[X] Close
You are about to erase all the values you have customized, search history, page format, etc.
Click here to RESET all values       Click here to GO BACK without resetting any value
Items 1 to 100 of about 289
41. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The OTT-MAL/RBM15-MKL1 fusion protein is the result of the recurrent translocation t(1;22) in acute megakaryocytic leukemia in infants.

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Immunity. 2003 Feb;18(2):301-12 [12594956.001]
  • [Cites] Mol Biol Cell. 2002 Dec;13(12):4167-78 [12475943.001]
  • [Cites] Genes Dev. 2003 Aug 1;17(15):1909-20 [12897056.001]
  • [Cites] Mol Cell Biol. 2003 Sep;23(18):6597-608 [12944485.001]
  • [Cites] EMBO J. 2004 Oct 13;23(20):3973-83 [15385960.001]
  • [Cites] Blood. 1991 Aug 1;78(3):748-52 [1859887.001]
  • [Cites] Mol Cell Biol. 1996 May;16(5):2473-82 [8628315.001]
  • [Cites] Cell. 1998 Feb 20;92(4):475-87 [9491889.001]
  • [Cites] Cell. 1999 Jul 23;98(2):159-69 [10428028.001]
  • [Cites] Biochemistry. 1999 Aug 17;38(33):10678-90 [10451362.001]
  • [Cites] J Biol Chem. 2005 Nov 4;280(44):36935-45 [16129689.001]
  • [Cites] Mol Cell Biol. 2006 Jun;26(11):4134-48 [16705166.001]
  • [Cites] Genetics. 2006 May;173(1):279-86 [16547102.001]
  • [Cites] Trends Cell Biol. 2006 Nov;16(11):588-96 [17035020.001]
  • [Cites] Curr Opin Genet Dev. 2007 Feb;17(1):52-9 [17178457.001]
  • [Cites] Cancer Cell. 2007 Feb;11(2):133-46 [17292825.001]
  • [Cites] Mol Cell Biol. 2007 Apr;27(8):3056-64 [17283045.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Apr 3;104(14):6001-6 [17376872.001]
  • [Cites] Science. 2007 Jun 22;316(5832):1749-52 [17588931.001]
  • [Cites] Am J Physiol Regul Integr Comp Physiol. 2000 Oct;279(4):R1455-66 [11004016.001]
  • [Cites] Nat Med. 2000 Nov;6(11):1278-81 [11062542.001]
  • [Cites] Genes Dev. 2001 May 1;15(9):1140-51 [11331609.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 May 8;98(10):5776-9 [11344311.001]
  • [Cites] Nat Genet. 2001 Jul;28(3):220-1 [11431691.001]
  • [Cites] Cell. 2001 Jun 29;105(7):851-62 [11439182.001]
  • [Cites] Genes Chromosomes Cancer. 2002 Jan;33(1):22-8 [11746984.001]
  • [Cites] Development. 2000 Apr;127(7):1517-29 [10704397.001]
  • [Cites] Curr Biol. 2000 Jul 27-Aug 10;10(15):943-6 [10959845.001]
  • [Cites] J Biol Chem. 2002 Aug 9;277(32):28853-60 [12019265.001]
  • [Cites] Nature. 2002 Sep 12;419(6903):182-5 [12226669.001]
  • [Cites] EMBO J. 2002 Oct 15;21(20):5417-26 [12374742.001]
  • [Cites] Cell. 2003 May 2;113(3):329-42 [12732141.001]
  • (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
  •  go-up   go-down


42. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

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

  • Genetic Alliance. consumer health - Acute Megakaryoblastic Leukemia.
  • COS Scholar Universe. author profiles.
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • SciCrunch. Marmoset Gene list: Data: Gene Annotation .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Genes Dev. 2005 Oct 1;19(19):2331-42 [16166372.001]
  • [Cites] Blood. 2008 Nov 15;112(10):4220-6 [18755984.001]
  • [Cites] Blood. 2005 Nov 15;106(10):3370-3 [16037387.001]
  • [Cites] Cell. 2006 Mar 10;124(5):973-83 [16530044.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Feb 28;103(9):3339-44 [16492768.001]
  • [Cites] FEBS Lett. 2006 May 22;580(12):2860-8 [16574107.001]
  • [Cites] Cancer Cell. 2006 Jul;10(1):65-75 [16843266.001]
  • [Cites] Nat Rev Mol Cell Biol. 2006 Sep;7(9):678-89 [16921404.001]
  • [Cites] Blood. 2006 Oct 15;108(8):2770-9 [16804112.001]
  • [Cites] Br J Haematol. 2006 Sep;134(5):453-66 [16856888.001]
  • [Cites] Leukemia. 2006 Nov;20(11):1967-77 [16990763.001]
  • [Cites] Blood. 2006 Nov 15;108(10):3472-6 [16868251.001]
  • [Cites] Cell Mol Life Sci. 2006 Nov;63(21):2460-76 [16909203.001]
  • [Cites] Blood. 2000 Mar 1;95(5):1633-41 [10688818.001]
  • [Cites] Blood. 2001 Apr 1;97(7):2023-30 [11264167.001]
  • [Cites] Mol Cell Biol. 2001 Apr;21(8):2659-70 [11283246.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 May 8;98(10):5776-9 [11344311.001]
  • [Cites] Blood. 2001 Jun 15;97(12):3727-32 [11389009.001]
  • [Cites] Nat Genet. 2001 Jul;28(3):220-1 [11431691.001]
  • [Cites] Genes Chromosomes Cancer. 2002 Jan;33(1):22-8 [11746984.001]
  • [Cites] Oncogene. 2002 May 13;21(21):3359-67 [12032774.001]
  • [Cites] J Clin Invest. 2002 Jun;109(12):1579-85 [12070305.001]
  • [Cites] Blood. 2002 Jul 15;100(2):618-26 [12091356.001]
  • [Cites] Nat Genet. 2002 Sep;32(1):148-52 [12172547.001]
  • [Cites] EMBO J. 2002 Oct 15;21(20):5417-26 [12374742.001]
  • [Cites] Mol Cell Biol. 2003 Jan;23(2):655-64 [12509463.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Jan 7;100(1):205-10 [12490656.001]
  • [Cites] Immunity. 2003 Feb;18(2):301-12 [12594956.001]
  • [Cites] Br J Haematol. 2003 Mar;120(6):930-8 [12648061.001]
  • [Cites] Cell. 2003 May 2;113(3):329-42 [12732141.001]
  • [Cites] Am J Hematol. 2003 Jun;73(2):71-80 [12749007.001]
  • [Cites] Genes Dev. 2003 Aug 1;17(15):1909-20 [12897056.001]
  • [Cites] Biostatistics. 2003 Apr;4(2):249-64 [12925520.001]
  • [Cites] Semin Cancer Biol. 2004 Oct;14(5):387-96 [15288264.001]
  • [Cites] Genome Biol. 2004;5(10):R80 [15461798.001]
  • [Cites] Science. 2004 Oct 8;306(5694):269-71 [15472075.001]
  • [Cites] Blood. 1992 Jun 15;79(12):3325-30 [1596573.001]
  • [Cites] Blood. 1999 Aug 15;94(4):1273-82 [10438715.001]
  • [Cites] Growth Factors. 2004 Sep;22(3):151-5 [15518238.001]
  • [Cites] Nat Immunol. 2005 Mar;6(3):314-22 [15665828.001]
  • [Cites] Nature. 2005 Apr 28;434(7037):1144-8 [15793561.001]
  • [Cites] Nat Genet. 2005 Jun;37(6):613-9 [15895080.001]
  • [Cites] PLoS Med. 2006 Jul;3(7):e270 [16834459.001]
  • [Cites] Curr Opin Genet Dev. 2007 Feb;17(1):52-9 [17178457.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Jan 30;104(5):1610-5 [17242367.001]
  • [Cites] Mol Cell Biol. 2007 Apr;27(8):3056-64 [17283045.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Apr 3;104(14):6001-6 [17376872.001]
  • [Cites] Immunity. 2007 Jul;27(1):100-10 [17658278.001]
  • [Cites] Immunity. 2007 Jul;27(1):89-99 [17658279.001]
  • [Cites] Stem Cells. 2008 Mar;26(3):621-9 [18055448.001]
  • [Cites] Cell Stem Cell. 2008 Sep 11;3(3):314-26 [18786418.001]
  • [Cites] Mol Cell Biol. 2008 Oct;28(20):6302-13 [18694962.001]
  • [Cites] Mol Cell Biol. 2008 Oct;28(20):6171-81 [18710951.001]
  • [Cites] Cell Stem Cell. 2007 Nov;1(5):541-54 [18345353.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Oct 25;102(43):15545-50 [16199517.001]
  • (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
  •  go-up   go-down


43. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

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


4
Advertisement
4. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

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

  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Blood. 2007 Aug 1;110(3):1077-9 [17644747.001]
  • [Cites] Br J Haematol. 2007 May;137(4):337-41 [17456055.001]
  • [Cites] Blood. 2008 Feb 15;111(4):2155-7 [18094329.001]
  • [Cites] Br J Haematol. 2008 May;141(5):681-8 [18397343.001]
  • [Cites] Immunol Rev. 2008 Jun;223:132-42 [18613833.001]
  • [Cites] Blood. 2008 Nov 15;112(10):4220-6 [18755984.001]
  • [Cites] Cytokine Growth Factor Rev. 2008 Oct-Dec;19(5-6):371-81 [18948053.001]
  • [Cites] Immunol Rev. 2009 Mar;228(1):273-87 [19290934.001]
  • [Cites] Blood. 2009 Mar 19;113(12):2746-54 [19139084.001]
  • [Cites] Nat Rev Immunol. 2009 Jul;9(7):480-90 [19543225.001]
  • [Cites] Am J Pathol. 2009 Aug;175(2):825-34 [19608866.001]
  • [Cites] Annu Rev Immunol. 2000;18:143-64 [10837055.001]
  • [Cites] Curr Opin Cell Biol. 2001 Apr;13(2):211-7 [11248555.001]
  • [Cites] Oncogene. 2003 Aug 21;22(35):5399-407 [12934099.001]
  • [Cites] Science. 2003 Oct 31;302(5646):875-8 [14593182.001]
  • [Cites] Oncogene. 2004 Apr 8;23(15):2617-29 [14968112.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 Jul 5;91(14):6374-8 [8022790.001]
  • [Cites] Science. 1995 Nov 3;270(5237):797-800 [7481768.001]
  • [Cites] Science. 1995 Nov 3;270(5237):800-2 [7481769.001]
  • [Cites] Curr Opin Immunol. 1997 Aug;9(4):541-7 [9287175.001]
  • [Cites] Blood. 2005 Aug 1;106(3):996-1002 [15831699.001]
  • [Cites] Cancer Cell. 2006 Jul;10(1):65-75 [16843266.001]
  • [Cites] Blood. 2006 Oct 15;108(8):2796-803 [16825495.001]
  • [Cites] Oncogene. 2007 Oct 15;26(47):6724-37 [17934481.001]
  • (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
  •  go-up   go-down


45. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

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

  • Genetic Alliance. consumer health - Down Syndrome.
  • MedlinePlus Health Information. consumer health - Down Syndrome.
  • COS Scholar Universe. author profiles.
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Gene. 2003 Oct 30;318:137-47 [14585506.001]
  • [Cites] Blood. 2003 Aug 1;102(3):981-6 [12649131.001]
  • [Cites] Nat Rev Genet. 2004 Oct;5(10):725-38 [15510164.001]
  • [Cites] Am J Med Genet. 1983 Oct;16(2):173-7 [6228141.001]
  • [Cites] Prog Clin Biol Res. 1990;360:263-80 [2147289.001]
  • [Cites] Am J Med Genet. 1993 Jun 15;46(5):510-2 [8322810.001]
  • [Cites] Am J Pediatr Hematol Oncol. 1993 Nov;15(4):392-9 [8214361.001]
  • [Cites] Arch Pediatr Adolesc Med. 1995 Jul;149(7):824-5 [7795778.001]
  • [Cites] Arch Biochem Biophys. 1997 Aug 15;344(2):424-32 [9264557.001]
  • [Cites] Nat Genet. 2005 Jun;37(6):613-9 [15895080.001]
  • [Cites] Ann N Y Acad Sci. 2005 Jun;1044:142-58 [15958708.001]
  • [Cites] Br J Haematol. 2000 Sep;110(3):512-24 [10997960.001]
  • [Cites] Nat Genet. 2002 Sep;32(1):148-52 [12172547.001]
  • [Cites] Lancet. 2003 May 10;361(9369):1617-20 [12747884.001]
  • [Cites] Blood. 2003 Jun 1;101(11):4298-300 [12560215.001]
  • [Cites] Blood. 2003 Jun 1;101(11):4333-41 [12576332.001]
  • [Cites] Blood. 2003 Jun 1;101(11):4301-4 [12586620.001]
  • [Cites] Blood. 2003 Oct 15;102(8):2960-8 [12816863.001]
  • [Cites] Science. 2005 Sep 23;309(5743):2033-7 [16179473.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Feb 28;103(9):3339-44 [16492768.001]
  • [Cites] Nat Genet. 2006 Jul;38(7):807-12 [16783379.001]
  • [Cites] Am J Med Genet A. 2007 Jan 1;143A(1):42-50 [17163522.001]
  • [Cites] Blood Cells Mol Dis. 2007 Sep-Oct;39(2):156-9 [17532652.001]
  • [Cites] Blood. 2008 Jan 15;111(2):767-75 [17901249.001]
  • [Cites] J Exp Med. 2008 Mar 17;205(3):585-94 [18299402.001]
  • [Cites] Learn Mem. 2008 Jul;15(7):492-500 [18626093.001]
  • [Cites] Br J Haematol. 2008 Oct;143(2):300-3 [18699852.001]
  • [Cites] Blood. 2008 Dec 1;112(12):4507-11 [18689547.001]
  • [Cites] Blood. 2008 Dec 1;112(12):4503-6 [18812473.001]
  • [Cites] Blood. 2009 Feb 26;113(9):1929-37 [19109561.001]
  • [Cites] Blood. 2009 Mar 19;113(12):2619-28 [19139078.001]
  • [Cites] Hum Mol Genet. 2009 Apr 15;18(8):1449-63 [19181682.001]
  • [Cites] Blood. 2009 Apr 2;113(14):3337-47 [19168790.001]
  • [Cites] Cancer Res. 2009 Jun 1;69(11):4665-73 [19487285.001]
  • [Cites] Blood. 2004 Apr 1;103(7):2480-9 [14656875.001]
  • (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
  •  go-up   go-down


91. Xu G, Kato K, Toki T, Takahashi Y, Terui K, Ito E: Development of acute megakaryoblastic leukemia from a minor clone in a Down syndrome patient with clinically overt transient myeloproliferative disorder. J Pediatr Hematol Oncol; 2006 Oct;28(10):696-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Development of acute megakaryoblastic leukemia from a minor clone in a Down syndrome patient with clinically overt transient myeloproliferative disorder.
  • A Down syndrome male showed leukocytosis from birth and was diagnosed as transient myeloproliferative disorder (TMD).
  • Eight months later, his condition had progressed to myelodysplastic syndrome after spontaneous resolution, and it then evolved to acute megakaryoblastic leukemia (AMKL) at the age of 20 months.
  • Sequencing analysis showed that the predominant TMD and AMKL clones had different GATA1 mutations, although a minor TMD clone identical to the AMKL clone was present at birth.
  • These observations suggest that a minor clone rather than the predominant clone at the time of TMD may give rise to AMKL later on.
  • [MeSH-major] Down Syndrome / genetics. GATA1 Transcription Factor / genetics. Leukemia, Megakaryoblastic, Acute / genetics. Myeloproliferative Disorders / genetics
  • [MeSH-minor] Cell Lineage. Clone Cells. DNA Mutational Analysis. Disease Progression. Humans. Immunophenotyping. Infant. Infant, Newborn. Leukocytosis / diagnosis. Leukocytosis / etiology. Male. Mutation. Risk Factors

  • Genetic Alliance. consumer health - Acute Megakaryoblastic Leukemia.
  • Genetic Alliance. consumer health - Down Syndrome.
  • MedlinePlus Health Information. consumer health - Down Syndrome.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17023834.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / GATA1 Transcription Factor
  •  go-up   go-down


