. Hemorrhage / prevention & control. Humans. Intercellular Signaling Peptides and Proteins / blood. Leukemia, Megakaryoblastic, Acute / blood. Leukemia, Megakaryoblastic, Acute / therapy. Leukemia, Promyelocytic, Acute / blood. Leukemia, Promyelocytic, Acute / therapy

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  • (PMID = 18217131.001).
  • [ISSN] 0340-6245
  • [Journal-full-title] Thrombosis and haemostasis
  • [ISO-abbreviation] Thromb. Haemost.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Cytokines; 0 / Intercellular Signaling Peptides and Proteins
  • [Number-of-references] 164
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52. Carmichael CL, Majewski IJ, Alexander WS, Metcalf D, Hilton DJ, Hewitt CA, Scott HS: Hematopoietic defects in the Ts1Cje mouse model of Down syndrome. Blood; 2009 Feb 26;113(9):1929-37
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  • Down syndrome (DS) persons are born with various hematopoietic abnormalities, ranging from relatively benign, such as neutrophilia and macrocytosis, to a more severe transient myeloproliferative disorder (TMD).
  • However, sometimes the TMD represents a premalignant disease that develops into acute megakaryocytic leukemia (AMKL), usually in association with acquired GATA1 mutations.
  • Despite these defects, the Ts1Cje mice do not develop disease resembling either TMD or AMKL, and this was not altered by a loss of function allele of Gata1.
  • Thus, loss of Gata1 and partial trisomy of chromosome 21 orthologs, when combined, do not appear to be sufficient to induce TMD or AMKL-like phenotypes in mice.
  • [MeSH-major] Disease Models, Animal. Down Syndrome / complications. Hematologic Diseases / etiology


53. Wright JT, Hart TC, Hart PS, Simmons D, Suggs C, Daley B, Simmer J, Hu J, Bartlett JD, Li Y, Yuan ZA, Seow WK, Gibson CW: Human and mouse enamel phenotypes resulting from mutation or altered expression of AMEL, ENAM, MMP20 and KLK4. Cells Tissues Organs; 2009;189(1-4):224-9
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  • [Title] Human and mouse enamel phenotypes resulting from mutation or altered expression of AMEL, ENAM, MMP20 and KLK4.
  • Amelogenesis imperfecta (AI) is caused by AMEL, ENAM, MMP20 and KLK4 gene mutations.
  • A total of 463 individuals from 54 families were evaluated and mutations in the AMEL, ENAM and KLK4 genes were identified.
  • The majority of human mutations for genes coding enamel nonproteinase proteins (AMEL and ENAM) resulted in variable hypoplasia ranging from local pitting to a marked, generalized enamel thinning.
  • Specific AMEL mutations were associated with abnormal mineralization and maturation defects.
  • Amel and Enam null murine models displayed marked enamel hypoplasia and a complete loss of prism structure.
  • The currently available Amel and Enam mouse models for AI exhibit enamel phenotypes (hypoplastic) that are generally similar to those seen in humans.

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  • [Copyright] Copyright 2008 S. Karger AG, Basel.
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  • (PMID = 18714142.001).
  • [ISSN] 1422-6421
  • [Journal-full-title] Cells, tissues, organs
  • [ISO-abbreviation] Cells Tissues Organs (Print)
  • [Language] ENG
  • [Grant] United States / NIDCR NIH HHS / DE / R01 DE012879-05; United States / NIDCR NIH HHS / DE / DE012879-05; United States / NIDCR NIH HHS / DE / R01 DE016276; United States / NIDCR NIH HHS / DE / DE01627; United States / NIDCR NIH HHS / DE / R01 DE016276-04; United States / NIDCR NIH HHS / DE / R56 DE011301; United States / NIDCR NIH HHS / DE / R01 DE011089; United States / NIDCR NIH HHS / DE / R01 DE011301-09; United States / NIDCR NIH HHS / DE / R01 DE012879; United States / NIDCR NIH HHS / DE / DE011301-09; United States / NIDCR NIH HHS / DE / R01 DE011301; United States / NIDCR NIH HHS / DE / R29 DE011301; United States / NIDCR NIH HHS / DE / DE11301; United States / NIDCR NIH HHS / DE / R01 DE011089-11; United States / NIDCR NIH HHS / DE / DE011089; United States / NIDCR NIH HHS / DE / DE12879
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Amelogenin; 0 / Dental Enamel Proteins; 0 / tuftelin; EC 3.4.21.- / Kallikreins; EC 3.4.21.- / kallikrein 4; EC 3.4.24.- / Matrix Metalloproteinase 20
  • [Other-IDs] NLM/ NIHMS131427; NLM/ PMC2754863
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54. Cushing T, Clericuzio CL, Wilson CS, Taub JW, Ge Y, Reichard KK, Winter SS: Risk for leukemia in infants without Down syndrome who have transient myeloproliferative disorder. J Pediatr; 2006 May;148(5):687-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Risk for leukemia in infants without Down syndrome who have transient myeloproliferative disorder.
  • Transient myeloproliferative disorder (TMD) occurs in 10% of infants with Down syndrome (DS).
  • Down syndrome infants with resolved TMD may later develop acute megakaryocytic leukemia (AMKL).
  • In these patients, AMKL is associated with somatic mutations in the X-linked transcription factor gene, GATA1.
  • AMKL also has been described after TMD in children without DS.
  • We report on a non-DS child identified with trisomy 21 mosaicism and a GATA1 mutation in the original blast cells who has been followed for 2 years without exhibiting AMKL.
  • Currently, the risk for such infants developing acute leukemia is uncertain.
  • [MeSH-major] GATA1 Transcription Factor / genetics. Leukemia, Megakaryoblastic, Acute / genetics. Myeloproliferative Disorders / genetics

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  • [CommentIn] J Pediatr. 2007 Mar;150(3):e34 [17307526.001]
  • (PMID = 16737888.001).
  • [ISSN] 0022-3476
  • [Journal-full-title] The Journal of pediatrics
  • [ISO-abbreviation] J. Pediatr.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / GATA1 Transcription Factor
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55. Wang M, Jin RM, Qiu YN, Lin W, Meng B: [Effects of ouabain at low concentrations on growth of leukemia cells]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2007 Dec;15(6):1165-8
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  • [Title] [Effects of ouabain at low concentrations on growth of leukemia cells].
  • This study was aimed to investigate the effects of ouabain at low concentrations on growth regulation in various leukemia cell lines and to determine the therapeutic potential of ouabain in leukemia.
  • By using MTT, flow cytometry (FCM), the changes in cell growth and cell cycle of leukemia cell lines were observed after treating with ouabain at low concentrations (<or=10 nmol/L).
  • The results showed that in megakaryocytic leukemia M07e and Meg-01 cell lines, the low concentrations of ouabain (<or=10 nmol/L) inhibited the cell growth, blocked the cell cycle at G1 phase, and decreased the protein expression of sodium pump alpha1 subunit.
  • The same concentrations of ouabain induced the proliferation of lymphocytic leukemia B95 and Jhhan cell lines, increased the percentage of cells at S phase and G2/M phase and up-regulated the expression of sodium pump alpha1 subunit.
  • It is concluded that the low concentrations of ouabain inhibit the cell growth of the megakaryocytic leukemia cell lines M07e and Meg-0, which may be related with the low expression of sodium pump alpha1 subunit of that cell lines and the negative regulation of the protein induced by ouabain.

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  • (PMID = 18088458.001).
  • [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] 5ACL011P69 / Ouabain; EC 3.6.3.9 / Sodium-Potassium-Exchanging ATPase
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56. Shimizu R, Engel JD, Yamamoto M: GATA1-related leukaemias. Nat Rev Cancer; 2008 Apr;8(4):279-87
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] GATA1-related leukaemias.
  • GATA1 is a prototypical lineage-restricted transcription factor that is central to the correct differentiation, proliferation and apoptosis of erythroid and megakaryocytic cells.
  • Mutations in GATA1 can generate a truncated protein, which contributes to the genesis of transient myeloproliferative disorder (TMD) and acute megakaryoblastic leukaemia (AMKL) in infants with Down syndrome.
  • Similarly, Gata1 knockdown to 5% of its wild-type level causes high incidence of erythroid leukaemia in mice.
  • The GATA1-related leukaemias in both human and mouse could provide important insights into the mechanism of multi-step leukaemogenesis.
  • Efforts are afoot to produce mouse models that are reflective of TMD and AMKL.
  • [MeSH-major] GATA1 Transcription Factor / physiology. Leukemia, Megakaryoblastic, Acute / metabolism. Myeloproliferative Disorders / metabolism
  • [MeSH-minor] Animals. Disease Progression. Humans. Mice

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  • (PMID = 18354416.001).
  • [ISSN] 1474-1768
  • [Journal-full-title] Nature reviews. Cancer
  • [ISO-abbreviation] Nat. Rev. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / GATA1 Transcription Factor
  • [Number-of-references] 93
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57. Zarina AL, Hamidah A, Yong SC, Rohana J, Hamidah NH, Azma RZ, Boo NY, Jamal R: Transient abnormal myelopoeisis in newborns with Down syndrome. Malays J Pathol; 2007 Dec;29(2):107-11
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  • Furthermore, even for those who do show spontaneous resolution, a significant percentage will develop acute megakaryoblastic leukaemia within the next few years of life.

