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6. 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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7. Ge Y, Elghetany MT: CD36: a multiligand molecule. Lab Hematol; 2005;11(1):31-7
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  • 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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8. Steensma DP, Gibbons RJ, Mesa RA, Tefferi A, Higgs DR: Somatic point mutations in RUNX1/CBFA2/AML1 are common in high-risk myelodysplastic syndrome, but not in myelofibrosis with myeloid metaplasia. Eur J Haematol; 2005 Jan;74(1):47-53
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  • [Title] Somatic point mutations in RUNX1/CBFA2/AML1 are common in high-risk myelodysplastic syndrome, but not in myelofibrosis with myeloid metaplasia.
  • OBJECTIVE: Acquired somatic point mutations in RUNX1/CBFA2/AML1 have recently been described in a subset of patients with myelodysplastic syndrome (MDS) and acute myeloid leukaemia (AML).
  • Given the importance of core-binding factor in megakaryocytic differentiation and platelet production, as well as the central role of megakaryocytes in the pathophysiology of myelofibrosis with myeloid metaplasia (MMM), we hypothesised that RUNX1 gene mutations might be common in MMM.
  • DHPLC is a useful technique for high-throughput analysis of RUNX1 mutation status in myeloid disorders, and may be complementary to screening via other methods.


9. Brière J: [Essential thrombocythemia. Contribution of the V617F JAK2 mutation to the pathophysiology, diagnosis and outcome]. Bull Acad Natl Med; 2007 Mar;191(3):535-48
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  • [Title] [Essential thrombocythemia. Contribution of the V617F JAK2 mutation to the pathophysiology, diagnosis and outcome].
  • [Transliterated title] Thrombocytémie essentielle. Apport de la mutation V617F de JAK2 pour la stratégie diagnostique, la physiopathologie et les modalités évolutives.
  • Secondary thrombocytosis is a reactive process in relation with acute or chronic inflammatory diseases, or asplenia.
  • However, the most frequent causes of chronic thrombocytosis in adults are the so-called chronic myeloproliferative syndromes (chronic myelocytic leukaemia, polycythemia vera, primary myelofibrosis, essential thrombocytemia), and to a lesser extent, myelodysplastic syndromes.
  • In the course of these disorders, thrombocytosis is often the first recognized abnormality.
  • Chronic myelocytic leukaemia is easily diagnosed owing to the presence of either the Philadelphia chromosome or the BCR-ABL fusion gene product.
  • The next step still relies upon a distinction according to the PVSG or the WHO criteria of Polycythemia Vera (PV) and Idiopathic myelo fibrosis (IMF) to finally confirm genuine Essential Thrombocythemia (ET).
  • However, this mutation is neither specific nor constant in any of the Philadelphia negative myeloproliferative disorders, which outlines the importance of the WHO criteria of megakaryocytic abnormalities on bone marrow biopsy as the hallmark of Ph negative MPDs.
  • The exclusion of PV and of IMF, including pre fibrotic and early fibrotic forms is still required for the diagnosis of "true" ET.
  • Disease stratification and treatment strategy are targeted on the evaluation and prevention of vascular complications.
  • Acute leukaemia or myelodysplasia, and other clonal progressions like myelofibrotic transformation, are infrequent and delayed events.
  • [MeSH-minor] Adult. Biopsy. Bone Marrow / pathology. Cohort Studies. Diagnosis, Differential. Disease Progression. Female. Humans. Male. Middle Aged. Mutation. Myeloproliferative Disorders / diagnosis. Myeloproliferative Disorders / genetics. Philadelphia Chromosome. Polycythemia Vera / diagnosis. Polycythemia Vera / genetics. Primary Myelofibrosis / diagnosis. Primary Myelofibrosis / genetics. Prognosis. Risk Factors. World Health Organization

