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1. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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2. 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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3. 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.

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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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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. Gluzman DF, Nadgornaya VA, Sklyarenko LM, Ivanovskaya TS, Poludnenko LY, Ukrainskaya NI: Immunocytochemical markers in acute leukaemias diagnosis. Exp Oncol; 2010 Sep;32(3):195-9
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  • [Title] Immunocytochemical markers in acute leukaemias diagnosis.
  • The study included 1742 patients with acute myeloblastic leukaemias (AML) and acute lymphoblastic leukaemias (ALL), Kyiv city residents and patients from 20 regions of Ukraine.
  • Bone marrow and blood smears were sent at diagnosis to Reference Center.
  • Immunocytochemical study was required especially in diagnosing of AML with minimal differentiation, acute megakaryoblastic leukaemia, acute erythroid leukaemia and acute leukaemias of ambiguous lineage.
  • Acute lymphoblastic leukaemias was broadly classified into B-lineage and T-lineage ALL.
  • Immunocytochemical examination was required to diagnose AL of ambiguous lineage with no clear evidence of lineage differentiation (acute undifferentiated leukaemia) or those with blasts that express markers of more than one lineage (mixed phenotype acute leukaemias).
  • [MeSH-major] Leukemia, Myeloid, Acute / immunology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology
  • [MeSH-minor] Acute Disease. Biomarkers, Tumor / immunology. Humans. Immunohistochemistry. Immunophenotyping. Lymphocyte Subsets / immunology. Lymphocyte Subsets / pathology

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  • (PMID = 21403617.001).
  • [ISSN] 1812-9269
  • [Journal-full-title] Experimental oncology
  • [ISO-abbreviation] Exp. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Ukraine
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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6. 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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7. 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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8. Ge Y, Elghetany MT: CD36: a multiligand molecule. Lab Hematol; 2005;11(1):31-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • CD36 is commonly expressed on blasts in acute monocytic leukemia, megakaryoblastic leukemia, and erythroleukemia.
  • As a receptor for thrombospondin 1, CD36 plays a role in the regulation of angiogenesis, which may be a therapeutic strategy for controlling the dissemination of malignant neoplasms.
  • [MeSH-minor] Antigens, CD / physiology. Blast Crisis / pathology. Ethnic Groups. Gene Expression Regulation / immunology. Humans. Leukemia / blood. Malaria / blood. Malaria / immunology. Neovascularization, Physiologic

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  • (PMID = 15790550.001).
  • [ISSN] 1080-2924
  • [Journal-full-title] Laboratory hematology : official publication of the International Society for Laboratory Hematology
  • [ISO-abbreviation] Lab Hematol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD36
  • [Number-of-references] 70
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9. 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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10. 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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11. 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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12. Morerio C, Rapella A, Tassano E, Rosanda C, Panarello C: MLL-MLLT10 fusion gene in pediatric acute megakaryoblastic leukemia. Leuk Res; 2005 Oct;29(10):1223-6
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  • [Title] MLL-MLLT10 fusion gene in pediatric acute megakaryoblastic leukemia.
  • The occurrence of MLL gene rearrangement in acute megakaryoblastic leukemia (AML-M7, acute myeloid leukemia, French-American-British type M7) is very rare and limited to pediatric age: in particular, MLL-MLLT10 fusion, previously reported as characteristic of monocytic leukemia, has been reported in only one case of pediatric megakaryoblastic leukemia.
  • We describe the second case with this association in light of the few reported cases of AML-M7 with MLL and/or 11q23 involvement.
  • [MeSH-major] Chromosomes, Human, Pair 11 / genetics. Leukemia, Megakaryoblastic, Acute / genetics. Oncogene Proteins, Fusion / genetics
  • [MeSH-minor] Child, Preschool. Female. Humans. In Situ Hybridization, Fluorescence. Karyotyping. Male. Myeloid-Lymphoid Leukemia Protein. Translocation, Genetic

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  • (PMID = 16111539.001).
  • [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; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / MLL-AF10 fusion protein, human; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
  • [Number-of-references] 15
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13. Pine SR, Guo Q, Yin C, Jayabose S, Druschel CM, Sandoval C: Incidence and clinical implications of GATA1 mutations in newborns with Down syndrome. Blood; 2007 Sep 15;110(6):2128-31
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  • Somatic mutations in the GATA1 gene are present in almost all cases of Down syndrome (DS)-associated acute megakaryoblastic leukemia (AMKL) and transient leukemia (TL).
  • Two newborns with a GATA1 mutation subsequently developed AMKL, and none of the infants without a functional GATA1 mutation were reported to have developed leukemia.
  • In addition to screening for TL, a GATA1 mutation at birth might serve as a biomarker for an increased risk of DS-related AMKL.
  • [MeSH-major] Down Syndrome / genetics. GATA1 Transcription Factor / genetics. Leukemia, Megakaryoblastic, Acute / genetics. Mutation / genetics

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  • (PMID = 17576817.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / GATA1 Transcription Factor; 0 / GATA1 protein, human
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14. Al-Ahmari A, Shah N, Sung L, Zipursky A, Hitzler J: Long-term results of an ultra low-dose cytarabine-based regimen for the treatment of acute megakaryoblastic leukaemia in children with Down syndrome. Br J Haematol; 2006 Jun;133(6):646-8
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  • [Title] Long-term results of an ultra low-dose cytarabine-based regimen for the treatment of acute megakaryoblastic leukaemia in children with Down syndrome.
  • Children with acute megakaryoblastic leukaemia (AMKL) and Down syndrome (DS) show a favourable response to chemotherapy, probably due to increased sensitivity of the leukaemic blasts to cytarabine.
  • The survival of children with AMKL and DS was retrospectively compared following treatment with a low-dose chemotherapy protocol, consisting of cytarabine (10 mg/m2/dose), retinylpalmitate and vincristine or standard chemotherapy.
  • Further reduction of treatment intensity in AMKL of children with DS, therefore, appears feasible.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Down Syndrome / drug therapy. Leukemia, Megakaryoblastic, Acute / drug therapy

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  • (PMID = 16704441.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study
  • [Publication-country] England
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; 11103-57-4 / Vitamin A; 1D1K0N0VVC / retinol palmitate; 5J49Q6B70F / Vincristine
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15. 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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16. Jarmuz M, Kroll R, Przybyłowicz-Chalecka A, Ratajczak B, Gniot M, Szyfter K, Komarnicki M: Megakaryocytic blast crisis in a chronic myeloid leukemia patient with a rare variant of Philadelphia rearrangement t(9;22;22) and a constitutional translocation t(3;7). Cancer Genet Cytogenet; 2010 May;199(1):45-7
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  • [Title] Megakaryocytic blast crisis in a chronic myeloid leukemia patient with a rare variant of Philadelphia rearrangement t(9;22;22) and a constitutional translocation t(3;7).
  • Megakaryocytic blast crisis occurs extremely rarely, accounting for <3% of cases of chronic myelogenous leukemia in blastic transformation.
  • In chronic myeloid leukemia, a variant Philadelphia translocation is reported in 2-10% of cases.
  • We report an unusual case of megakaryocytic blast crisis with the Philadelphia variant rearrangement t(9;22;22) and a constitutional translocation t(3;7).
  • The chromosome region 22q13 harbors MKL1 gene, which is engaged in a specific translocation associated with acute megakaryoblastic leukemia.
  • Study of deregulation of these four genes could contribute to better understanding of the effects of the t(9;22;22) rearrangement in a megakaryocytic blast crisis.
  • [MeSH-major] Blast Crisis / genetics. Blast Crisis / pathology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Megakaryocytes / pathology. Philadelphia Chromosome


17. Klusmann JH, Reinhardt D, Hasle H, Kaspers GJ, Creutzig U, Hahlen K, van den Heuvel-Eibrink MM, Zwaan CM: Janus kinase mutations in the development of acute megakaryoblastic leukemia in children with and without Down's syndrome. Leukemia; 2007 Jul;21(7):1584-7
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  • [Title] Janus kinase mutations in the development of acute megakaryoblastic leukemia in children with and without Down's syndrome.
  • [MeSH-major] Down Syndrome / complications. Janus Kinases / genetics. Leukemia, Megakaryoblastic, Acute / etiology


18. Muntean AG, Ge Y, Taub JW, Crispino JD: Transcription factor GATA-1 and Down syndrome leukemogenesis. Leuk Lymphoma; 2006 Jun;47(6):986-97
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  • Recently, acquired mutations in the megakaryocytic regulator GATA1 have been found in essentially all cases of acute megakaryoblastic leukemia (AMkL) in children with Down syndrome and in the closely related malignancy transient myeloproliferative disorder.
  • Because GATA-1s retains both DNA binding zinc fingers, but is missing the N-terminal transactivation domain, it has been predicted that the inability of GATA-1s to regulate its normal class of megakaryocytic target genes is the mechanism by which mutations in GATA1 contribute to the disease.
  • Indeed, several recent reports have confirmed that GATA-1s fails to properly regulate the growth of megakaryocytic precursors, likely through aberrant transcriptional regulation.
  • Finally, the inability of GATA-1s to promote expression of important metabolic genes, such as cytadine deaminase, likely contributes to the remarkable hypersensitivity of AMkL blasts to cytosine arabinoside.