92. Orazi A: Histopathology in the diagnosis and classification of acute myeloid leukemia, myelodysplastic syndromes, and myelodysplastic/myeloproliferative diseases. Pathobiology; 2007;74(2):97-114
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Histopathology in the diagnosis and classification of acute myeloid leukemia, myelodysplastic syndromes, and myelodysplastic/myeloproliferative diseases.
  • In spite of the impressive advances in the area of molecular pathology, bone marrow morphology remains the diagnosis cornerstone to identify the various subtypes of myeloid neoplasms.
  • Particular emphasis is being given to the correct identification of cases of myeloid neoplasms associated with myelofibrosis and for which the bone marrow biopsy represents the only available diagnostic mean.
  • Such cases include two subtypes of acute myeloid leukemia which typically cause diagnostic difficulties: acute megakaryoblastic leukemia and acute panmyelosis with myelofibrosis (acute myelosclerosis).
  • Acute myeloid leukemia with multilineage dysplasia, therapy-related myelodysplastic syndrome/therapy-related acute myeloid leukemia and de novo myelodysplastic syndromes (MDS) will also be discussed.
  • In MDS, in particular, bone marrow biopsy may help in confirming a suspected diagnosis by excluding reactive conditions in which dyshematopoietic changes may also be observed.
  • Among the alterations detected by bone marrow biopsy, a prognostically important finding is the presence of aggregates or clusters of immature myeloid precursor cells (myeloblasts and promyelocytes).
  • These can also be identified by immunohistochemistry with CD34, an antigen expressed in progenitor and early precursor marrow cells, which can be used to demonstrate pathological accumulations of blasts in aggressive subtypes of myeloid neoplasms.
  • In both of these variants, the presence of reticulin fibrosis or fatty changes in the bone marrow can make accurate disease characterization very difficult or impossible using bone marrow aspirates.
  • [MeSH-major] Bone Marrow / pathology. Leukemia, Myeloid / diagnosis. Myelodysplastic Syndromes / diagnosis. Myeloproliferative Disorders / diagnosis
  • [MeSH-minor] Acute Disease. Antigens, CD34 / analysis. Antineoplastic Agents / adverse effects. Biopsy / methods. Diagnosis, Differential. Humans. Immunohistochemistry. Leukemia, Megakaryoblastic, Acute / diagnosis. Leukemia, Megakaryoblastic, Acute / pathology. Primary Myelofibrosis / diagnosis. Primary Myelofibrosis / pathology. Prognosis. Reticulin / analysis


93. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

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

  • Genetic Alliance. consumer health - Tuberculosis.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


94. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

  • The Weizmann Institute of Science GeneCards and MalaCards databases. gene/protein/disease-specific - MalaCards for megakaryocytic leukemia .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


95. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

  • Genetic Alliance. consumer health - Down Syndrome.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • MedlinePlus Health Information. consumer health - Down Syndrome.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [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


98. Alioglu B, Avci Z, Canan O, Ozcay F, Demirhan B, Ozbek N: Invasive esophageal aspergillosis associated with acute myelogenous leukemia: successful therapy with combination caspofungin and liposomal amphotericin B. Pediatr Hematol Oncol; 2007 Jan-Feb;24(1):63-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Invasive esophageal aspergillosis associated with acute myelogenous leukemia: successful therapy with combination caspofungin and liposomal amphotericin B.
  • Aspergillosis is one of the most common invasive fungal infections in patients with leukemia.
  • The lungs are most often affected, but the esophagus can also be involved.The authors report the case of a child with leukemia who developed invasive esophageal aspergillosis.
  • The patient was already receiving empirical liposomal amphotericin B when the diagnosis was made, so a second antifungal (caspofungin) was added to the regimen.
  • [MeSH-major] Amphotericin B / therapeutic use. Antifungal Agents / therapeutic use. Aspergillosis / drug therapy. Esophageal Diseases / drug therapy. Leukemia, Megakaryoblastic, Acute / complications. Peptides, Cyclic / therapeutic use


99. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [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.