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  • (PMID = 19108403.001).
  • [ISSN] 0126-8635
  • [Journal-full-title] The Malaysian journal of pathology
  • [ISO-abbreviation] Malays J Pathol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Malaysia
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58. Sembon S, Suzuki S, Fuchimoto D, Iwamoto M, Kawarasaki T, Onishi A: Sex identification of pigs using polymerase chain reaction amplification of the amelogenin gene. Zygote; 2008 Nov;16(4):327-32
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  • The amelogenin (AMEL) gene exists on both sex chromosomes of various mammalian species and the length and sequence of the noncoding regions differ between the two chromosome-specific alleles.
  • Because both forms can be amplified using a single primer set, the use of AMEL in polymerase chain reaction (PCR)-based methods has facilitated sex identification in various mammalian species, including cattle, sheep and humans.
  • In this study, we designed PCR primers to yield different-sized products from the AMEL genes on the X (AMELX) and Y (AMELY) chromosomes of pigs.
  • We then tested the use of PCR of AMEL for sex identification of in vitro-produced (IVP) porcine embryos sampled at 2 or 5 to 6 days after fertilization; germinal vesicle (GV)-stage oocytes and electroactivated embryos were used as controls.
  • Our findings show that PCR analysis of the AMEL gene is reliable for sex identification of pigs and porcine embryos.

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  • (PMID = 18616845.001).
  • [ISSN] 0967-1994
  • [Journal-full-title] Zygote (Cambridge, England)
  • [ISO-abbreviation] Zygote
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Amelogenin; 0 / DNA Primers; 9007-49-2 / DNA
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59. Halene S, Gao Y, Hahn K, Massaro S, Italiano JE Jr, Schulz V, Lin S, Kupfer GM, Krause DS: Serum response factor is an essential transcription factor in megakaryocytic maturation. Blood; 2010 Sep 16;116(11):1942-50
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  • [Title] Serum response factor is an essential transcription factor in megakaryocytic maturation.
  • Mkl1, a cofactor of Srf, is part of the t(1;22) translocation in acute megakaryoblastic leukemia, and plays a critical role in megakaryopoiesis.
  • To test the role of Srf in megakaryocyte development, we crossed Pf4-Cre mice, which express Cre recombinase in cells committed to the megakaryocytic lineage, to Srf(F/F) mice in which functional Srf is no longer expressed after Cre-mediated excision.

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  • (PMID = 20525922.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Databank-accession-numbers] GEO/ GSE21859
  • [Grant] United States / NIDDK NIH HHS / DK / P30 DK072442; United States / NHLBI NIH HHS / HL / HL63357; United States / NHLBI NIH HHS / HV / N01-HV-28186; United States / NIDDK NIH HHS / DK / K08 DK073366; United States / NHLBI NIH HHS / HL / N01HV28186; United States / NHLBI NIH HHS / HL / P01 HL063357; United States / NHLBI NIH HHS / HL / R01 HL068130; United States / NHLBI NIH HHS / HL / HL68130; United States / NCI NIH HHS / CA / P30 CA016359; United States / NIDDK NIH HHS / DK / DK072442; United States / NIDDK NIH HHS / DK / R01 DK086267; United States / NCI NIH HHS / CA / CA016359
  • [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 / Luminescent Proteins; 0 / Serum Response Factor; 0 / Transcription Factors; 37270-94-3 / Platelet Factor 4
  • [Other-IDs] NLM/ PMC3173990
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60. Chang HH, Lu MY, Jou ST, Lin KH, Tien HF, Wu ET, Lin DT: Neoplastic disorders of hematopoiesis in children with Down's syndrome--a single institution experience in Taiwan. J Formos Med Assoc; 2005 May;104(5):333-40
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  • METHODS: All DS patients aged < 18 years of age with a diagnosis of leukemia or myelodysplastic syndrome (MDS) from 1990 to 2002 were included in this retrospective study.
  • The clinical and laboratory characteristics of patients, including age at diagnosis, gender, initial hemogram, cytogenetic findings, immunophenotype, treatment regimen and outcomes were analyzed.
  • Among them, 9 patients (56%) had acute myeloid leukemia (AML), mainly of the megakaryoblastic subtype.
  • Among the 6 patients (38%) who developed transient myeloproliferative disorder, 2 were lost to follow-up, 2 died from DS-associated congenital heart abnormalities and 2 survived without any AML changes.
  • CONCLUSIONS: This study found that AML is the most common hematologic neoplasm in Taiwanese children with DS, especially megakaryoblastic leukemia.
  • This finding is comparable to the reported results from related studies in different countries.


61. Widmer C, Toussaint NC, Altun Y, Rätsch G: Inferring latent task structure for Multitask Learning by Multiple Kernel Learning. BMC Bioinformatics; 2010;11 Suppl 8:S5
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  • This is done by formulating the Multitask Learning problem as Multiple Kernel Learning, using the recently published q-Norm MKL algorithm.

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  • (PMID = 21034430.001).
  • [ISSN] 1471-2105
  • [Journal-full-title] BMC bioinformatics
  • [ISO-abbreviation] BMC Bioinformatics
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2966292
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62. Ishikawa M, Nishijima N, Shiota J, Sakagami H, Tsuchida K, Mizukoshi M, Fukuchi M, Tsuda M, Tabuchi A: Involvement of the serum response factor coactivator megakaryoblastic leukemia (MKL) in the activin-regulated dendritic complexity of rat cortical neurons. J Biol Chem; 2010 Oct 22;285(43):32734-43
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  • [Title] Involvement of the serum response factor coactivator megakaryoblastic leukemia (MKL) in the activin-regulated dendritic complexity of rat cortical neurons.
  • Dynamic changes in neuronal morphology and transcriptional regulation play crucial roles in the neuronal network and function.
  • Accumulating evidence suggests that the megakaryoblastic leukemia (MKL) family members, which function not only as actin-binding proteins but also as serum response factor (SRF) transcriptional coactivators, regulate neuronal morphology.
  • However, the extracellular ligands and signaling pathways, which activate MKL-mediated morphological changes in neurons, remain unresolved.
  • Activin promoted dendritic complexity in a SRF- and MKL-dependent manner without drastically affecting MKL localization and protein levels.
  • In contrast, activin promoted the nuclear export of suppressor of cancer cell invasion (SCAI), which is a corepressor for SRF and MKL.
  • Collectively, these results strongly suggest that activin-SCAI-MKL signaling is a novel pathway that regulates the dendritic morphology of rat cortical neurons by excluding SCAI from the nucleus and activating MKL/SRF-mediated gene expression.

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  • (PMID = 20709749.001).
  • [ISSN] 1083-351X
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MKL1 protein, mouse; 0 / Trans-Activators; 0 / Transcription Factors; 0 / myocardin-related transcription factor B, mouse; 104625-48-1 / Activins
  • [Other-IDs] NLM/ PMC2963415
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63. Wong KF, Yu PH: Erythrophagocytic megakaryoblasts in acute megakaryoblastic leukaemia. Br J Haematol; 2010 Mar;148(5):672
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  • [Title] Erythrophagocytic megakaryoblasts in acute megakaryoblastic leukaemia.
  • [MeSH-major] Leukemia, Megakaryoblastic, Acute / diagnosis. Megakaryocyte Progenitor Cells / pathology. Phagocytosis

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  • (PMID = 19663828.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
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64. Evelyn CR, Wade SM, Wang Q, Wu M, Iñiguez-Lluhí JA, Merajver SD, Neubig RR: CCG-1423: a small-molecule inhibitor of RhoA transcriptional signaling. Mol Cancer Ther; 2007 Aug;6(8):2249-60
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  • Lysophosphatidic acid receptors stimulate a Galpha(12/13)/RhoA-dependent gene transcription program involving the serum response factor (SRF) and its coactivator and oncogene, megakaryoblastic leukemia 1 (MKL1).
  • The ability of CCG-1423 to block transcription activated by MKL1, but not that induced by SRF-VP16 or GAL4-VP16, suggests a mechanism targeting MKL/SRF-dependent transcriptional activation that does not involve alterations in DNA binding.