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  • (PMID = 16840187.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01-CA101774; United States / NCI NIH HHS / CA / R01-CA092308; United States / NCI NIH HHS / CA / R01 CA101774; United States / NCI NIH HHS / CA / CA101774-04; United States / NCI NIH HHS / CA / R01 CA101774-04
  • [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; 0 / GATA1 protein, human; 9007-49-2 / DNA
  • [Number-of-references] 91
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19. Roy A, Roberts I, Norton A, Vyas P: Acute megakaryoblastic leukaemia (AMKL) and transient myeloproliferative disorder (TMD) in Down syndrome: a multi-step model of myeloid leukaemogenesis. Br J Haematol; 2009 Oct;147(1):3-12
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  • [Title] Acute megakaryoblastic leukaemia (AMKL) and transient myeloproliferative disorder (TMD) in Down syndrome: a multi-step model of myeloid leukaemogenesis.
  • Children with Down syndrome (DS) have a marked increase in susceptibility to Acute Megakaryoblastic Leukaemia (DS-AMKL) and the closely linked neonatal preleukaemic syndrome, Transient Myeloproliferative Disorder (DS-TMD).
  • The distinct stages of DS-TMD and DS-AMKL provide an excellent tractable model to study leukaemogenesis.
  • This review focuses on recent studies describing clinical, haematological and biological features of DS-AMKL and DS-TMD.
  • The findings from these studies suggest that mutations in the key haemopoietic regulator GATA1 (GATA binding protein 1) in DS-AMKL and DS-TMD may be useful in diagnosis and assessing minimal residual disease.
  • These findings raise the possibility of population-based screening strategies for DS-TMD and the development of treatment to eliminate the preleukaemic TMD clone to prevent DS-AMKL.
  • These findings have implications for leukaemia biology more broadly given the frequency of acquired trisomy in other human leukaemias.
  • [MeSH-major] Cell Transformation, Neoplastic / genetics. Down Syndrome / genetics. Leukemia, Megakaryoblastic, Acute / genetics. Models, Genetic. Myeloproliferative Disorders / genetics

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  • (PMID = 19594743.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Grant] United Kingdom / Department of Health / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / GATA1 Transcription Factor; 0 / GATA1 protein, human; 0 / Neoplasm Proteins
  • [Number-of-references] 91
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20. 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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21. 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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  • (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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22. Taketani T, Taki T, Sako M, Ishii T, Yamaguchi S, Hayashi Y: MNX1-ETV6 fusion gene in an acute megakaryoblastic leukemia and expression of the MNX1 gene in leukemia and normal B cell lines. Cancer Genet Cytogenet; 2008 Oct 15;186(2):115-9
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  • [Title] MNX1-ETV6 fusion gene in an acute megakaryoblastic leukemia and expression of the MNX1 gene in leukemia and normal B cell lines.
  • Patients with infant acute myeloid leukemia (AML) who carry a t(7;12)(q36;p13) translocation have been reported to have a poor clinical outcome.
  • A 23-month-old girl with acute megakaryoblastic leukemia (AMKL) exhibited chromosome abnormalities, including add(7)(q22), and del(12)(p12p13).
  • This represents a novel case of an AMKL patient with MNX1-ETV6 fusion transcripts who had a good prognosis.
  • [MeSH-major] B-Lymphocytes / metabolism. Gene Fusion. Homeodomain Proteins / genetics. Leukemia / genetics. Leukemia, Megakaryoblastic, Acute / genetics. Proto-Oncogene Proteins c-ets / genetics. Repressor Proteins / genetics. Transcription Factors / genetics

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  • (PMID = 18940475.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ETS translocation variant 6 protein; 0 / Homeodomain Proteins; 0 / MNX1 protein, human; 0 / Proto-Oncogene Proteins c-ets; 0 / Repressor Proteins; 0 / Transcription Factors
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23. 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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24. Bhargava P, Kallakury BV, Ross JS, Azumi N, Bagg A: CD79a is heterogeneously expressed in neoplastic and normal myeloid precursors and megakaryocytes in an antibody clone-dependent manner. Am J Clin Pathol; 2007 Aug;128(2):306-13
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  • [Title] CD79a is heterogeneously expressed in neoplastic and normal myeloid precursors and megakaryocytes in an antibody clone-dependent manner.
  • The reported frequency of CD79a expression in acute myeloid leukemias (AML) ranges from 0% to 90%.
  • Of 7 acute promyelocytic leukemia (APL) cases, 6 (86%) stained for CD79a with clones HM47/A9 (Novocastra, Newcastle Upon Tyne, England) and HM57 (DAKO, Carpinteria, CA) but were negative with clones 11E3 (Novocastra), and JCB117 (DAKO).
  • Half of 6 acute megakaryoblastic leukemia (AMKL) cases and normal megakaryocytes in 14 (67%) of 21 cases were immunoreactive using clone 11D10 (Novocastra).
  • Approximately one third of non-APL/non-AMKL AML and myeloid precursors in normal marrow specimens stained with clones HM57 and 11D10.
  • This heterogeneity of CD79a expression in AML, megakaryocytes, and myeloid precursors is MoAb clone-dependent, likely owing to different epitope detection, and may be of diagnostic usefulness.
  • [MeSH-major] Antigens, CD79 / analysis. Bone Marrow Cells / chemistry. Leukemia, Myeloid, Acute / metabolism. Megakaryocytes / chemistry

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  • (PMID = 17638667.001).
  • [ISSN] 0002-9173
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD79; 0 / CD79A protein, human
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25. Crispino JD: GATA1 in normal and malignant hematopoiesis. Semin Cell Dev Biol; 2005 Feb;16(1):137-47
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  • [Title] GATA1 in normal and malignant hematopoiesis.
  • Furthermore, few would have guessed that missense mutations in GATA1 would cause inherited blood disorders, while acquired mutations would be found associated with essentially all cases of acute megakaryoblastic leukemia (AMKL) in children with Down syndrome (DS).
  • With respect to the latter disorder, the presence of a GATA1 mutation is now arguably the defining feature of this leukemia.
  • In this review, I will summarize our current knowledge of the role of GATA-1 in normal development, and discuss how mutations in GATA1 lead to abnormal and malignant hematopoiesis.

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  • (PMID = 15659348.001).
  • [ISSN] 1084-9521
  • [Journal-full-title] Seminars in cell & developmental biology
  • [ISO-abbreviation] Semin. Cell Dev. Biol.
  • [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; United States / NIDDK NIH HHS / DK / R01-DK61464
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] England
  • [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] 94
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26. Gu TL, Mercher T, Tyner JW, Goss VL, Walters DK, Cornejo MG, Reeves C, Popova L, Lee K, Heinrich MC, Rush J, Daibata M, Miyoshi I, Gilliland DG, Druker BJ, Polakiewicz RD: A novel fusion of RBM6 to CSF1R in acute megakaryoblastic leukemia. Blood; 2007 Jul 1;110(1):323-33
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  • [Title] A novel fusion of RBM6 to CSF1R in acute megakaryoblastic leukemia.
  • Activated tyrosine kinases have been frequently implicated in the pathogenesis of cancer, including acute myeloid leukemia (AML), and are validated targets for therapeutic intervention with small-molecule kinase inhibitors.
  • This method revealed the presence of an activated colony-stimulating factor 1 receptor (CSF1R) kinase in the acute megakaryoblastic leukemia (AMKL) cell line MKPL-1.
  • DNA sequence analysis of cDNA generated by 5'RACE from CSF1R coding sequences identified a novel fusion of the RNA binding motif 6 (RBM6) gene to CSF1R gene generated presumably by a t(3;5)(p21;q33) translocation.
  • Expression of the RBM6-CSF1R fusion protein conferred interleukin-3 (IL-3)-independent growth in BaF3 cells, and induces a myeloid proliferative disease (MPD) with features of megakaryoblastic leukemia in a murine transplant model.

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  • (PMID = 17360941.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA066996; United States / NCI NIH HHS / CA / R01 CA66996
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Oncogene Proteins, Fusion; 0 / RBM6 protein, human; 0 / RNA-Binding Proteins; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor, Macrophage Colony-Stimulating Factor
  • [Other-IDs] NLM/ PMC1896120
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27. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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28. Ciovacco WA, Raskind WH, Kacena MA: Human phenotypes associated with GATA-1 mutations. Gene; 2008 Dec 31;427(1-2):1-6
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  • These five human diseases are: X-linked thrombocytopenia (XLT), X-linked thrombocytopenia with thalassemia (XLTT), congenital erythropoietic porphyria (CEP), transient myeloproliferative disorder (TMD) and acute megarakaryoblastic leukemia (AMKL) associated with Trisomy 21, and, lastly, a particular subtype of anemia associated with the production of GATA-1s, a shortened, mutant isoform of the wild-type GATA-1.