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  • (PMID = 18072652.001).
  • [ISSN] 0001-4079
  • [Journal-full-title] Bulletin de l'Académie nationale de médecine
  • [ISO-abbreviation] Bull. Acad. Natl. Med.
  • [Language] fre
  • [Publication-type] Comparative Study; English Abstract; Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2
  • [Number-of-references] 56
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10. 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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11. Webb DK: Optimizing therapy for myeloid disorders of Down syndrome. Br J Haematol; 2005 Oct;131(1):3-7
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  • [Title] Optimizing therapy for myeloid disorders of Down syndrome.
  • Children with Down syndrome (DS) are at increased risk of leukaemia.
  • Myeloid disorders include transient abnormal myelopoiesis (TAM), myelodysplasia (MDS) and acute myeloid leukaemia (AML).
  • Mutations in the GATA-1 gene, which encodes for a transcription factor central to the normal development of the erythroid and megakaryocytic lineages, are found in cases of TAM, MDS and AML in DS children.
  • DS children with MDS/AML mostly present between the ages of 1 and 4 years, and have a large predominance of megakaryoblastic disease (French-American-British type M7).
  • The MDS and AML are part of a single disease entity (myeloid leukaemia of Down syndrome) that is extremely sensitive to chemotherapy.
  • Resistant disease and relapse are rare, but treatment-related toxicity is high, and deaths in remission have exceeded those due to disease in most series.
  • [MeSH-major] Down Syndrome / complications. Down Syndrome / therapy. Leukemia, Myeloid / complications. Leukemia, Myeloid / therapy
  • [MeSH-minor] Acute Disease. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child, Preschool. Drug Administration Schedule. Humans. Infant. Megakaryocytes / immunology. Neural Tube Defects / complications. Neural Tube Defects / therapy


12. 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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13. 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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4. 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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15. 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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16. 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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17. 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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18. 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


19. 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


20. 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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21. 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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22. 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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23. 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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24. 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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25. 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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26. 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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27. 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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28. Daniëls L, Guerti K, Vermeulen K, De Raeve H, Van Assche E, Van de Velde AL, Berneman ZN, Van Der Planken M: Acute myeloid leukaemia of mixed megakaryocytic and erythroid origin: a case report and review of the literature. Acta Clin Belg; 2007 Sep-Oct;62(5):308-14
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  • [Title] Acute myeloid leukaemia of mixed megakaryocytic and erythroid origin: a case report and review of the literature.
  • We report the case of a 78-year-old man who presented with acute myeloid leukaemia showing subpopulations of cells expressing platelet-associated markers and the presence of a pan-myeloid component, besides glycophorin A-positive cells.
  • Most of the immature cells had a proerythroblast-like morphology and we classified this case as an FAB-M6 variant, as suggested by Bain (1).
  • According to the WHO classification, this leukaemia fulfilled the criteria of'AML with multilineage dysplasia' (2).
  • Immunophenotyping characteristics showed two distinct aberrant subpopulations, a young pan-myeloid (CD45+ with low density, CD34+, CD117+, CD13+, CD33+, partial cytoplasmic myeloperoxidase (MPO)+) population with platelet-associated markers (CD41+, CD42+, CD61+) and a CD45+, CD117+, CD34- population with partial CD235a positivity indicative for erythroid maturation.
  • This case belongs to the group of 'early' erythroblastic leukaemias where a subset of progenitor cells present with erythroid-megakaryocyte bipotentiality or are blocked at an early BFU-E (burst-forming unit erythrocyte)-like stage of erythroid differentiation (11, 12, 13).
  • [MeSH-major] Bone Marrow Cells / pathology. Leukemia, Erythroblastic, Acute / diagnosis. Leukemia, Megakaryoblastic, Acute / diagnosis
  • [MeSH-minor] Aged. Biopsy, Needle. Diagnosis, Differential. Fatal Outcome. Humans. Immunophenotyping. Male