  • MedlinePlus Health Information. consumer health - Blood Thinners.
  • MedlinePlus Health Information. consumer health - Pancreatic Cancer.
  • MedlinePlus Health Information. consumer health - Skin Cancer.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Clin Cancer Res. 2001 May;7(5):1299-305 [11350898.001]
  • [Cites] Clin Exp Metastasis. 2009;26(3):171-8 [19067186.001]
  • [Cites] Eur Surg Res. 2002 Jan-Apr;34(1-2):83-91 [11867907.001]
  • [Cites] Arterioscler Thromb Vasc Biol. 2003 Nov 1;23(11):2110-5 [12920044.001]
  • [Cites] Semin Thromb Hemost. 2004 Feb;30 Suppl 1:25-30 [15085463.001]
  • [Cites] Nat Med. 2004 May;10(5):502-9 [15098027.001]
  • [Cites] J Clin Oncol. 2004 May 15;22(10):1944-8 [15143088.001]
  • [Cites] J Thromb Haemost. 2004 Aug;2(8):1266-71 [15304029.001]
  • [Cites] Thromb Haemost. 2004 Sep;92(3):627-33 [15351861.001]
  • [Cites] Microvasc Res. 1974 Jan;7(1):131-43 [4821168.001]
  • [Cites] Res Exp Med (Berl). 1980;177(2):125-34 [7003665.001]
  • [Cites] Blood. 1987 Aug;70(2):551-7 [2955820.001]
  • [Cites] Science. 1989 Mar 17;243(4897):1490-3 [2467380.001]
  • [Cites] Haemostasis. 1993 Mar;23 Suppl 1:141-9 [7684350.001]
  • [Cites] Biochem Biophys Res Commun. 1994 Sep 15;203(2):1339-47 [7522446.001]
  • [Cites] Microvasc Res. 1995 Mar;49(2):212-26 [7541506.001]
  • [Cites] Int J Microcirc Clin Exp. 1996 Jan-Feb;16(1):8-15 [8739219.001]
  • [Cites] J Cell Physiol. 1997 Jul;172(1):69-78 [9207927.001]
  • [Cites] Int J Microcirc Clin Exp. 1997 Nov-Dec;17(6):314-21 [9527522.001]
  • [Cites] J Cardiovasc Pharmacol. 1999 Feb;33(2):223-8 [10028929.001]
  • [Cites] Cancer Res. 1999 Jul 15;59(14):3433-41 [10416607.001]
  • [Cites] Int J Exp Pathol. 2000 Jun;81(3):191-8 [10971740.001]
  • [Cites] Cancer Res. 2000 Nov 1;60(21):6196-200 [11085545.001]
  • [Cites] Pharmacol Rev. 2001 Mar;53(1):93-105 [11171940.001]
  • [Cites] Biochim Biophys Acta. 2001 Mar 21;1471(3):M99-108 [11250066.001]
  • [Cites] Circ Res. 2005 Feb 4;96(2):172-9 [15625285.001]
  • [Cites] J Clin Oncol. 2005 Apr 1;23(10):2130-5 [15699479.001]
  • [Cites] Fertil Steril. 2005 Oct;84 Suppl 2:1199-209 [16210012.001]
  • [Cites] Anal Quant Cytol Histol. 2005 Oct;27(5):284-90 [16447821.001]
  • [Cites] Crit Rev Oncol Hematol. 2007 Mar;61(3):195-207 [17074500.001]
  • [Cites] J Surg Oncol. 2007 May 1;95(6):507-12 [17192920.001]
  • [Cites] Thromb Res. 2007;120 Suppl 2:S121-7 [18023705.001]
  • [Cites] Thromb Res. 2008;121(5):637-45 [17692905.001]
  • [Cites] Expert Opin Investig Drugs. 2008 Jul;17(7):1029-37 [18549339.001]
  • [Cites] APMIS. 2008 Jul-Aug;116(7-8):695-715 [18834413.001]
  • [Cites] Nat Clin Pract Oncol. 2009 Feb;6(2):74-84 [18957949.001]
  • [Cites] Inflamm Res. 2001 Dec;50(12):581-4 [11822782.001]
  • (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


100. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [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

  • Genetic Alliance. consumer health - Acute Megakaryoblastic Leukemia.
  • Genetic Alliance. consumer health - Down Syndrome.
  • MedlinePlus Health Information. consumer health - Down Syndrome.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down






Advertisement