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  • (PMID = 18930124.001).
  • [ISSN] 0378-1119
  • [Journal-full-title] Gene
  • [ISO-abbreviation] Gene
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / P30 DK072442; United States / NIAMS NIH HHS / AR / AR055269-02; United States / NIAMS NIH HHS / AR / R03 AR055269-02; United States / NIAMS NIH HHS / AR / R03 AR055269; United States / NIDDK NIH HHS / DK / DK0724429; United States / NIAMS NIH HHS / AR / AR055269; United States / NIDDK NIH HHS / DK / DK072442-02; United States / NIDDK NIH HHS / DK / P30 DK072442-02; United States / NIAMS NIH HHS / AR / R03 AR055269-01; United States / NIAMS NIH HHS / AR / AR055269-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / GATA1 Transcription Factor; 0 / GATA1 protein, human
  • [Other-IDs] NLM/ NIHMS80104; NLM/ PMC2601579
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29. 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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30. 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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  • [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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31. Lei Q, Liu Y, Tang SQ: [Childhood acute megakaryoblastic leukemia]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2007 Jun;15(3):528-32
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  • [Title] [Childhood acute megakaryoblastic leukemia].
  • The aim of this study was to investigate the clinical, pathological and biological features of acute megakaryoblastic leukemia in childhood.
  • The morphology of cells was observed by means of bone marrow smear; the immunophenotype was detected by flow cytometry and immunohistochemistry assay.
  • At the time of diagnosis, the bone marrow had more than 30% megakaryoblasts in nucleated cells.
  • According to all above mentioned results, this case was diagnosed as acute megakaryoblastic leukemia.
  • In conclusion, childhood acute megakaryoblastic leukemia is a rare and easily misdiagnosed disease with poor prognosis.
  • Flow cytometry analysis and immunohistochemistry assay of bone marrow can help in detecting this leukemia subtype and evaluating its prognosis.

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  • (PMID = 17605859.001).
  • [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 / Platelet Glycoprotein GPIb-IX Complex
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32. 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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33. 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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34. 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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35. Nishii K, Nanbu R, Lorenzo V F, Monma F, Kato K, Ryuu H, Katayama N: Expression of the JAK2 V617F mutation is not found in de novo AML and MDS but is detected in MDS-derived leukemia of megakaryoblastic nature. Leukemia; 2007 Jun;21(6):1337-8
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  • [Title] Expression of the JAK2 V617F mutation is not found in de novo AML and MDS but is detected in MDS-derived leukemia of megakaryoblastic nature.
  • [MeSH-major] Janus Kinase 2 / genetics. Leukemia, Megakaryoblastic, Acute / genetics
  • [MeSH-minor] Acute Disease. Humans. Leukemia, Myeloid / genetics. Mutation, Missense. Myelodysplastic Syndromes / genetics

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  • (PMID = 17344916.001).
  • [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] EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2
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36. 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
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Amelogenin
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37. 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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38. 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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39. 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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40. Mercher T, Raffel GD, Moore SA, Cornejo MG, Baudry-Bluteau D, Cagnard N, Jesneck JL, Pikman Y, Cullen D, Williams IR, Akashi K, Shigematsu H, Bourquin JP, Giovannini M, Vainchenker W, Levine RL, Lee BH, Bernard OA, Gilliland DG: The OTT-MAL fusion oncogene activates RBPJ-mediated transcription and induces acute megakaryoblastic leukemia in a knockin mouse model. J Clin Invest; 2009 Apr;119(4):852-64
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  • [Title] The OTT-MAL fusion oncogene activates RBPJ-mediated transcription and induces acute megakaryoblastic leukemia in a knockin mouse model.
  • Acute megakaryoblastic leukemia (AMKL) is a form of acute myeloid leukemia (AML) associated with a poor prognosis.
  • The genetics and pathophysiology of AMKL are not well understood.
  • We generated a knockin mouse model of the one twenty-two-megakaryocytic acute leukemia (OTT-MAL) fusion oncogene that results from the t(1;22)(p13;q13) translocation specifically associated with a subtype of pediatric AMKL.
  • Furthermore, cooperation between OTT-MAL and an activating mutation of the thrombopoietin receptor myeloproliferative leukemia virus oncogene (MPL) efficiently induced a short-latency AMKL that recapitulated all the features of human AMKL, including megakaryoblast hyperproliferation and maturation block, thrombocytopenia, organomegaly, and extensive fibrosis.
  • Our results establish that concomitant activation of RBPJ (Notch signaling) and MPL (cytokine signaling) transforms cells of the megakaryocytic lineage and suggest that specific targeting of these pathways could be of therapeutic value for human AMKL.

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  • (PMID = 19287095.001).
  • [ISSN] 1558-8238
  • [Journal-full-title] The Journal of clinical investigation
  • [ISO-abbreviation] J. Clin. Invest.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA66996; United States / NCI NIH HHS / CA / U01 CA105423; United States / NIDDK NIH HHS / DK / DK50654; United States / NCI NIH HHS / CA / P01 CA066996; United States / NCI NIH HHS / CA / K08 CA111399; United States / NIDDK NIH HHS / DK / P01 DK050654
  • [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 / Immunoglobulin J Recombination Signal Sequence-Binding Protein; 0 / Mpl protein, mouse; 0 / OTT-MAL fusion protein, human; 0 / Oncogene Proteins, Fusion; 0 / Rbpj protein, mouse; 0 / Receptors, Notch; 0 / Receptors, Thrombopoietin
  • [Other-IDs] NLM/ PMC2662544
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41. 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


42. Cornejo MG, Boggon TJ, Mercher T: JAK3: a two-faced player in hematological disorders. Int J Biochem Cell Biol; 2009 Dec;41(12):2376-9
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  • Recent data indicate that abnormal activation of JAK3 due to activating mutations is also found in human hematological malignancies, including acute megakaryoblastic leukemia (AMKL) and cutaneous T cell lymphoma (CTCL).

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  • (PMID = 19747563.001).
  • [ISSN] 1878-5875
  • [Journal-full-title] The international journal of biochemistry & cell biology
  • [ISO-abbreviation] Int. J. Biochem. Cell Biol.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / AI075133-03; United States / NIAID NIH HHS / AI / R01 AI075133; United States / NIAID NIH HHS / AI / R01 AI075133-03
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Interleukin Receptor Common gamma Subunit; 0 / Piperidines; 0 / Pyrimidines; 0 / Pyrroles; 0 / Receptors, Cytokine; 87LA6FU830 / tofacitinib; EC 2.7.10.2 / Janus Kinase 3
  • [Number-of-references] 24
  • [Other-IDs] NLM/ NIHMS190724; NLM/ PMC2853879
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43. Alford KA, Slender A, Vanes L, Li Z, Fisher EM, Nizetic D, Orkin SH, Roberts I, Tybulewicz VL: Perturbed hematopoiesis in the Tc1 mouse model of Down syndrome. Blood; 2010 Apr 08;115(14):2928-37
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  • Trisomy of human chromosome 21 (Hsa21) results in Down syndrome (DS), a disorder that affects many aspects of physiology, including hematopoiesis.
  • DS children have greatly increased rates of acute lymphoblastic leukemia and acute megakaryoblastic leukemia (AMKL); DS newborns present with transient myeloproliferative disorder (TMD), a preleukemic form of AMKL.
  • TMD and DS-AMKL almost always carry an acquired mutation in GATA1 resulting in exclusive synthesis of a truncated protein (GATA1s), suggesting that both trisomy 21 and GATA1 mutations are required for leukemogenesis.
  • We show that although Tc1 mice do not develop leukemia, they have macrocytic anemia and increased extramedullary hematopoiesis.
  • Introduction of GATA1s into Tc1 mice resulted in a synergistic increase in megakaryopoiesis, but did not result in leukemia or a TMD-like phenotype, demonstrating that GATA1s and trisomy of approximately 80% of Hsa21 perturb megakaryopoiesis but are insufficient to induce leukemia.
  • [MeSH-minor] Anemia, Macrocytic / genetics. Anemia, Macrocytic / metabolism. Anemia, Macrocytic / physiopathology. Animals. Disease Models, Animal. GATA1 Transcription Factor / genetics. GATA1 Transcription Factor / metabolism. Humans. Leukemia, Megakaryoblastic, Acute / genetics. Leukemia, Megakaryoblastic, Acute / metabolism. Leukemia, Megakaryoblastic, Acute / physiopathology. Mice. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / physiopathology

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  • (PMID = 20154221.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G0601056; United Kingdom / Medical Research Council / / MC/ U117527252; United States / NHLBI NIH HHS / HL / R01 HL032259; United Kingdom / Medical Research Council / / U117527252
  • [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 / Gata1 protein, mouse
  • [Other-IDs] NLM/ PMC2854435
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44. 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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45. 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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46. Yanagida M, Osato M, Yamashita N, Liqun H, Jacob B, Wu F, Cao X, Nakamura T, Yokomizo T, Takahashi S, Yamamoto M, Shigesada K, Ito Y: Increased dosage of Runx1/AML1 acts as a positive modulator of myeloid leukemogenesis in BXH2 mice. Oncogene; 2005 Jun 30;24(28):4477-85
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  • [Title] Increased dosage of Runx1/AML1 acts as a positive modulator of myeloid leukemogenesis in BXH2 mice.
  • The RUNX1/AML1 gene on chromosome 21 is most frequently inactivated in human leukemias.
  • In addition, an increased dose of RUNX1 is suggested as a basis for several kinds of leukemias.
  • Amplifications of chromosome 21 or the RUNX1 gene are shown to be associated with leukemias with lymphoid lineage, whereas its involvement in myeloid lineage remains unclear.
  • In this study, we generated GATA-1 promoter-driven Runx1 transgenic (Tg) mice, which showed a transient mild increase of megakaryocyte marker-positive myeloid cells but no spontaneous leukemia.
  • These mice were then crossed with BXH2 mice, which have a replication-competent retrovirus in the mouse and develop myeloid leukemia due to insertional mutagenesis by random integration of the virus.
  • Overexpressed Runx1 transgene in BXH2 mice resulted in shortening of the latency of leukemia with increased frequency of megakaryoblastic leukemia, suggesting that increased Runx1 dosage is leukemogenic in myeloid lineage.
  • Identifications of retroviral integration sites revealed the genetic alterations that may cooperate with Runx1 overdose in myeloid leukemogenesis.
  • This mouse model may be useful for analysing the pathogenesis of myeloid leukemias with RUNX1 overdose, especially to examine whether an extra-copy of RUNX1 by trisomy 21 is causally related to Down's syndrome-related acute megakaryoblastic leukemia (DS-AMKL).
  • [MeSH-major] DNA-Binding Proteins / genetics. Gene Dosage. Leukemia, Myeloid / genetics. Proto-Oncogene Proteins / genetics. Transcription Factors / genetics
  • [MeSH-minor] Animals. Core Binding Factor Alpha 2 Subunit. DNA Transposable Elements. Disease Models, Animal. Erythroid-Specific DNA-Binding Factors. GATA1 Transcription Factor. Gene Expression Regulation, Leukemic. Humans. Integrin beta3 / genetics. Integrin beta3 / immunology. Leukocytes / immunology. Leukocytes / pathology. Mice. Mice, Mutant Strains. Mice, Transgenic. Promoter Regions, Genetic. Retroviridae / genetics