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  • (PMID = 17699722.001).
  • [ISSN] 1535-7163
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / R01 DK061656; United States / NIDDK NIH HHS / DK / R01 DK061656-02; United States / NIDDK NIH HHS / DK / DK061656-05; United States / NCI NIH HHS / CA / R01CA77612; United States / NIDDK NIH HHS / DK / DK061656-04; United States / NIDDK NIH HHS / DK / R01DK61615; United States / NIGMS NIH HHS / GM / R01GM39561; United States / NIDDK NIH HHS / DK / DK061656-03; United States / NIDDK NIH HHS / DK / R01 DK061656-04; United States / NIDDK NIH HHS / DK / R01 DK061656-03; United States / NIDDK NIH HHS / DK / DK061656-02; United States / NIDDK NIH HHS / DK / DK061656-01; United States / NIDDK NIH HHS / DK / R01 DK061656-05; United States / NIDDK NIH HHS / DK / R01 DK061656-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anilides; 0 / Antineoplastic Agents; 0 / Benzamides; 0 / CCG 1423; EC 1.13.12.- / Luciferases; EC 3.6.5.2 / rhoA GTP-Binding Protein
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65. Ge Y, Stout ML, Tatman DA, Jensen TL, Buck S, Thomas RL, Ravindranath Y, Matherly LH, Taub JW: GATA1, cytidine deaminase, and the high cure rate of Down syndrome children with acute megakaryocytic leukemia. J Natl Cancer Inst; 2005 Feb 2;97(3):226-31
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  • [Title] GATA1, cytidine deaminase, and the high cure rate of Down syndrome children with acute megakaryocytic leukemia.
  • Down syndrome children with acute megakaryocytic leukemia (AMkL) have higher cure rates than non-Down syndrome acute myeloid leukemia (AML) patients treated with cytosine arabinoside (ara-C).
  • Somatic mutations in the GATA1 transcription factor have been detected exclusively and almost uniformly in Down syndrome AMkL patients, suggesting a potential linkage to the chemotherapy sensitivity of Down syndrome megakaryoblasts.
  • Stable transfection of wild-type GATA1 cDNA into the Down syndrome AMkL cell line CMK resulted in decreased (8- to 17-fold) ara-C sensitivity and a threefold-lower generation of the active ara-C metabolite ara-CTP compared with that for mock-transfected CMK cells.
  • These results suggest that GATA1 transcriptionally upregulates cytidine deaminase and that the presence or absence of GATA1 mutations in AML blasts likely confers differences in ara-C sensitivities due to effects on cytidine deaminase gene expression, which, in turn, contributes to the high cure rate of Down syndrome AMkL patients.
  • [MeSH-major] Cytidine Deaminase / metabolism. DNA-Binding Proteins / metabolism. Down Syndrome / complications. Down Syndrome / metabolism. Leukemia, Megakaryoblastic, Acute / metabolism. Transcription Factors / metabolism

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  • (PMID = 15687366.001).
  • [ISSN] 1460-2105
  • [Journal-full-title] Journal of the National Cancer Institute
  • [ISO-abbreviation] J. Natl. Cancer Inst.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA92308
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / DNA-Binding Proteins; 0 / Erythroid-Specific DNA-Binding Factors; 0 / GATA1 Transcription Factor; 0 / GATA1 protein, human; 0 / Transcription Factors; 04079A1RDZ / Cytarabine; 13191-15-6 / Arabinofuranosylcytosine Triphosphate; 3083-77-0 / Arabinofuranosyluracil; EC 3.5.4.5 / Cytidine Deaminase
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66. Ru YX, Zhao SY, Liu JH, Mi YC, Zhu XF, Wang HJ, Wang JX: [Ultrastructural characteristics of megakaryocytes in 11 patients with acute megakaryocytic leukemia]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2007 Aug;15(4):720-3
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  • [Title] [Ultrastructural characteristics of megakaryocytes in 11 patients with acute megakaryocytic leukemia].
  • The purpose of study was to investigate the ultrastructural features of leukemic megakarocyte (LMK) in patients with acute megakaryocytic leukemia (M(7)).

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  • (PMID = 17708790.001).
  • [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] EC 1.11.1.7 / Peroxidase
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67. Salek-Ardakani S, Smooha G, de Boer J, Sebire NJ, Morrow M, Rainis L, Lee S, Williams O, Izraeli S, Brady HJ: ERG is a megakaryocytic oncogene. Cancer Res; 2009 Jun 1;69(11):4665-73
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  • [Title] ERG is a megakaryocytic oncogene.
  • Truncated forms of ERG are associated with multiple cancers such as Ewing's sarcoma, prostate cancer, and leukemia as part of oncogenic fusion translocations.
  • Increased expression of ERG is highly indicative of poor prognosis in acute myeloid leukemia and ERG is expressed in acute megakaryoblastic leukemia (AMKL); however, it is unclear if expression of ERG per se has a leukemogenic activity.
  • We show that ectopic expression of ERG in fetal hematopoietic progenitors promotes megakaryopoiesis and that ERG alone acts as a potent oncogene in vivo leading to rapid onset of leukemia in mice.
  • We observe that the endogenous ERG is required for the proliferation and maintenance of AMKL cell lines.
  • ERG also strongly cooperates with the GATA1s mutated protein, found in Down syndrome AMKL, to immortalize megakaryocyte progenitors, suggesting that the additional copy of ERG in trisomy 21 may have a role in Down syndrome AMKL.
  • These data suggest that ERG is a hematopoietic oncogene that may play a direct role in myeloid leukemia pathogenesis.
  • [MeSH-major] Leukemia, Megakaryoblastic, Acute / genetics. Megakaryocytes / physiology. Oncogenes / physiology. Thrombopoiesis / genetics. Trans-Activators / physiology

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  • (PMID = 19487285.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 1R01CA120772-01A2
  • [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 / ERG protein, human; 0 / Interleukin-3; 0 / Trans-Activators
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68. Ge Y, Dombkowski AA, LaFiura KM, Tatman D, Yedidi RS, Stout ML, Buck SA, Massey G, Becton DL, Weinstein HJ, Ravindranath Y, Matherly LH, Taub JW: Differential gene expression, GATA1 target genes, and the chemotherapy sensitivity of Down syndrome megakaryocytic leukemia. Blood; 2006 Feb 15;107(4):1570-81
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  • [Title] Differential gene expression, GATA1 target genes, and the chemotherapy sensitivity of Down syndrome megakaryocytic leukemia.
  • Children with Down syndrome (DS) with acute megakaryocytic leukemia (AMkL) have very high survival rates compared with non-DS AMkL patients.
  • Somatic mutations identified in the X-linked transcription factor gene, GATA1, in essentially all DS AMkL cases result in the synthesis of a shorter (40 kDa) protein (GATA1s) with altered transactivation activity and may lead to altered expression of GATA1 target genes.
  • Using the Affymetrix U133A microarray chip, we identified 551 differentially expressed genes between DS and non-DS AMkL samples.
  • Transcripts for the bone marrow stromal-cell antigen 2 (BST2) gene, encoding a transmembrane glycoprotein potentially involved in interactions between leukemia cells and bone marrow stromal cells, were 7.3-fold higher (validated by real-time polymerase chain reaction) in the non-DS compared with the DS group.
  • Our results demonstrate that genes that account for differences in survival between DS and non-DS AMkL cases may be identified by microarray analysis and that differential gene expression may reflect relative transactivation capacities of the GATA1s and full-length GATA1 proteins.

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  • (PMID = 16249385.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NIEHS NIH HHS / ES / P30 ES06639; United States / NCI NIH HHS / CA / R01 CA92308
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; 0 / GATA1 Transcription Factor; 0 / GATA1 protein, human; 04079A1RDZ / Cytarabine; EC 1.13.12.- / Luciferases
  • [Other-IDs] NLM/ PMC1895418
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69. Morita T, Mayanagi T, Sobue K: Reorganization of the actin cytoskeleton via transcriptional regulation of cytoskeletal/focal adhesion genes by myocardin-related transcription factors (MRTFs/MAL/MKLs). Exp Cell Res; 2007 Oct 1;313(16):3432-45
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  • It also regulates the nuclear translocation of myocardin-related transcription factor-A and -B (MRTF-A/B, MAL or MKL 1/2), which are co-activators of serum response factor (SRF).