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  • (PMID = 18229464.001).
  • [ISSN] 1784-3286
  • [Journal-full-title] Acta clinica Belgica
  • [ISO-abbreviation] Acta Clin Belg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Belgium
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29. 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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  • 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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30. 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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31. Ge Y, Stout ML, Tatman DA, Jensen TL, Buck S, Thomas RL, Ravindranath Y, Matherly LH, Taub JW: GATA1, cytidine deaminase, and the high cure rate of Down syndrome children with acute megakaryocytic leukemia. J Natl Cancer Inst; 2005 Feb 2;97(3):226-31
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  • [Title] GATA1, cytidine deaminase, and the high cure rate of Down syndrome children with acute megakaryocytic leukemia.
  • Down syndrome children with acute megakaryocytic leukemia (AMkL) have higher cure rates than non-Down syndrome acute myeloid leukemia (AML) patients treated with cytosine arabinoside (ara-C).
  • Somatic mutations in the GATA1 transcription factor have been detected exclusively and almost uniformly in Down syndrome AMkL patients, suggesting a potential linkage to the chemotherapy sensitivity of Down syndrome megakaryoblasts.
  • Stable transfection of wild-type GATA1 cDNA into the Down syndrome AMkL cell line CMK resulted in decreased (8- to 17-fold) ara-C sensitivity and a threefold-lower generation of the active ara-C metabolite ara-CTP compared with that for mock-transfected CMK cells.
  • These results suggest that GATA1 transcriptionally upregulates cytidine deaminase and that the presence or absence of GATA1 mutations in AML blasts likely confers differences in ara-C sensitivities due to effects on cytidine deaminase gene expression, which, in turn, contributes to the high cure rate of Down syndrome AMkL patients.
  • [MeSH-major] Cytidine Deaminase / metabolism. DNA-Binding Proteins / metabolism. Down Syndrome / complications. Down Syndrome / metabolism. Leukemia, Megakaryoblastic, Acute / metabolism. Transcription Factors / metabolism

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  • (PMID = 15687366.001).
  • [ISSN] 1460-2105
  • [Journal-full-title] Journal of the National Cancer Institute
  • [ISO-abbreviation] J. Natl. Cancer Inst.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA92308
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / DNA-Binding Proteins; 0 / Erythroid-Specific DNA-Binding Factors; 0 / GATA1 Transcription Factor; 0 / GATA1 protein, human; 0 / Transcription Factors; 04079A1RDZ / Cytarabine; 13191-15-6 / Arabinofuranosylcytosine Triphosphate; 3083-77-0 / Arabinofuranosyluracil; EC 3.5.4.5 / Cytidine Deaminase
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32. 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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33. 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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34. 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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35. 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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36. 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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37. 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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38. 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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39. 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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  • [ISSN] 1573-4978
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40. Tefferi A: JAK and MPL mutations in myeloid malignancies. Leuk Lymphoma; 2008 Mar;49(3):388-97
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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41. 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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42. 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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43. 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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44. 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


45. 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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96. 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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97. 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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  • 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


98. 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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  • 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
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99. 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

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  • (PMID = 16628190.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / GATA1 Transcription Factor; 0 / GATA1 protein, human; 0 / Platelet Glycoprotein GPIb-IX Complex; 0 / RUNX1 protein, human
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100. Kiyoi H, Yamaji S, Kojima S, Naoe T: JAK3 mutations occur in acute megakaryoblastic leukemia both in Down syndrome children and non-Down syndrome adults. Leukemia; 2007 Mar;21(3):574-6
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  • [Title] JAK3 mutations occur in acute megakaryoblastic leukemia both in Down syndrome children and non-Down syndrome adults.
  • [MeSH-major] Down Syndrome / complications. Janus Kinase 3 / genetics. Leukemia, Megakaryoblastic, Acute / genetics. Myeloproliferative Disorders / genetics. Neoplasm Proteins / genetics
  • [MeSH-minor] Adult. Binding Sites / genetics. Child. DNA Mutational Analysis. DNA, Neoplasm / genetics. Disease Progression. Enzyme Activation / genetics. Female. GATA1 Transcription Factor / genetics. Genes, ras. Genetic Predisposition to Disease. Humans. Interleukin Receptor Common gamma Subunit / metabolism. Male. Protein Structure, Tertiary. Structure-Activity Relationship. Tumor Suppressor Protein p53 / genetics. fms-Like Tyrosine Kinase 3 / genetics

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  • (PMID = 17252020.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Comparative Study; Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / GATA1 Transcription Factor; 0 / GATA1 protein, human; 0 / Interleukin Receptor Common gamma Subunit; 0 / JAK3 protein, human; 0 / Neoplasm Proteins; 0 / Tumor Suppressor Protein p53; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 2.7.10.2 / Janus Kinase 3
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