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  • (PMID = 15856017.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / DNA Transposable Elements; 0 / DNA-Binding Proteins; 0 / Erythroid-Specific DNA-Binding Factors; 0 / GATA1 Transcription Factor; 0 / GATA1 protein, human; 0 / Gata1 protein, mouse; 0 / Integrin beta3; 0 / Proto-Oncogene Proteins; 0 / RUNX1 protein, human; 0 / Runx1 protein, mouse; 0 / Transcription Factors
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47. Xu JW, Jin RM, Li EQ, Wang YR, Bai Y: Signal pathways in ouabain-induced proliferation of leukemia cells. World J Pediatr; 2009 May;5(2):140-5
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  • [Title] Signal pathways in ouabain-induced proliferation of leukemia cells.
  • We explored the participation of ouabain-activated signaling pathways in growth regulation of leukemia cells.
  • METHODS: Lymphocytic leukemia Jhhan cells and megakaryocytic leukemia M07e cells were incubated at different concentrations of ouabain (0, 1 and 10 nmol) for 24 hours.
  • The expression of Na(+)/K(+)-ATPase alpha1 subunit of leukemia cells was evaluated by RT-PCR and Western blotting.
  • CONCLUSION: Ouabain activates Src and ERK1/2 pathways and regulates the proliferation of leukemia cells.
  • [MeSH-major] Enzyme Inhibitors / pharmacology. Leukemia, Lymphoid / metabolism. Leukemia, Megakaryoblastic, Acute / metabolism. Ouabain / pharmacology. Signal Transduction / drug effects. Tumor Cells, Cultured / drug effects

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  • (PMID = 19718538.001).
  • [ISSN] 1708-8569
  • [Journal-full-title] World journal of pediatrics : WJP
  • [ISO-abbreviation] World J Pediatr
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 5ACL011P69 / Ouabain; EC 3.6.3.9 / Sodium-Potassium-Exchanging ATPase
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48. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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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49. Tosi S, Ballabio E, Teigler-Schlegel A, Boultwood J, Bruch J, Harbott J: Characterization of 6q abnormalities in childhood acute myeloid leukemia and identification of a novel t(6;11)(q24.1;p15.5) resulting in a NUP98-C6orf80 fusion in a case of acute megakaryoblastic leukemia. Genes Chromosomes Cancer; 2005 Nov;44(3):225-32
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  • [Title] Characterization of 6q abnormalities in childhood acute myeloid leukemia and identification of a novel t(6;11)(q24.1;p15.5) resulting in a NUP98-C6orf80 fusion in a case of acute megakaryoblastic leukemia.
  • Chromosome abnormalities of 6q are not frequently observed in myeloid disorders.
  • In this article, we report the incidence of these chromosome changes in childhood myeloid leukemia as 2%-4% based on the cytogenetic database of a single institution.
  • We applied fluorescence in situ hybridization (FISH) to characterize precisely the types of 6q abnormalities in seven patients (six with acute myeloid leukemia and one with myelodysplastic syndrome).
  • Among these, we identified a novel translocation, t(6;11)(q24.1;p15.5), in a patient with acute megakaryoblastic leukemia.
  • Further studies will aim to fully characterize C6orf80 and will elucidate the role of this new NUP98 fusion in myeloid leukemia.
  • [MeSH-major] Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 6 / genetics. Leukemia, Myeloid / genetics. Nuclear Pore Complex Proteins / genetics. Oncogene Proteins, Fusion / genetics. Translocation, Genetic
  • [MeSH-minor] Acute Disease. Adolescent. Amino Acid Sequence. Base Sequence. Child. Child, Preschool. Chromosome Breakage. Chromosomes, Artificial, Bacterial. Cytogenetic Analysis. DNA, Neoplasm / analysis. Humans. In Situ Hybridization, Fluorescence. Infant. Molecular Sequence Data. RNA, Neoplasm / analysis. Reverse Transcriptase Polymerase Chain Reaction

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  • [Copyright] (c) 2005 Wiley-Liss, Inc.
  • (PMID = 16028218.001).
  • [ISSN] 1045-2257
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / Nuclear Pore Complex Proteins; 0 / Oncogene Proteins, Fusion; 0 / RNA, Neoplasm; 0 / nuclear pore complex protein 98
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50. Carpenter E, Valverde-Garduno V, Sternberg A, Mitchell C, Roberts I, Vyas P, Vora A: GATA1 mutation and trisomy 21 are required only in haematopoietic cells for development of transient myeloproliferative disorder. Br J Haematol; 2005 Feb;128(4):548-51
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  • [Title] GATA1 mutation and trisomy 21 are required only in haematopoietic cells for development of transient myeloproliferative disorder.
  • Trisomy 21 [Down's syndrome (DS)] and mutations in transcription factor GATA1 predispose neonates to a transient myeloproliferative disorder (TMD) and/or acute megakaryocytic leukaemia (AMKL).
  • We previously reported two rare neonates without DS who had TMD, one of whom progressed to AMKL.
  • Trisomy 21 was detected only in blood cells at presentation with TMD/AMKL and disappeared with disease resolution.
  • We now show that the blood cells at presentation of TMD harboured GATA1 genomic DNA mutations, suggesting a requirement for trisomy 21 in haematopoietic cells, rather than other cell types, for development of TMD/AMKL.
  • [MeSH-minor] Base Sequence. DNA Mutational Analysis. DNA, Neoplasm / genetics. Erythroid-Specific DNA-Binding Factors. Female. GATA1 Transcription Factor. Humans. Infant, Newborn. Leukemia, Megakaryoblastic, Acute / genetics. Male. Molecular Sequence Data. Neoplasm Proteins / genetics

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  • (PMID = 15686466.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / DNA-Binding Proteins; 0 / Erythroid-Specific DNA-Binding Factors; 0 / GATA1 Transcription Factor; 0 / GATA1 protein, human; 0 / Neoplasm Proteins; 0 / Transcription Factors
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51. Walters DK, Mercher T, Gu TL, O'Hare T, Tyner JW, Loriaux M, Goss VL, Lee KA, Eide CA, Wong MJ, Stoffregen EP, McGreevey L, Nardone J, Moore SA, Crispino J, Boggon TJ, Heinrich MC, Deininger MW, Polakiewicz RD, Gilliland DG, Druker BJ: Activating alleles of JAK3 in acute megakaryoblastic leukemia. Cancer Cell; 2006 Jul;10(1):65-75
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  • [Title] Activating alleles of JAK3 in acute megakaryoblastic leukemia.
  • Tyrosine kinases are aberrantly activated in numerous malignancies, including acute myeloid leukemia (AML).
  • This allowed the identification of an activating mutation (A572V) in the JAK3 pseudokinase domain in the acute megakaryoblastic leukemia (AMKL) cell line CMK.
  • Subsequent analysis identified two additional JAK3 alleles, V722I and P132T, in AMKL patients.
  • JAK3(A572V), JAK3(V722I), and JAK3(P132T) each transform Ba/F3 cells to factor-independent growth, and JAK3(A572V) confers features of megakaryoblastic leukemia in a murine model.