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  • (PMID = 17714703.001).
  • [ISSN] 0014-4827
  • [Journal-full-title] Experimental cell research
  • [ISO-abbreviation] Exp. Cell Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Actins; 0 / MKL1 protein, mouse; 0 / Serum Response Factor; 0 / Trans-Activators; 0 / Transcription Factors; 0 / myocardin-related transcription factor B, mouse; EC 3.6.5.2 / rhoA GTP-Binding Protein
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70. Nam C, Case AJ, Hostager BS, O'Dorisio MS: The role of vasoactive intestinal peptide (VIP) in megakaryocyte proliferation. J Mol Neurosci; 2009 Feb;37(2):160-7
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  • Megakaryocytopoiesis is a multistage process that involves differentiation of hematopoietic stem cells through the myeloid lineage, ultimately producing megakaryocytes and platelets.
  • The present study was designed to investigate whether the type 1 VIP receptor, VPAC1, mediates VIP effects on megakaryocytopoiesis.
  • The human megakaryoblastic leukemia cell line (CMK) was transfected with VPAC1 and the transgene expression was confirmed by qualitative polymerase chain reaction and immunohistochemistry.
  • [MeSH-major] Megakaryocytes / cytology. Megakaryocytes / physiology. Receptors, Vasoactive Intestinal Polypeptide, Type I / metabolism. Vasoactive Intestinal Peptide / metabolism
  • [MeSH-minor] Autocrine Communication / physiology. Cell Division / physiology. Cell Line, Tumor. Gene Expression / physiology. Humans. Leukemia, Megakaryoblastic, Acute. Reverse Transcriptase Polymerase Chain Reaction. Transfection. Up-Regulation / physiology

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  • (PMID = 18663606.001).
  • [ISSN] 0895-8696
  • [Journal-full-title] Journal of molecular neuroscience : MN
  • [ISO-abbreviation] J. Mol. Neurosci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptors, Vasoactive Intestinal Polypeptide, Type I; 37221-79-7 / Vasoactive Intestinal Peptide
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71. Crispino JD: GATA1 mutations in Down syndrome: implications for biology and diagnosis of children with transient myeloproliferative disorder and acute megakaryoblastic leukemia. Pediatr Blood Cancer; 2005 Jan;44(1):40-4
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  • [Title] GATA1 mutations in Down syndrome: implications for biology and diagnosis of children with transient myeloproliferative disorder and acute megakaryoblastic leukemia.
  • Although physicians have known for many decades that children with Down syndrome are predisposed to developing transient myeloproliferative disorder (TMD) and acute megakaryoblastic leukemia (AMKL), many questions regarding these disorders remain unresolved.
  • First, what is the relationship between TMD and AMKL?
  • Finally, what factors lead to the increased predisposition to these myeloid disorders?
  • In this review I will summarize important new insights into the biology of TMD and AMKL gained from the recent discovery that GATA1, a gene that encodes an essential hematopoietic transcription factor, is mutated in the leukemic blasts from nearly all patients with these malignancies.
  • In addition, I will discuss whether assaying for the presence of a GATA1 mutation can aid in the diagnosis of these and related megakaryoblastic leukemias.
  • Future research aimed at defining the activity of mutant GATA-1 protein and identifying interacting factors encoded by chromosome 21 will likely lead to an even greater understanding of this intriguing leukemia.

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  • [Copyright] (c) 2004 Wiley-Liss, Inc.
  • (PMID = 15390312.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA101774-03; United States / NCI NIH HHS / CA / R01 CA101774; United States / NCI NIH HHS / CA / R01 CA101774-03
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / Erythroid-Specific DNA-Binding Factors; 0 / GATA1 Transcription Factor; 0 / GATA1 protein, human; 0 / Transcription Factors
  • [Number-of-references] 30
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72. Berger R, Busson M, Dastugue N, Radford-Weiss I, Michaux L, Hagemeijer A, Quilichini B, Benattar L, Bernard O, Romana SP: Acute megakaryoblastic leukemia and loss of the RUNX1 gene. Cancer Genet Cytogenet; 2006 Jan 1;164(1):71-3
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  • [Title] Acute megakaryoblastic leukemia and loss of the RUNX1 gene.
  • Since the RUNX1 gene contributes to megakaryopoiesis and acquired trisomy 21 is the most frequent numerical chromosome anomaly in acute megakaryoblastic leukemia (AMLK), a systematic study of RUNX1 abnormalities was performed by fluorescence in situ hybridization in AMLK patients.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / genetics. Gene Deletion. Leukemia, Megakaryoblastic, Acute / genetics

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  • (PMID = 16364766.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / RUNX1 protein, human
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73. Wang L, Guan X, Yin H, Moradian-Oldak J, Nancollas GH: Mimicking the Self-Organized Microstructure of Tooth Enamel. J Phys Chem C Nanomater Interfaces; 2008 Mar 22;112(15):5892-5899
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  • Under near-physiological pH, temperature, and ionic strength, amelogenin (Amel) accelerates hydroxyapatite (HAP) nucleation kinetics, decreasing the induction time in a concentration-dependent manner.
  • Hierarchically organized apatite microstructures are achieved by self-assembly involving nucleated nanocrystallites and Amel oligomers and nanospheres at low supersaturations and protein concentrations in a slow and well-controlled constant composition (CC) system.
  • The nanorod building blocks form spontaneously by synergistic interactions between flexible Amel protein assemblies and rigid calcium phosphate nanocrystallites.
  • This in vitro observation provides direct evidence that Amel promotes apatite crystallization and organization.
  • We interpret our observations to propose that in vivo Amel may maximally exert an influence on the structural control of developing enamel crystals at the earliest nucleation stages.

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  • (PMID = 19169386.001).
  • [ISSN] 1932-7447
  • [Journal-full-title] The journal of physical chemistry. C, Nanomaterials and interfaces
  • [ISO-abbreviation] J Phys Chem C Nanomater Interfaces
  • [Language] ENG
  • [Grant] United States / NIDCR NIH HHS / DE / DE015644-04; United States / NIDCR NIH HHS / DE / R01 DE003223; United States / NIDCR NIH HHS / DE / R01 DE013414; United States / NIDCR NIH HHS / DE / R01 DE020099; United States / NIDCR NIH HHS / DE / R01 DE015644; United States / NIDCR NIH HHS / DE / R37 DE003223
  • [Publication-type] JOURNAL ARTICLE
  • [Publication-country] United States
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74. Sharma S, Nangia A, Jain Malhotra S, Narayan S, Harbhajanka A, Singh S: Clinico-haematological profile of acute megakaryoblastic leukaemia: report of five cases. Adv Hematol; 2009;2009:461912
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  • [Title] Clinico-haematological profile of acute megakaryoblastic leukaemia: report of five cases.
  • Acute megakaryoblastic leukemia (AMKL) is a rare subtype of acute myeloid leukemia.
  • We herein present the clinical, morphological, cytochemical, and immunocytochemical features of five cases of AMKL.
  • Certain morphological features such as presence of abnormal platelet count, giant platelets, and cytoplasmic blebbing in blasts were found to be important pointers towards the diagnosis.
  • However, none of the features were found to be consistent and thus morphological diagnosis has to be confirmed by cytochemistry and immunocytochemistry.

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  • (PMID = 19960061.001).
  • [ISSN] 1687-9112
  • [Journal-full-title] Advances in hematology
  • [ISO-abbreviation] Adv Hematol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Egypt
  • [Other-IDs] NLM/ PMC2778566
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75. Kalita K, Kharebava G, Zheng JJ, Hetman M: Role of megakaryoblastic acute leukemia-1 in ERK1/2-dependent stimulation of serum response factor-driven transcription by BDNF or increased synaptic activity. J Neurosci; 2006 Sep 27;26(39):10020-32
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  • [Title] Role of megakaryoblastic acute leukemia-1 in ERK1/2-dependent stimulation of serum response factor-driven transcription by BDNF or increased synaptic activity.