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  • (PMID = 16843266.001).
  • [ISSN] 1535-6108
  • [Journal-full-title] Cancer cell
  • [ISO-abbreviation] Cancer Cell
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA101774-04; United States / NCI NIH HHS / CA / R01 CA101774; United States / NCI NIH HHS / CA / R01 CA101774-04
  • [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 / Benzamides; 0 / JAK3 protein, human; 0 / Mutant Proteins; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Proto-Oncogene Proteins; 0 / Pyrimidines; 0 / RNA, Small Interfering; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Jak2 protein, mouse; EC 2.7.10.2 / Jak3 protein, mouse; EC 2.7.10.2 / Janus Kinase 2; EC 2.7.10.2 / Janus Kinase 3; EC 2.7.10.2 / TYK2 Kinase; EC 2.7.10.2 / TYK2 protein, human
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52. 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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53. 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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54. Ge Y, LaFiura KM, Dombkowski AA, Chen Q, Payton SG, Buck SA, Salagrama S, Diakiw AE, Matherly LH, Taub JW: The role of the proto-oncogene ETS2 in acute megakaryocytic leukemia biology and therapy. Leukemia; 2008 Mar;22(3):521-9
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  • [Title] The role of the proto-oncogene ETS2 in acute megakaryocytic leukemia biology and therapy.
  • Acute myeloid leukemia (AML) in Down syndrome (DS) children has several unique features including a predominance of the acute megakaryocytic leukemia (AMkL) phenotype, higher event-free survivals compared to non-DS children using cytosine arabinoside (ara-C)/anthracycline-based protocols and a uniform presence of somatic mutations in the X-linked transcription factor gene, GATA1.
  • Several chromosome 21-localized transcription factor oncogenes including ETS2 may contribute to the unique features of DS AMkL.
  • In a doxycycline-inducible erythroleukemia cell line, K562pTet-on/ETS2, induction of ETS2 resulted in an erythroid to megakaryocytic phenotypic switch independent of GATA1 levels.
  • Microarray analysis of doxycycline-induced and doxycycline-uninduced cells revealed an upregulation by ETS2 of cytokines (for example, interleukin 1 and CSF2) and transcription factors (for example, TAL1), which are key regulators of megakaryocytic differentiation.
  • These results suggest that ETS2 expression is linked to the biology of AMkL in both DS and non-DS children, and that ETS2 acts by regulating expression of hematopoietic lineage and transcription factor genes involved in erythropoiesis and megakaryopoiesis, and in chemotherapy sensitivities.

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  • (PMID = 18094719.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA092308; United States / NCI NIH HHS / CA / R01 CA92308; United States / NIEHS NIH HHS / ES / P30 ES06639; United States / NIEHS NIH HHS / ES / P30 ES006639; United States / NCI NIH HHS / CA / T32 CA009531; United States / NCI NIH HHS / CA / R01 CA120772
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / ETS2 protein, human; 0 / GATA1 Transcription Factor; 0 / GATA1 protein, human; 0 / Neoplasm Proteins; 0 / Proto-Oncogene Protein c-ets-2; 04079A1RDZ / Cytarabine; ZS7284E0ZP / Daunorubicin
  • [Other-IDs] NLM/ NIHMS505525; NLM/ PMC3809919
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55. Kitoh T, Taki T, Hayashi Y, Nakamura K, Irino T, Osaka M: Transient abnormal myelopoiesis in a Down syndrome newborn followed by acute myeloid leukemia: identification of the same chromosomal abnormality in both stages. Cancer Genet Cytogenet; 2009 Jan 15;188(2):99-102
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  • [Title] Transient abnormal myelopoiesis in a Down syndrome newborn followed by acute myeloid leukemia: identification of the same chromosomal abnormality in both stages.
  • Ten months after the patient achieved remission, the transient abnormal myelopoiesis evolved to an acute megakaryoblastic leukemia.
  • Cytogenetic study revealed only a single clonal abnormality, 47,XY,der(7)t(1;7)(q25;p15),+21c, identical to one of the structural changes seen at birth.
  • It may be that the der(7)t(1;7)(q25;p15) abnormality played some selective role in the development of acute megakaryoblastic leukemia in this patient.
  • To our knowledge, the present case is unique in demonstrating a subclone with der(7)t(1;7)(q25;p15) evolving to acute leukemia.
  • [MeSH-major] Chromosome Aberrations. Down Syndrome / genetics. Leukemia, Myeloid, Acute / genetics. Myelopoiesis / genetics

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  • [ErratumIn] Cancer Genet Cytogenet. 2009 Apr 15;190(2):134
  • (PMID = 19100513.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Codon, Terminator; 0 / GATA1 Transcription Factor; 0 / GATA1 protein, human
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56. 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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57. Kim IS, Park ES, Lim JY, Ki CS, Chi HS: A novel mutation in the GATA1 gene associated with acute megakaryoblastic leukemia in a Korean Down syndrome patient. J Korean Med Sci; 2008 Dec;23(6):1105-8
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  • [Title] A novel mutation in the GATA1 gene associated with acute megakaryoblastic leukemia in a Korean Down syndrome patient.
  • Although acquired mutations in the GATA1 gene have been reported for Down syndrome-related acute megakaryoblastic leukemia (DS-AMKL) in Caucasians, this is the first report of a Korean Down syndrome patient with AMKL carrying a novel mutation of the GATA1 gene.
  • The findings of a peripheral blood smear and bone marrow study were compatible with the presence of AMKL.
  • This case demonstrates that a leukemogenic mechanism for DS-AMKL is contributed by a unique collaboration between overexpressed genes from trisomy 21 and an acquired GATA1 mutation previously seen in Caucasians and now in a Korean patient.
  • [MeSH-major] Down Syndrome / genetics. GATA1 Transcription Factor / genetics. Leukemia, Megakaryoblastic, Acute / genetics. Mutation

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  • (PMID = 19119459.001).
  • [ISSN] 1011-8934
  • [Journal-full-title] Journal of Korean medical science
  • [ISO-abbreviation] J. Korean Med. Sci.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / GATA1 Transcription Factor; 0 / GATA1 protein, human
  • [Other-IDs] NLM/ PMC2610649
  • [Keywords] NOTNLM ; Down Syndrome / GATA1 Transcription Factor / Korea / Leukemia, Megakaryoblastic, Acute
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58. 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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59. Chong LA, Josephine P, Ariffin H: Malignant myeloid transformation in a child with severe congenital neutropenia (Kostmann's syndrome). Med J Malaysia; 2006 Jun;61(2):236-8
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  • [Title] Malignant myeloid transformation in a child with severe congenital neutropenia (Kostmann's syndrome).
  • She subsequently developed acute megakaryoblastic leukemia at the age of 17 years and succumbed during induction chemotherapy.
  • The role of G-CSF in the pathogenesis of her malignant transformation to AML is complicated as this disorder has a propensity for myelodysplasia or AML as part of its natural history.
  • [MeSH-major] Cell Transformation, Neoplastic / pathology. Leukemia, Myeloid / pathology. Neutropenia / congenital

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  • (PMID = 16898320.001).
  • [ISSN] 0300-5283
  • [Journal-full-title] The Medical journal of Malaysia
  • [ISO-abbreviation] Med. J. Malaysia
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Malaysia
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60. Orazi A, O'Malley DP, Jiang J, Vance GH, Thomas J, Czader M, Fang W, An C, Banks PM: Acute panmyelosis with myelofibrosis: an entity distinct from acute megakaryoblastic leukemia. Mod Pathol; 2005 May;18(5):603-14
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  • [Title] Acute panmyelosis with myelofibrosis: an entity distinct from acute megakaryoblastic leukemia.
  • The WHO criteria for diagnosing acute panmyelosis with myelofibrosis are somewhat distinct from those for acute megakaryoblastic leukemia.
  • To determine the potential importance of bone marrow biopsy supplemented by immunohistochemistry in distinguishing between these two conditions, we studied 17 bone marrow biopsies of well-characterized cases of acute panmyelosis with myelofibrosis (six cases) and acute megakaryoblastic leukemia (11 cases).
  • We compared blast frequency, reticulin content, CD34 expression, and the degree of megakaryocytic differentiation of the blast cells in these two conditions.
  • Acute panmyelosis with myelofibrosis is characterized by a multilineage myeloid proliferation with a less numerous population of blasts than acute megakaryoblastic leukemia (P<0.01).
  • In the former condition, blasts are always positive with CD34, while in acute megakaryoblastic leukemia they express CD34 in 60% of the cases.
  • The blasts in acute panmyelosis with myelofibrosis only rarely express megakaryocytic antigens.
  • By contrast, acute megakaryoblastic leukemia has a significantly higher proportion of blasts expressing megakaryocytic antigens (P<0.01 with CD42b).
  • [MeSH-major] Bone Marrow Cells / pathology. Leukemia, Megakaryoblastic, Acute / pathology. Primary Myelofibrosis / pathology
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Aged, 80 and over. Antigens, CD / analysis. Child. Child, Preschool. Chromosome Aberrations. Diagnosis, Differential. Female. Flow Cytometry. Humans. Karyotyping. Male. Middle Aged