  • Gene Ontology. gene/protein/disease-specific - Gene Ontology annotations from this paper .
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  • (PMID = 17005865.001).
  • [ISSN] 1529-2401
  • [Journal-full-title] The Journal of neuroscience : the official journal of the Society for Neuroscience
  • [ISO-abbreviation] J. Neurosci.
  • [Language] eng
  • [Grant] United States / NINDS NIH HHS / NS / NS047341-01; United States / NCRR NIH HHS / RR / RR015576-06
  • [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 / Amides; 0 / Brain-Derived Neurotrophic Factor; 0 / Butadienes; 0 / Chromones; 0 / Cyr61 protein, rat; 0 / Cysteine-Rich Protein 61; 0 / Immediate-Early Proteins; 0 / Intercellular Signaling Peptides and Proteins; 0 / Morpholines; 0 / Nitriles; 0 / Proto-Oncogene Proteins c-fos; 0 / Proto-Oncogene Proteins c-jun; 0 / Pyridines; 0 / Serum Response Factor; 0 / Transcription Factors; 0 / U 0126; 138381-45-0 / Y 27632; 154447-36-6 / 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one; 6384-92-5 / N-Methylaspartate; 660YQ98I10 / Potassium Chloride; BH3B64OKL9 / 4-Aminopyridine; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3; Y37615DVKC / Bicuculline
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76. Okabayash S, Ohno C, Yasutomi Y: Acute megakaryocytic leukaemia (AMKL)-like disease in a cynomolgus monkey (Macaca fascicularis). J Comp Pathol; 2009 Feb-Apr;140(2-3):212-6
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  • [Title] Acute megakaryocytic leukaemia (AMKL)-like disease in a cynomolgus monkey (Macaca fascicularis).
  • Microscopically, numerous atypical cells resembling myeloid cells were observed in the bone marrow, and myelofibrosis was present.
  • A diagnosis of acute megakaryocytic leukaemia (AMKL)-like disease was made.
  • This would appear to be the first report of AMKL-like disease in non-human primates.
  • This monkey was infected with simian retrovirus type D and it is possible that this viral infection was associated with the development of neoplasia.
  • [MeSH-major] Leukemia, Megakaryoblastic, Acute / pathology. Leukemia, Megakaryoblastic, Acute / veterinary. Monkey Diseases / pathology

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  • (PMID = 19159898.001).
  • [ISSN] 1532-3129
  • [Journal-full-title] Journal of comparative pathology
  • [ISO-abbreviation] J. Comp. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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77. Kanezaki R, Toki T, Xu G, Narayanan R, Ito E: Cloning and characterization of the novel chimeric gene p53/FXR2 in the acute megakaryoblastic leukemia cell line CMK11-5. Tohoku J Exp Med; 2006 Jul;209(3):169-80
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  • [Title] Cloning and characterization of the novel chimeric gene p53/FXR2 in the acute megakaryoblastic leukemia cell line CMK11-5.
  • Western blot analyses have shown that the p53/FXR2 protein is indeed expressed in a Down syndrome-related acute megakaryoblastic leukemia cell line, CMK11-5 cells.
  • The p53/FXR2 protein was expressed at high levels in the cytoplasm, whereas wild-type p53 and FXR2 were localized primarily in the nucleus and in the periphery of the nucleus, respectively.
  • These results suggest that the p53/FXR2 fusion protein lacks the ability of wild-type p53 to function as a transcription factor.
  • [MeSH-major] Genes, p53 / genetics. Leukemia, Megakaryoblastic, Acute / genetics. Mutant Chimeric Proteins / genetics. RNA-Binding Proteins / genetics

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  • (PMID = 16778363.001).
  • [ISSN] 0040-8727
  • [Journal-full-title] The Tohoku journal of experimental medicine
  • [ISO-abbreviation] Tohoku J. Exp. Med.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / CDKN1A protein, human; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / FXR2 protein, human; 0 / Mutant Chimeric Proteins; 0 / RNA-Binding Proteins; 0 / Topoisomerase II Inhibitors; 6PLQ3CP4P3 / Etoposide
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78. Bourquin JP, Subramanian A, Langebrake C, Reinhardt D, Bernard O, Ballerini P, Baruchel A, Cavé H, Dastugue N, Hasle H, Kaspers GL, Lessard M, Michaux L, Vyas P, van Wering E, Zwaan CM, Golub TR, Orkin SH: Identification of distinct molecular phenotypes in acute megakaryoblastic leukemia by gene expression profiling. Proc Natl Acad Sci U S A; 2006 Feb 28;103(9):3339-44
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  • [Title] Identification of distinct molecular phenotypes in acute megakaryoblastic leukemia by gene expression profiling.
  • Individuals with Down syndrome (DS) are predisposed to develop acute megakaryoblastic leukemia (AMKL), characterized by expression of truncated GATA1 transcription factor protein (GATA1s) due to somatic mutation.
  • The treatment outcome for DS-AMKL is more favorable than for AMKL in non-DS patients.
  • To gain insight into gene expression differences in AMKL, we compared 24 DS and 39 non-DS AMKL samples.
  • We found that non-DS-AMKL samples cluster in two groups, characterized by differences in expression of HOX/TALE family members.
  • Both of these groups are distinct from DS-AMKL, independent of chromosome 21 gene expression.
  • Genes repressed after GATA1 induction in the murine system, most notably GATA-2, MYC, and KIT, show increased expression in DS-AMKL, suggesting that GATA1s fail to repress this class of genes.
  • Only a subset of genes that are up-regulated upon GATA1 induction in the murine system show increased expression in DS-AMKL, including GATA1 and BACH1, a probable negative regulator of megakaryocytic differentiation located on chromosome 21.
  • Surprisingly, expression of the chromosome 21 gene RUNX1, a known regulator of megakaryopoiesis, was not elevated in DS-AMKL.
  • Our results identify relevant signatures for distinct AMKL entities and provide insight into gene expression changes associated with these related leukemias.
  • [MeSH-major] Gene Expression Profiling. Leukemia, Megakaryoblastic, Acute / genetics

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  • (PMID = 16492768.001).
  • [ISSN] 0027-8424
  • [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
  • [Databank-accession-numbers] OMIM/ GSE4119
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / GATA1 Transcription Factor; 0 / GATA1 protein, human; 0 / RUNX1 protein, human; 0 / Transcription Factors
  • [Other-IDs] NLM/ PMC1413912
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79. Hollanda LM, Lima CS, Cunha AF, Albuquerque DM, Vassallo J, Ozelo MC, Joazeiro PP, Saad ST, Costa FF: An inherited mutation leading to production of only the short isoform of GATA-1 is associated with impaired erythropoiesis. Nat Genet; 2006 Jul;38(7):807-12
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  • Acquired somatic mutations in exon 2 of the hematopoietic transcription factor GATA-1 have been found in individuals with Down syndrome with both transient myeloproliferative disorder and acute megakaryoblastic leukemia.
  • Moreover, this is the first study to indicate that a germline splicing mutation does not lead to leukemia in the absence of other cooperating events, such as Down syndrome.

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  • [CommentIn] Nat Genet. 2006 Jul;38(7):741-2 [16804537.001]
  • (PMID = 16783379.001).
  • [ISSN] 1061-4036
  • [Journal-full-title] Nature genetics
  • [ISO-abbreviation] Nat. Genet.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / GATA1 Transcription Factor; 0 / GATA1 protein, human; 0 / Protein Isoforms
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80. Bercovich D, Ganmore I, Scott LM, Wainreb G, Birger Y, Elimelech A, Shochat C, Cazzaniga G, Biondi A, Basso G, Cario G, Schrappe M, Stanulla M, Strehl S, Haas OA, Mann G, Binder V, Borkhardt A, Kempski H, Trka J, Bielorei B, Avigad S, Stark B, Smith O, Dastugue N, Bourquin JP, Tal NB, Green AR, Izraeli S: Mutations of JAK2 in acute lymphoblastic leukaemias associated with Down's syndrome. Lancet; 2008 Oct 25;372(9648):1484-92
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  • [Title] Mutations of JAK2 in acute lymphoblastic leukaemias associated with Down's syndrome.
  • BACKGROUND: Children with Down's syndrome have a greatly increased risk of acute megakaryoblastic and acute lymphoblastic leukaemias.
  • Acute megakaryoblastic leukaemia in Down's syndrome is characterised by a somatic mutation in GATA1.
  • Constitutive activation of the JAK/STAT (Janus kinase and signal transducer and activator of transcription) pathway occurs in several haematopoietic malignant diseases.
  • We tested the hypothesis that mutations in JAK2 might be a common molecular event in acute lymphoblastic leukaemia associated with Down's syndrome.
  • METHODS: JAK2 DNA mutational analysis was done on diagnostic bone marrow samples obtained from 88 patients with Down's syndrome-associated acute lymphoblastic leukaemia; and 216 patients with sporadic acute lymphoblastic leukaemia, Down's syndrome-associated acute megakaryoblastic leukaemia, and essential thrombocythaemia.
  • FINDINGS: Somatically acquired JAK2 mutations were identified in 16 (18%) patients with Down's syndrome-associated acute lymphoblastic leukaemia.
  • The only patient with non-Down's syndrome-associated leukaemia but with a JAK2 mutation had an isochromosome 21q.
  • Children with a JAK2 mutation were younger (mean [SE] age 4.5 years [0.86] vs 8.6 years [0.59], p<0.0001) at diagnosis.
  • INTERPRETATION: A specific genotype-phenotype association exists between the type of somatic mutation within the JAK2 pseudokinase domain and the development of B-lymphoid or myeloid neoplasms.
  • Somatically acquired R683 JAK2 mutations define a distinct acute lymphoblastic leukaemia subgroup that is uniquely associated with trisomy 21.
  • JAK2 inhibitors could be useful for treatment of this leukaemia.
  • [MeSH-major] Down Syndrome / complications. Down Syndrome / genetics. GATA1 Transcription Factor / genetics. Janus Kinase 2 / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics


81. Silva ML, Pombo-de-Oliveira MS, Raimondi SC, Mkrtchyan H, Abdelhay E, de Figueiredo AF, de Souza MT, Garcia DR, de Ventura EM, de Sousa AM, Liehr T: Unbalanced chromosome 1 abnormalities leading to partial trisomy 1q in four infants with Down syndrome and acute megakaryocytic leukemia. Mol Cytogenet; 2009;2:7
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  • [Title] Unbalanced chromosome 1 abnormalities leading to partial trisomy 1q in four infants with Down syndrome and acute megakaryocytic leukemia.
  • BACKGROUND: Children with Down syndrome (DS) have an increased risk of childhood acute leukemia, especially acute megakaryoblastic leukemia (AMKL) also called acute myeloid leukemia (AML) type M7.
  • CONCLUSION: Our results corroborate that abnormalities of chromosome 1 are common in DS-associated AMKL.
  • Whether this chromosomal region contains gene(s) involved in hematopoietic malignant transformation remains to be determined.

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  • (PMID = 19228396.001).
  • [ISSN] 1755-8166
  • [Journal-full-title] Molecular cytogenetics
  • [ISO-abbreviation] Mol Cytogenet
  • [Language] eng
  • [Publication-type] Editorial
  • [Publication-country] United States
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82. Ameri M, Wilkerson MJ, Stockham SL, Almes KM, Patton KM, Jackson T: Acute megakaryoblastic leukemia in a German Shepherd dog. Vet Clin Pathol; 2010 Mar;39(1):39-45
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  • [Title] Acute megakaryoblastic leukemia in a German Shepherd dog.
  • Based on microscopic and immunophenotypic findings, a diagnosis of acute megakaryoblastic leukemia (AMegL) was made.
  • To our knowledge, this is the first report of AMegL in a domestic animal in which immunophenotyping by flow cytometry and a panel of antibodies against CD41/61, CD61, and CD62P were used to support the diagnosis.

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  • (PMID = 19793230.001).
  • [ISSN] 1939-165X
  • [Journal-full-title] Veterinary clinical pathology
  • [ISO-abbreviation] Vet Clin Pathol
  • [Language] ENG
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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83. Spinelli SL, Casey AE, Pollock SJ, Gertz JM, McMillan DH, Narasipura SD, Mody NA, King MR, Maggirwar SB, Francis CW, Taubman MB, Blumberg N, Phipps RP: Platelets and megakaryocytes contain functional nuclear factor-kappaB. Arterioscler Thromb Vasc Biol; 2010 Mar;30(3):591-8
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  • Moreover, inhibition of I-kappaB-alpha phosphorylation (BAY-11-7082) reverted fully spread platelets back to a spheroid morphology.

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  • (PMID = 20042710.001).
  • [ISSN] 1524-4636
  • [Journal-full-title] Arteriosclerosis, thrombosis, and vascular biology
  • [ISO-abbreviation] Arterioscler. Thromb. Vasc. Biol.
  • [Language] ENG
  • [Grant] United States / NIDCR NIH HHS / DE / T32-DE07165; United States / NHLBI NIH HHS / HL / R21 HL086367; United States / NHLBI NIH HHS / HL / HL086367; United States / NINDS NIH HHS / NS / R01 NS054578; United States / NHLBI NIH HHS / HL / RC1 HL100051; United States / NIDCR NIH HHS / DE / DE011390; United States / NHLBI NIH HHS / HL / R01 HL078603-04; United States / NIEHS NIH HHS / ES / ES01247; United States / NHLBI NIH HHS / HL / HL095467-01A1; United States / NIEHS NIH HHS / ES / P30 ES001247; United States / NIEHS NIH HHS / ES / P30 ES001247-269015; United States / NHLBI NIH HHS / HL / R01 HL095467; United States / NHLBI NIH HHS / HL / HL095467; United States / NIDCR NIH HHS / DE / R01 DE011390; United States / NHLBI NIH HHS / HL / RC1 HL100051-01; United States / NINDS NIH HHS / NS / NS054578; United States / NHLBI NIH HHS / HL / RC1HL100051; United States / NHLBI NIH HHS / HL / HL078603-04; United States / NHLBI NIH HHS / HL / R01 HL078603; United States / NIDCR NIH HHS / DE / T32 DE007165; United States / NHLBI NIH HHS / HL / R01 HL095467-01A1; United States / NHLBI NIH HHS / HL / HL078603; United States / CCR NIH HHS / RC / HL100051-01; United States / NIEHS NIH HHS / ES / ES001247-269015; United States / NIDCR NIH HHS / DE / R01 DE011390-22; United States / NIDCR NIH HHS / DE / DE011390-22
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 3-(4-methylphenylsulfonyl)-2-propenenitrile; 0 / NF-kappa B; 0 / NF-kappa B p50 Subunit; 0 / Nitriles; 0 / Sulfones; 0 / Transcription Factor RelA
  • [Other-IDs] NLM/ NIHMS172813; NLM/ PMC2853005
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84. Sekikawa T, Iwase S, Saito S, Arakawa Y, Agawa M, Horiguchi-Yamada J, Yamada H: JAS-R, a new megakaryo-erythroid leukemic cell line that secretes erythropoietin. Anticancer Res; 2006 Mar-Apr;26(2A):843-50
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  • Leukemic cell lines derived from megakaryocytic leukemia are valuable reagents for studies on these events.
  • MATERIALS AND METHODS: A new cell line, JAS-R, was established from a 64-year-old patient with acute megakaryocytic leukemia (AML M7).
  • [MeSH-major] Cell Line, Tumor / pathology. Erythropoietin / secretion. Leukemia, Erythroblastic, Acute / pathology. Leukemia, Megakaryoblastic, Acute / pathology

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  • (PMID = 16619478.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 11096-26-7 / Erythropoietin
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85. Durmaz R, Zozio T, Gunal S, Allix C, Fauville-Dufaux M, Rastogi N: Population-based molecular epidemiological study of tuberculosis in Malatya, Turkey. J Clin Microbiol; 2007 Dec;45(12):4027-35
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  • The most prevalent spoligotype was SIT41 (LAM7-TUR) with 33 (23.9%) isolates.
  • The repartition of strains according to major M. tuberculosis clades (in decreasing order) was as follows: ill-defined T clade (45.7%) > Latin American and Mediterranean (LAM; 29%) > Haarlem (15.9%).
  • We conclude that our patient population is infected by diverse M. tuberculosis populations; however, the majority of the ongoing transmission is due to "evolutionary recent" tuberculosis lineages belonging to principal genetic group 2 (PGG2; Haarlem and LAM) and PGG3 (ill-defined T clade), and most of it is attributable to the LAM7-TUR sublineage with an enhanced phylogeographical specificity for Turkey.