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  • (PMID = 15578075.001).
  • [ISSN] 0893-3952
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD
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61. 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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62. Lam HK, Li K, Chik KW, Yang M, Liu VC, Li CK, Fok TF, Ng PC, Shing MM, Chuen CK, Yuen PM: Arsenic trioxide mediates intrinsic and extrinsic pathways of apoptosis and cell cycle arrest in acute megakaryocytic leukemia. Int J Oncol; 2005 Aug;27(2):537-45
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  • [Title] Arsenic trioxide mediates intrinsic and extrinsic pathways of apoptosis and cell cycle arrest in acute megakaryocytic leukemia.
  • Arsenic trioxide (ATO) induces apoptosis in a range of solid tumors and leukemia cells, and has been clinically applied for the treatment of acute promyelocytic leukemia with confirmed efficacy.
  • Acute megakaryocytic leukemia (AMKL) is an aggressive malignancy with poor prognosis, if bone marrow transplantation is not possible.
  • In this study, we applied flow cytometry, Western blot analysis and microarray techniques to investigate the effects of ATO on apoptosis and the cell division cycle of AMKL cell lines CHRF-288-11 and MEG-01.
  • Our data demonstrated that ATO is a potent agent against AMKL as indicated by apoptotic markers, Annexin V and caspase-3.
  • ATO induced delays of cell cycle progression at S phase and arrest at G2/M phase of AMKL cells, but caspase-3 expression appeared not to be phase-specific.
  • The multiple-signaling mechanism of ATO warrants it a potential agent to incorporate in the treatment regimen of AMKL.
  • [MeSH-minor] Antigens, CD / genetics. Antigens, CD / metabolism. Antigens, CD137. Antigens, CD95 / genetics. Antigens, CD95 / metabolism. Caspase 8. Caspase 9. Caspases / genetics. Caspases / metabolism. Cell Line, Tumor. Cell Proliferation / drug effects. Dose-Response Relationship, Drug. Flow Cytometry. Gene Expression Regulation, Neoplastic / drug effects. Gene Expression Regulation, Neoplastic / genetics. Humans. Intracellular Membranes / drug effects. Intracellular Membranes / physiology. Leukemia, Megakaryoblastic, Acute / genetics. Leukemia, Megakaryoblastic, Acute / metabolism. Leukemia, Megakaryoblastic, Acute / pathology. Membrane Potentials / drug effects. Mitochondria / drug effects. Mitochondria / physiology. Oligonucleotide Array Sequence Analysis / methods. Proto-Oncogene Proteins c-bcl-2 / genetics. Proto-Oncogene Proteins c-bcl-2 / metabolism. RNA, Messenger / genetics. RNA, Messenger / metabolism. Receptors, Cell Surface / genetics. Receptors, Cell Surface / metabolism. Receptors, Nerve Growth Factor / genetics. Receptors, Nerve Growth Factor / metabolism. Receptors, Tumor Necrosis Factor / genetics. Receptors, Tumor Necrosis Factor / metabolism. Signal Transduction / drug effects. Time Factors

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  • (PMID = 16010437.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD137; 0 / Antigens, CD95; 0 / Arsenicals; 0 / Oxides; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / RNA, Messenger; 0 / Receptors, Cell Surface; 0 / Receptors, Nerve Growth Factor; 0 / Receptors, Tumor Necrosis Factor; 0 / TNFRSF9 protein, human; EC 3.4.22.- / CASP8 protein, human; EC 3.4.22.- / CASP9 protein, human; EC 3.4.22.- / Caspase 8; EC 3.4.22.- / Caspase 9; EC 3.4.22.- / Caspases; S7V92P67HO / arsenic trioxide
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63. Bhat R, Malinge S, Gamis AS, Sorrell AD, Hilden JM, Ketterling RP, Paietta E, Tallman MS, Crispino JD: Mutational analysis of candidate tumor-associated genes in acute megakaryoblastic leukemia. Leukemia; 2009 Nov;23(11):2159-60
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  • [Title] Mutational analysis of candidate tumor-associated genes in acute megakaryoblastic leukemia.

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  • [CommentOn] Leukemia. 2009 May;23(5):852-5 [19194467.001]
  • (PMID = 19657363.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA101774; United States / NCI NIH HHS / CA / U10 CA098413; United States / NCI NIH HHS / CA / CA101774; United States / NCI NIH HHS / CA / U10 CA098543; United States / NCI NIH HHS / CA / U24 CA114737
  • [Publication-type] Comment; Letter; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Transcription Factors
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64. Bernard OA, Gilliland DG, Mercher T: [The OTT-MAL fusion oncogene: another Notch in megakaryoblastic leukemia]. Med Sci (Paris); 2009 Aug-Sep;25(8-9):676-8
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  • [Title] [The OTT-MAL fusion oncogene: another Notch in megakaryoblastic leukemia].
  • [Transliterated title] Activation de la voie Notch par OTT-MAL dans les leucémies aiguës mégacaryoblastiques.
  • [MeSH-major] Leukemia, Megakaryoblastic, Acute / genetics. Oncogene Fusion. Oncogene Proteins, Fusion / genetics

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  • (PMID = 19765378.001).
  • [ISSN] 0767-0974
  • [Journal-full-title] Médecine sciences : M/S
  • [ISO-abbreviation] Med Sci (Paris)
  • [Language] fre
  • [Publication-type] News
  • [Publication-country] France
  • [Chemical-registry-number] 0 / OTT-MAL fusion protein, human; 0 / Oncogene Proteins, Fusion; 0 / Receptors, Thrombopoietin
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65. Kanegane H, Watanabe S, Nomura K, Xu G, Ito E, Miyawaki T: Distinct clones are associated with the development of transient myeloproliferative disorder and acute megakaryocytic leukemia in a patient with Down syndrome. Int J Hematol; 2007 Oct;86(3):250-2
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  • [Title] Distinct clones are associated with the development of transient myeloproliferative disorder and acute megakaryocytic leukemia in a patient with Down syndrome.
  • Children with Down syndrome (DS) have an approximately 20-fold higher incidence of leukemia than unaffected children, and most leukemia cases with DS present as acute megakaryocytic leukemia (AMKL).
  • At least 10% of neonates with DS develop transient myeloproliferative disorder (TMD), and 20% to 30% of patients with TMD develop AMKL.
  • Mutations in the GATA1 gene are identified not only in AMKL patients but also in TMD patients; however, sequential analysis of GATA1 is not often performed in the same patients.
  • We describe a child with DS who developed TMD followed by AMKL and have identified different mutations in the GATA1 gene during the course of TMD and AMKL.
  • Distinct clones were associated with the development of TMD and AMKL in this patient.
  • [MeSH-major] Down Syndrome / complications. Leukemia, Megakaryoblastic, Acute / etiology. Myeloproliferative Disorders / complications

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  • (PMID = 17988992.001).
  • [ISSN] 0925-5710
  • [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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66. 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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67. 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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68. Takita J, Motomura A, Koh K, Ida K, Taki T, Hayashi Y, Igarashi T: Acute megakaryoblastic leukemia in a child with the MLL-AF4 fusion gene. Eur J Haematol; 2009 Aug;83(2):149-53
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  • [Title] Acute megakaryoblastic leukemia in a child with the MLL-AF4 fusion gene.
  • Mixed-lineage leukemia (MLL) rearrangements are commonly observed in childhood acute lymphoblastic and myeloid leukemia, as well as therapy-related leukemia.
  • However, the occurrence of MLL rearrangements in acute megakaryoblastic leukemia (AMKL) is very rare.
  • We report a pediatric case of AMKL with the MLL-AF4 fusion transcript.
  • MLL-AF4 is derived from t(4;11)(q21:q23) and occurs exclusively in B-cell lineage leukemia.
  • To our knowledge, MLL-AF4 as well as t(4;11)(q21:q23) has not been reported in adult and childhood AMKL.
  • Thus, our case provides new insight into the molecular mechanisms of MLL-AF4-associated leukemia.
  • [MeSH-major] Leukemia, Megakaryoblastic, Acute / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Oncogene Proteins, Fusion / genetics

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  • (PMID = 19459927.001).
  • [ISSN] 1600-0609
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / MLL-AF4 fusion protein, human; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
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69. Larussa D, Grisetti S, Pilozzi E, Concorsi P, Pisa R, Ruco L, Antinori A: Acute megakaryoblastic leukemia in a patient receiving HAART. Am J Hematol; 2005 Sep;80(1):89-90
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  • [Title] Acute megakaryoblastic leukemia in a patient receiving HAART.
  • [MeSH-major] Acquired Immunodeficiency Syndrome / drug therapy. Antiretroviral Therapy, Highly Active / adverse effects. Leukemia, Megakaryoblastic, Acute / chemically induced


70. 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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71. 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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72. Ito E: [The role of GATA1 mutation in acute megakaryocytic leukemia]. Rinsho Ketsueki; 2006 Nov;47(11):1415-22
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [The role of GATA1 mutation in acute megakaryocytic leukemia].
  • [MeSH-major] GATA1 Transcription Factor / genetics. Leukemia, Megakaryoblastic, Acute / genetics. Mutation

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  • (PMID = 17176883.001).
  • [ISSN] 0485-1439
  • [Journal-full-title] [Rinshō ketsueki] The Japanese journal of clinical hematology
  • [ISO-abbreviation] Rinsho Ketsueki
  • [Language] jpn
  • [Publication-type] Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / GATA1 Transcription Factor; 0 / GATA1 protein, human
  • [Number-of-references] 53
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73. Constantinescu SN, Girardot M, Pecquet C: Mining for JAK-STAT mutations in cancer. Trends Biochem Sci; 2008 Mar;33(3):122-31
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • JAK2 and JAK3 mutations have also been identified in a minority of polycythemia vera and acute megakaryoblastic leukemia patients, and it is predicted that further JAK-STAT mutations will be identified in different cancers.

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  • (PMID = 18291658.001).
  • [ISSN] 0968-0004
  • [Journal-full-title] Trends in biochemical sciences
  • [ISO-abbreviation] Trends Biochem. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / STAT Transcription Factors; EC 2.7.10.2 / Janus Kinases
  • [Number-of-references] 77
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74. Lichtman MA: Chronic megakaryocytic leukemia, misnamed chronic idiopathic myelofibrosis, has neoplastic not hyperplastic megakaryocytopoiesis. Blood; 2007 Oct 15;110(8):3085-6
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  • [Title] Chronic megakaryocytic leukemia, misnamed chronic idiopathic myelofibrosis, has neoplastic not hyperplastic megakaryocytopoiesis.
  • [MeSH-major] Leukemia, Megakaryoblastic, Acute / pathology. Megakaryocytes / pathology. Primary Myelofibrosis / pathology. Terminology as Topic
  • [MeSH-minor] Chronic Disease. Humans. Hyperplasia

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  • [CommentOn] Blood. 2007 Aug 1;110(3):986-93 [17473062.001]
  • (PMID = 17916755.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Comment; Letter
  • [Publication-country] United States
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75. 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.


76. 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


77. Raffel GD, Mercher T, Shigematsu H, Williams IR, Cullen DE, Akashi K, Bernard OA, Gilliland DG: Ott1(Rbm15) has pleiotropic roles in hematopoietic development. Proc Natl Acad Sci U S A; 2007 Apr 3;104(14):6001-6
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  • OTT1(RBM15) was originally described as a 5' translocation partner of the MAL(MKL1) gene in t(1,22)(p13;q13) infant acute mega karyocytic leukemia.
  • To define the role of OTT1 in hematopoiesis and help elucidate the mechanism of t(1,22) acute megakaryocytic leukemia pathogenesis, a conditional allele of Ott1 was generated in mice.
  • There is myeloid and megakaryocytic expansion in spleen and bone marrow, an increase in the Lin(-)Sca-1(+)c-Kit(+) compartment that includes hematopoietic stem cells, and a shift in progenitor fate toward granulocyte differentiation.
  • These data show a requirement for Ott1 in B lymphopoiesis, and inhibitory roles in the myeloid, megakaryocytic, and progenitor compartments.

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  • (PMID = 17376872.001).
  • [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
  • [Grant] United States / NCI NIH HHS / CA / K08 CA111399; United States / NCI NIH HHS / CA / P01 CA066996; United States / NCI NIH HHS / CA / R01 CA66996
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Drosophila Proteins; 0 / RNA-Binding Proteins; 0 / Rbm15 protein, mouse
  • [Other-IDs] NLM/ PMC1851606
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78. Yamada H, Sekikawa T, Iwase S, Arakawa Y, Suzuki H, Agawa M, Akiyama M, Takeda N, Horiguchi-Yamada J: Segregation of megakaryocytic or erythroid cells from a megakaryocytic leukemia cell line (JAS-R) by adhesion during culture. Leuk Res; 2007 Nov;31(11):1537-43
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  • [Title] Segregation of megakaryocytic or erythroid cells from a megakaryocytic leukemia cell line (JAS-R) by adhesion during culture.
  • We previously reported a new megakaryocytic-erythroid cell line, JAS-R.
  • One type (designated as JAS-RAD cells) adhered to the substratum of the culture dishes, while the other (JAS-REN cells) grew as a single-cell suspension.
  • The two phenotypes were reciprocally exchangeable by selecting adherent or suspended cells from each type of culture.
  • These findings indicate that adhesion via integrins is related to the phenotypic shift of JAS-R cells between megakaryocytic and erythroid lineages.
  • [MeSH-major] Cell Adhesion. Erythrocytes / pathology. Leukemia, Megakaryoblastic, Acute / pathology. Megakaryocytes / pathology

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  • (PMID = 17383723.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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79. 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


80. 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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81. 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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82. Pérez-Vera P, Montero-Ruíz O, Paredes-Aguilera R, Romero-Guzmán L: [Three-way translocation t(3;12;21)(q26.2;q24.1;q22) in a girl with de novo acute megakaryoblastic leukemia]. Rev Invest Clin; 2008 Mar-Apr;60(2):181-2
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  • [Title] [Three-way translocation t(3;12;21)(q26.2;q24.1;q22) in a girl with de novo acute megakaryoblastic leukemia].
  • [Transliterated title] Triple translocación t(3;12;21)(q26.2;q24.1;q22) en una niña con leucemia aguda megacarioblástica de novo.
  • [MeSH-major] Leukemia, Megakaryoblastic, Acute / genetics. Translocation, Genetic

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  • (PMID = 18637574.001).
  • [ISSN] 0034-8376
  • [Journal-full-title] Revista de investigación clínica; organo del Hospital de Enfermedades de la Nutrición
  • [ISO-abbreviation] Rev. Invest. Clin.
  • [Language] spa
  • [Publication-type] Case Reports; Letter
  • [Publication-country] Mexico
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83. Li-Thiao-Te V, Bourges-Petit E, Capiod JC, Horle B, Micheli J, Morin G, Maingourd Y, Pautard B: [Congenital transient leukemia: a case report]. Arch Pediatr; 2008 Jan;15(1):33-6
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  • [Title] [Congenital transient leukemia: a case report].
  • [Transliterated title] Un cas de leucémie congénitale transitoire.
  • Neonates with Down's syndrome have an increased risk for congenital leukaemia, particularly acute megakaryoblastic leukaemia (FAB, M7) which most often resolves spontaneously and is called transient leukaemia.
  • OBSERVATION: We report a transient leukaemia with an isolated pericardial effusion in a phenotypically normal neonate.
  • DISCUSSION: Congenital leukaemias, with trisomy 21 on blasts cells have a good prognosis that justifies observation before using chemotherapy.
  • [MeSH-major] Down Syndrome / complications. Leukemia, Megakaryoblastic, Acute / congenital

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  • (PMID = 18162385.001).
  • [ISSN] 0929-693X
  • [Journal-full-title] Archives de pédiatrie : organe officiel de la Sociéte française de pédiatrie
  • [ISO-abbreviation] Arch Pediatr
  • [Language] fre
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Antigens, CD
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84. Rabin KR, Whitlock JA: Malignancy in children with trisomy 21. Oncologist; 2009 Feb;14(2):164-73
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  • Patients with Down syndrome (DS) display a unique spectrum of malignancies, with a 10- to 20-fold higher risk of acute leukemias, and a markedly lower incidence of solid tumors.
  • This review discusses the current understanding of the basis for this distinctive pattern of cancer incidence and the clinical and biologic features of the malignant disorders most frequent in DS individuals: transient myeloproliferative disease, acute megakaryoblastic leukemia, and acute lymphoblastic leukemia.
  • We also review distinctive pharmacogenetic issues, highlighting the differential chemosensitivity and toxicity profiles of DS patients compared with the general population, and epidemiologic studies of protective and adverse environmental risk factors for the development of leukemia.

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  • (PMID = 19176633.001).
  • [ISSN] 1549-490X
  • [Journal-full-title] The oncologist
  • [ISO-abbreviation] Oncologist
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U10 CA098543-06; United States / NCI NIH HHS / CA / K12 CA090433; United States / NCI NIH HHS / CA / U10 CA098543; United States / NCI NIH HHS / CA / 1 U10 CA098543-01; United States / NCI NIH HHS / CA / K12 CA090433-06; None / None / / U10 CA098543-06; United States / NCI NIH HHS / CA / CA90433-06
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 91
  • [Other-IDs] NLM/ NIHMS113124; NLM/ PMC2761094
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85. Heald B, Hilden JM, Zbuk K, Norton A, Vyas P, Theil KS, Eng C: Severe TMD/AMKL with GATA1 mutation in a stillborn fetus with Down syndrome. Nat Clin Pract Oncol; 2007 Jul;4(7):433-8
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  • [Title] Severe TMD/AMKL with GATA1 mutation in a stillborn fetus with Down syndrome.
  • BACKGROUND: A 34-year-old woman was referred for evaluation of a recent stillborn male fetus, gestational age 27 6/7 weeks, found to have congenital myeloid leukemia at autopsy.
  • DIAGNOSIS: Down syndrome with in utero onset of GATA1 mutation-positive severe transient myeloproliferative disorder/acute megakaryoblastic leukemia.
  • [MeSH-major] Down Syndrome / genetics. GATA1 Transcription Factor / genetics. Leukemia, Megakaryoblastic, Acute / genetics. Myeloproliferative Disorders / genetics. Stillbirth

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  • (PMID = 17597708.001).
  • [ISSN] 1743-4262
  • [Journal-full-title] Nature clinical practice. Oncology
  • [ISO-abbreviation] Nat Clin Pract Oncol
  • [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; 0 / GATA1 protein, human
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86. Creutzig U, Reinhardt D, Diekamp S, Dworzak M, Stary J, Zimmermann M: AML patients with Down syndrome have a high cure rate with AML-BFM therapy with reduced dose intensity. Leukemia; 2005 Aug;19(8):1355-60
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  • Despite improved prognosis in acute myelogenous leukaemia (AML) children with Down syndrome (DS), therapy-related toxicity remained a problem.
  • AML-DS patients were in median 1.8 years old, and 102/118 (86%) showed the typical morphology of acute megakaryoblastic leukaemia.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Down Syndrome / complications. Leukemia, Myeloid, Acute / drug therapy
  • [MeSH-minor] Adolescent. Age Factors. Child. Child, Preschool. Cytarabine / administration & dosage. Disease-Free Survival. Etoposide / administration & dosage. Female. Humans. Idarubicin / administration & dosage. Infant. Leukemia, Megakaryoblastic, Acute / pathology. Male. Survival Rate. Treatment Outcome