86. Garderet L, Labopin M, Gorin NC, Polge E, Baruchel A, Meloni G, Ortega J, Vossen J, Bunjes D, Leverger G, Blaise D, Ferrant A, Brune M, Dore E, Gadner H, Zintl F, Yaniv I, Dini G, Frassoni F, Acute Leukemia Working Party and Pediatric Working Party of the European Group for Blood and Marrow Transplantation: Hematopoietic stem cell transplantation for de novo acute megakaryocytic leukemia in first complete remission: a retrospective study of the European Group for Blood and Marrow Transplantation (EBMT). Blood; 2005 Jan 1;105(1):405-9
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  • [Title] Hematopoietic stem cell transplantation for de novo acute megakaryocytic leukemia in first complete remission: a retrospective study of the European Group for Blood and Marrow Transplantation (EBMT).
  • Acute megakaryoblastic leukemia (M7 AML) is a highly aggressive disease.
  • We evaluated outcomes in 57 children (11 with Down syndrome) and 69 adults with M7 AML after first complete remission (CR1) following autologous or HLA-identical allogeneic transplantation.
  • Results for autologous transplantation were (children and adults, respectively): engraftment, 90% and 100%; 3-year treatment-related mortality (TRM) rate, 3% and 8%; relapse rate, 45% and 64%; leukemia-free survival (LFS) rate, 52% and 27%; overall survival (OS) rate, 61% and 30%.
  • We conclude that M7 AML patients in CR1 (except children with Down syndrome, who already have better outcomes) can benefit from transplantation.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Leukemia, Megakaryoblastic, Acute / pathology. Leukemia, Megakaryoblastic, Acute / surgery
  • [MeSH-minor] Adolescent. Adult. Aged. Child. Child, Preschool. Disease-Free Survival. Down Syndrome / complications. Europe. Female. Graft vs Host Disease / immunology. Humans. Infant. Male. Middle Aged. Prognosis. Recurrence. Retrospective Studies. Survival Rate. Transplantation, Autologous / adverse effects. Transplantation, Homologous / adverse effects

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  • (PMID = 15191953.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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87. Elmaagacli AH, Koldehoff M, Zakrzewski JL, Steckel NK, Ottinger H, Beelen DW: Growth factor-independent 1B gene (GFI1B) is overexpressed in erythropoietic and megakaryocytic malignancies and increases their proliferation rate. Br J Haematol; 2007 Jan;136(2):212-9
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  • [Title] Growth factor-independent 1B gene (GFI1B) is overexpressed in erythropoietic and megakaryocytic malignancies and increases their proliferation rate.
  • Growth factor-independent 1B (GFI1B) is a transcription factor essential for the development and differentiation of erythroid and megakaryocytic lineages.
  • We evaluated the GFI1B expression in erythroleukaemia and megakaryocytic leukaemia, as well as in patients with other subtypes of acute myeloid leukaemia (AML), acute lymphoblastic leukaemia (ALL), chronic myeloid leukaemia (CML), myelodysplastic syndrome (MDS), severe aplastic anaemia (SAA), myelofibrosis with myeloid metaplasia (MMM) and in healthy volunteers.
  • GFI1B expression was increased at least threefold in patients with erythroleukaemia (P < 0.01 compared with controls) and megakaryocytic leukaemia (P < 0.05) as well as in their corresponding leukaemic cell lines HEL, K562, CMK and M-07e.
  • Our data indicate that GFI1B plays a major role in AML-M6 and AML-M7 and qualifies as a target for anti-leukaemic strategies in these malignancies.
  • [MeSH-major] Gene Expression Regulation, Neoplastic. Leukemia / metabolism. Proto-Oncogene Proteins / genetics. Repressor Proteins / genetics
  • [MeSH-minor] Anemia, Aplastic / metabolism. Antigens, CD34 / immunology. Apoptosis. Case-Control Studies. Cell Cycle. Cell Line, Tumor. Gene Expression. Genes, myc. Humans. Immunophenotyping. Leukemia, Erythroblastic, Acute / metabolism. Leukemia, Megakaryoblastic, Acute / metabolism. RNA Interference. RNA, Messenger / analysis. RNA, Small Interfering / genetics. Reverse Transcriptase Polymerase Chain Reaction. Statistics, Nonparametric. Transfection / methods. rho GTP-Binding Proteins / genetics

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  • (PMID = 17156408.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / GFI1B protein, human; 0 / Proto-Oncogene Proteins; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 0 / Repressor Proteins; EC 3.6.5.2 / rho GTP-Binding Proteins
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88. Huang Z, Dore LC, Li Z, Orkin SH, Feng G, Lin S, Crispino JD: GATA-2 reinforces megakaryocyte development in the absence of GATA-1. Mol Cell Biol; 2009 Sep;29(18):5168-80
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  • Dysregulation of GATA-2 is a hallmark of acute megakaryoblastic leukemia in children with Down syndrome, a malignancy that is defined by the combination of trisomy 21 and a GATA1 mutation.
  • Surprisingly, GATA-2 also negatively regulates the expression of crucial myeloid transcription factors, such as Sfpi1 and Cebpa.
  • In the absence of GATA-1, GATA-2 prevents induction of a latent myeloid gene expression program.

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  • (PMID = 19620289.001).
  • [ISSN] 1098-5549
  • [Journal-full-title] Molecular and cellular biology
  • [ISO-abbreviation] Mol. Cell. Biol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA101774-07; United States / NIGMS NIH HHS / GM / P50 GM081892; United States / NCI NIH HHS / CA / R01 CA101774; United States / NCI NIH HHS / CA / R01 CA101774-07
  • [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 / CCAAT-Enhancer-Binding Protein-alpha; 0 / GATA1 Transcription Factor; 0 / GATA2 Transcription Factor; 0 / Gata1 protein, mouse; 0 / Gata2 protein, mouse; 0 / Proto-Oncogene Proteins; 0 / Trans-Activators; 0 / proto-oncogene protein Spi-1
  • [Other-IDs] NLM/ PMC2738300
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89. Lee SJ, Yoon JH, Song KS: Chrysin inhibited stem cell factor (SCF)/c-Kit complex-induced cell proliferation in human myeloid leukemia cells. Biochem Pharmacol; 2007 Jul 15;74(2):215-25
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  • [Title] Chrysin inhibited stem cell factor (SCF)/c-Kit complex-induced cell proliferation in human myeloid leukemia cells.
  • However, the mechanism by which SCF induces cell proliferation in the human megakaryoblastic leukemia cell line, MO7e, and the signaling molecules involved, especially in downstream signaling of c-Kit, remain unclear.
  • [MeSH-major] Flavonoids / pharmacology. Leukemia, Myeloid / pathology. Stem Cell Factor / antagonists & inhibitors


90. Malaivijitnond S, Hamada Y, Suryobroto B, Takenaka O: Female long-tailed macaques with scrotum-like structure. Am J Primatol; 2007 Jul;69(7):721-35
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  • We recently observed another type of sexual swelling in long-tailed macaques inhabiting localities north of the Isthmus of Kra, Thailand.
  • The sex of the monkeys possessing the scrotum-like swelling was examined at the chromosomal and gonadal levels by determining the presence of two sex-related genes (the SRY and the AMEL), and sex-steroid hormone levels, respectively.
  • For chromosomal sex, polymerase chain reaction (PCR)-based assays suggested the absence of the Y-linked SRY and AMEL loci but the presence of the X-linked AMEL locus in the scrotum-like monkeys, consistent with them being XX and not XY.

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  • (PMID = 17245765.001).
  • [ISSN] 0275-2565
  • [Journal-full-title] American journal of primatology
  • [ISO-abbreviation] Am. J. Primatol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Amelogenin; 3XMK78S47O / Testosterone; 4TI98Z838E / Estradiol
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91. Steensma DP, McClure RF, Karp JE, Tefferi A, Lasho TL, Powell HL, DeWald GW, Kaufmann SH: JAK2 V617F is a rare finding in de novo acute myeloid leukemia, but STAT3 activation is common and remains unexplained. Leukemia; 2006 Jun;20(6):971-8
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  • [Title] JAK2 V617F is a rare finding in de novo acute myeloid leukemia, but STAT3 activation is common and remains unexplained.
  • Recently, several groups identified a recurrent somatic point mutation constitutively activating the hematopoietic growth factor receptor-associated JAK2 tyrosine kinase in diverse chronic myeloid disorders - most commonly classic myeloproliferative disorders (MPD), especially polycythemia vera.
  • We hypothesized that the JAK2 V617F mutation might also be present in samples from patients with acute myeloid leukemia (AML), especially erythroleukemia (AML-M6) or megakaryoblastic leukemia (AML-M7), where it might mimic erythropoietin or thrombopoietin signaling.
  • Immunoperoxidase staining confirmed phosphorylated STAT3 in malignant myeloblasts (21% of cases, including all AML-M3 samples tested).
  • We then analyzed genomic DNA from 162 AML, 30 B-cell lymphoma, and 10 chronic lymphocytic leukemia (CLL) samples for JAK2 mutations, and assayed a subset for SOCS1 and FLT3 mutations.
  • Janus kinase2 V617F was present in 13/162 AML samples (8%): 10/13 transformed MPD, and three apparent de novo AML (one of 12 AML-M6, one of 24 AML-M7, and one AML-M2 - all mixed clonality).
  • Lymphoproliferative disorder samples were both JAK2 and SOCS1 wild type.
  • Thus, while JAK2 V617F is uncommon in de novo AML and probably does not occur in lymphoid malignancy, unexplained STAT3 activation is common in AML.
  • [MeSH-major] Leukemia, Myeloid / genetics. Protein-Tyrosine Kinases / genetics. Proto-Oncogene Proteins / genetics. STAT3 Transcription Factor / metabolism
  • [MeSH-minor] Acute Disease. Blotting, Western. Humans. Janus Kinase 2. Phosphorylation. Point Mutation. Signal Transduction / genetics. Suppressor of Cytokine Signaling Proteins / genetics. fms-Like Tyrosine Kinase 3 / genetics