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  • [Copyright] Leukemia (2005) 19, 1355-1360.
  • (PMID = 15920490.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; 6PLQ3CP4P3 / Etoposide; ZRP63D75JW / Idarubicin; ICE protocol 4
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87. 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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  • 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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88. 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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  • 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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89. Hao X, Shin MS, Zhou JX, Lee CH, Qi CF, Naghashfar Z, Hartley JW, Fredrickson TN, Ward JM, Morse HC 3rd: Histologic and molecular characterizations of megakaryocytic leukemia in mice. Leuk Res; 2006 Apr;30(4):397-406
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  • [Title] Histologic and molecular characterizations of megakaryocytic leukemia in mice.
  • Six cases of megakaryocytic leukemia (MKL) were identified and analyzed for morphology and molecular features.
  • MKL were composed of megakaryocyte lineage cells ranging from immature to quite mature cells.
  • VWF, GATA1 and RUNX1 were strongly expressed in megakaryocytes in both normal spleen and MKL as analyzed by immunohistochemistry (IHC).
  • Altered expression of Meis1, Pbx1 and Psen2 and Lef1 in MKL detected with oligonucleotide microarrays was confirmed by qPCR and IHC.
  • This is the first report of spontaneous MKL in mice, defining VWF as a biomarker for diagnosis and suggesting possible involvement of a series of genes in disease pathogenesis.
  • [MeSH-major] Leukemia, Megakaryoblastic, Acute / genetics. Leukemia, Megakaryoblastic, Acute / pathology

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  • (PMID = 16219351.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / DNA Primers; 0 / GATA1 Transcription Factor; 0 / GATA1 protein, human; 0 / Integrin beta3; 0 / Ki-67 Antigen; 0 / RUNX1 protein, human; 0 / von Willebrand Factor
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90. 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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  • The major shared types were ST 53 (n = 55, 25%), ST 41 (LAM7-TUR; n = 19, 8.6%), and ST 284 (n = 15, 6.8%).
  • The major clades observed ranked in the following order: ill-defined T superfamily (n = 112, 50.9%); Latino-American-Mediterranean (LAM; n = 33, 15%); Haarlem (n = 24, 10.9%); and the S family (n = 9, 4.1%).

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  • (PMID = 19845107.001).
  • [ISSN] 1121-7138
  • [Journal-full-title] The new microbiologica
  • [ISO-abbreviation] New Microbiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / DNA, Viral
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91. Qayed M, Ahmed I, Valentini RP, Cushing B, Rajpurkar M: Hypercalcemia in pediatric acute megakaryocytic leukemia: case report and review of the literature. J Pediatr Hematol Oncol; 2009 May;31(5):373-6
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  • [Title] Hypercalcemia in pediatric acute megakaryocytic leukemia: case report and review of the literature.
  • Here, we report an 8-month-old non-Down syndrome infant with acute megakaryocytic leukemia and severe hypercalcemia at presentation.
  • A review of the literature reveals that this is the first case of hypercalcemia complicating acute megakaryocytic leukemia reported in the pediatric literature.
  • [MeSH-major] Hypercalcemia / etiology. Leukemia, Megakaryoblastic, Acute / complications

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  • (PMID = 19415024.001).
  • [ISSN] 1536-3678
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Bone Density Conservation Agents; 0 / Diphosphonates; OYY3447OMC / pamidronate
  • [Number-of-references] 34
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92. Zalzal SF, Smith CE, Nanci A: Ameloblastin and amelogenin share a common secretory pathway and are co-secreted during enamel formation. Matrix Biol; 2008 May;27(4):352-9
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  • The epithelially-derived ameloblasts secrete two main categories of extracellular matrix proteins, amelogenins (AMEL) and nonamelogenins.
  • Dual-immunogold labeling was used to visualize the presence of AMEL and ameloblastin (AMBN), the major nonamelogenin, and quantify the proportion of secretory granules containing one or both of these proteins in ameloblasts during the phase of appositional growth of the enamel layer in continuously-erupting rat incisors.
  • The results show that nearly 70% of granules contain both AMEL and AMBN, 13% label only for AMBN and 1% only for AMEL.
  • These proportions reach 98% (AMEL+AMBN) and 2% (AMBN only) following BFA treatment.
  • The observation that AMEL is almost always packaged with AMBN suggests a functional association between these two proteins.

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  • (PMID = 18281204.001).
  • [ISSN] 0945-053X
  • [Journal-full-title] Matrix biology : journal of the International Society for Matrix Biology
  • [ISO-abbreviation] Matrix Biol.
  • [Language] ENG
  • [Grant] None / None / / 64178-1; Canada / Canadian Institutes of Health Research / / 64178-1
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Ambn protein, rat; 0 / Amelogenin; 0 / Dental Enamel Proteins
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93. Xavier AC, Ge Y, Taub J: Unique clinical and biological features of leukemia in Down syndrome children. Expert Rev Hematol; 2010 Apr;3(2):175-86
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  • [Title] Unique clinical and biological features of leukemia in Down syndrome children.
  • Acute leukemias in children with Down syndrome (DS) are characterized by unique clinical and biological features.
  • Notable among DS children with acute myeloid leukemia (AML), is the high frequency of the acute megakaryocytic leukemia (AMkL) subtype, which uniformly harbor somatic mutations in the transcription factor GATA1 gene.
  • DS patients with AML, and in particular AMkL, have event-free survival rates of 80-100% in contrast to event-free survival rates of less than 35% for non-DS children with AMkL.
  • DS children with acute lymphoblastic leukemia have a more heterogeneous disease, with approximately 30% of the patients having somatic JAK2 mutations, heightened methotrexate sensitivity and higher rates of treatment-related toxicities.
  • These features highlight a striking relationship between genes localized to chromosome 21, leukemogenesis and sensitivity to leukemia chemotherapy agents.
  • [MeSH-major] Down Syndrome / complications. Leukemia, Myeloid, Acute / diagnosis

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  • (PMID = 21083461.001).
  • [ISSN] 1747-4094
  • [Journal-full-title] Expert review of hematology
  • [ISO-abbreviation] Expert Rev Hematol
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA 120772
  • [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; 0 / GATA1 protein, human; EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2
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94. Li Z, Godinho FJ, Klusmann JH, Garriga-Canut M, Yu C, Orkin SH: Developmental stage-selective effect of somatically mutated leukemogenic transcription factor GATA1. Nat Genet; 2005 Jun;37(6):613-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Acquired mutations in the hematopoietic transcription factor GATA binding protein-1 (GATA1) are found in megakaryoblasts from nearly all individuals with Down syndrome with transient myeloproliferative disorder (TMD, also called transient leukemia) and the related acute megakaryoblastic leukemia (DS-AMKL, also called DS-AML M7).
  • To understand the biological properties of GATA1s and its relation to DS-AMKL and TMD, we used gene targeting to generate Gata1 alleles that express GATA1s in mice.
  • We show that the dominant action of GATA1s leads to hyperproliferation of a unique, previously unrecognized yolk sac and fetal liver progenitor, which we propose accounts for the transient nature of TMD and the restriction of DS-AMKL to infants.
  • Our observations raise the possibility that the target cells in other leukemias of infancy and early childhood are distinct from those in adult leukemias and underscore the interplay between specific oncoproteins and potential target cells.
  • [MeSH-minor] Adult. Age Factors. Animals. Cell Differentiation. Cells, Cultured. Down Syndrome / genetics. Embryo, Mammalian. Erythroid-Specific DNA-Binding Factors. GATA1 Transcription Factor. Gene Targeting. Hematopoiesis / genetics. Humans. Infant. Leukemia, Megakaryoblastic, Acute / genetics. Liver / cytology. Liver / embryology. Megakaryocytes. Mice. Transfection


95. Debergh I, Van Damme N, Pattyn P, Peeters M, Ceelen WP: The low-molecular-weight heparin, nadroparin, inhibits tumour angiogenesis in a rodent dorsal skinfold chamber model. Br J Cancer; 2010 Mar 2;102(5):837-43
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • METHODS: AMel-3 and HAP-T1 tumours were grown in donor animals and fragments implanted in the window chambers.

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  • (PMID = 20125158.001).
  • [ISSN] 1532-1827
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anticoagulants; 0 / Nadroparin
  • [Other-IDs] NLM/ PMC2833243
  •  go-up   go-down


96. Xu G, Kanezaki R, Toki T, Watanabe S, Takahashi Y, Terui K, Kitabayashi I, Ito E: Physical association of the patient-specific GATA1 mutants with RUNX1 in acute megakaryoblastic leukemia accompanying Down syndrome. Leukemia; 2006 Jun;20(6):1002-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Physical association of the patient-specific GATA1 mutants with RUNX1 in acute megakaryoblastic leukemia accompanying Down syndrome.
  • Mutations of the GATA1 gene on chromosome X have been found in almost all cases of transient myeloproliferative disorder and acute megakaryoblastic leukemia (AMKL) accompanying Down syndrome (DS).
  • It has been suggested that loss of the N-terminal portion of GATA1 might interfere with physiological interactions with the critical megakaryocytic transcription factor RUNX1, and this would imply that GATA1s is not able to interact properly with RUNX1.
  • All of the patient-specific GATA1 mutants interacted efficiently with RUNX1 and retained their ability to act synergistically with RUNX1 on the megakaryocytic GP1balpha promoter, whereas the levels of transcriptional activities were diverse among the mutants.
  • Thus, our data indicate that physical interaction and synergy between GATA1 and RUNX1 are retained in DS-AMKL, although it is still possible that increased RUNX1 activity plays a role in the development of leukemia in DS.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / genetics. Down Syndrome / complications. Down Syndrome / genetics. GATA1 Transcription Factor / genetics. Leukemia, Megakaryoblastic, Acute / complications. Leukemia, Megakaryoblastic, Acute / genetics