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  • (PMID = 16598306.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / K12 CA90628; United States / NCI NIH HHS / CA / P50 CA97274; United States / NCI NIH HHS / CA / R01 CA69008
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins; 0 / SOCS1 protein, human; 0 / STAT3 Transcription Factor; 0 / STAT3 protein, human; 0 / Suppressor of Cytokine Signaling Proteins; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2
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92. Massey GV, Zipursky A, Chang MN, Doyle JJ, Nasim S, Taub JW, Ravindranath Y, Dahl G, Weinstein HJ, Children's Oncology Group (COG): A prospective study of the natural history of transient leukemia (TL) in neonates with Down syndrome (DS): Children's Oncology Group (COG) study POG-9481. Blood; 2006 Jun 15;107(12):4606-13
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  • [Title] A prospective study of the natural history of transient leukemia (TL) in neonates with Down syndrome (DS): Children's Oncology Group (COG) study POG-9481.
  • A unique transient leukemia (TL) has been described in newborns with Down syndrome (DS; or trisomy 21 mosaics).
  • This leukemia has a high incidence of spontaneous remission; however, early death and subsequent development of acute megakaryoblastic leukemia (AMKL) have been reported.
  • We prospectively evaluated 48 infants with DS and TL to determine the natural history and biologic characteristics of this disease, identify the clinical characteristics associated with early death or subsequent leukemia, and assess the incidence of subsequent leukemia.
  • Blast cells associated with TL in DS infants exhibited FAB M(7) morphology and phenotype.
  • Most infants (74%) had trisomy 21 (or mosaicism) as the only cytogenetic abnormality in the blast cells.
  • Early death occurred in 17% of infants and was significantly correlated with higher white blood cell count at diagnosis (P < .001), increased bilirubin and liver enzymes (P < .005), and a failure to normalize the blood count (P = .001).
  • Recurrence of leukemia occurred in 19% of infants at a mean of 20 months.
  • Development of leukemia was significantly correlated with karyotypic abnormalities in addition to trisomy 21 (P = .037).
  • Ongoing collaborative clinical studies are needed to determine the optimal role of chemotherapy for infants at risk for increased mortality or disease recurrence and to further the knowledge of the unique biologic features of this TL.
  • [MeSH-major] Chromosomes, Human, Pair 21. Down Syndrome. Leukemia, Megakaryoblastic, Acute. Mosaicism. Trisomy

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  • [CommentIn] Blood. 2006 Dec 1;108(12):3952-3; author reply 3953 [17114573.001]
  • (PMID = 16469874.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Enzymes; RFM9X3LJ49 / Bilirubin
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93. Kim BH, Jee JG, Yin CH, Sandoval C, Jayabose S, Kitamura D, Bach EA, Baeg GH: NSC114792, a novel small molecule identified through structure-based computational database screening, selectively inhibits JAK3. Mol Cancer; 2010;9:36
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  • BACKGROUND: Human or animals lacking either JAK3 or the common gamma chain (gammac) expression display severe combined immunodeficiency disease, indicating the crucial role of JAK3 in T-cell development and the homeostasis of the immune system.
  • Recent studies identified activating JAK3 mutations in patients with various hematopoietic malignancies, including acute megakaryoblastic leukemia.

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  • (PMID = 20149240.001).
  • [ISSN] 1476-4598
  • [Journal-full-title] Molecular cancer
  • [ISO-abbreviation] Mol. Cancer
  • [Language] eng
  • [Grant] United States / NIGMS NIH HHS / GM / R01 GM085075
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / 10,13-dimethyl-17-(2-(6-sulfanylidene-3H-purin-9-yl)acetyl)-1,2,6,7,8,9,11,12,14,15,16,17-dodecahydrocyclopenta(a)phenanthren-3-one; 0 / Antineoplastic Agents; 0 / Apoptosis Regulatory Proteins; 0 / Diterpenes; 0 / Interleukin-2; 0 / Protein Kinase Inhibitors; 0 / Purines; 0 / STAT5 Transcription Factor; 0 / Small Molecule Libraries; EC 2.7.10.2 / Janus Kinase 3
  • [Other-IDs] NLM/ PMC2830973
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94. Voisin V, Legault P, Ospina DP, Ben-David Y, Rassart E: Gene profiling of the erythro- and megakaryoblastic leukaemias induced by the Graffi murine retrovirus. BMC Med Genomics; 2010 Jan 26;3:2
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  • [Title] Gene profiling of the erythro- and megakaryoblastic leukaemias induced by the Graffi murine retrovirus.
  • BACKGROUND: Acute erythro- and megakaryoblastic leukaemias are associated with very poor prognoses and the mechanism of blastic transformation is insufficiently elucidated.
  • The murine Graffi leukaemia retrovirus induces erythro- and megakaryoblastic leukaemias when inoculated into NFS mice and represents a good model to study these leukaemias.
  • METHODS: To expand our understanding of genes specific to these leukaemias, we compared gene expression profiles, measured by microarray and RT-PCR, of all leukaemia types induced by this virus.
  • RESULTS: The transcriptome level changes, present between the different leukaemias, led to the identification of specific cancerous signatures.
  • The expression pattern of these genes has been further tested by RT-PCR in different samples, in a Friend erythroleukaemic model and in human leukaemic cell lines.We also screened the megakaryoblastic leukaemias for viral integrations and identified genes targeted by these integrations and potentially implicated in the onset of the disease.
  • CONCLUSIONS: Taken as a whole, the data obtained from this global gene profiling experiment have provided a detailed characterization of Graffi virus induced erythro- and megakaryoblastic leukaemias with many genes reported specific to the transcriptome of these leukaemias for the first time.

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  • (PMID = 20102610.001).
  • [ISSN] 1755-8794
  • [Journal-full-title] BMC medical genomics
  • [ISO-abbreviation] BMC Med Genomics
  • [Language] ENG
  • [Grant] Canada / Canadian Institutes of Health Research / / MOP-37994; Canada / Canadian Institutes of Health Research / / MOP-84460
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2843641
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95. Zhang HQ, Yang ZQ, Liu FE, Zhang J, Zhao WM: [Homologous amelogenin gene test of archaeological samples]. Fa Yi Xue Za Zhi; 2006 Jun;22(3):213-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • RESULTS: Seven in sixteen samples from eight graves showed positive results and the targeted segments were visible: a male with two bands of 106bp (Amel-X) and 112 bp (Amel-Y), while a female with only one band of 106 bp (Amel-X).

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  • (PMID = 16856347.001).
  • [ISSN] 1004-5619
  • [Journal-full-title] Fa yi xue za zhi
  • [ISO-abbreviation] Fa Yi 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 / Amelogenin; 0 / DNA Primers; 0 / Dental Enamel Proteins; 9007-49-2 / DNA
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96. Kearney L, Gonzalez De Castro D, Yeung J, Procter J, Horsley SW, Eguchi-Ishimae M, Bateman CM, Anderson K, Chaplin T, Young BD, Harrison CJ, Kempski H, So CW, Ford AM, Greaves M: Specific JAK2 mutation (JAK2R683) and multiple gene deletions in Down syndrome acute lymphoblastic leukemia. Blood; 2009 Jan 15;113(3):646-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Specific JAK2 mutation (JAK2R683) and multiple gene deletions in Down syndrome acute lymphoblastic leukemia.
  • Children with Down syndrome (DS) have a greatly increased risk of acute megakaryoblastic leukemia (AMKL) and acute lymphoblastic leukemia (ALL).
  • Both DS-AMKL and the related transient myeloproliferative disorder (TMD) have GATA1 mutations as obligatory, early events.
  • [MeSH-major] Down Syndrome / genetics. Janus Kinase 2 / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics


97. Otlu B, Durmaz R, Gunal S, Sola C, Zozio T, Rastogi N: Beijing/W and major spoligotype families of Mycobacterium tuberculosis strains isolated from tuberculosis patients in Eastern Turkey. New Microbiol; 2009 Jul;32(3):255-63
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