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Blood, 15 November 2005, Vol. 106, No. 10, pp. 3621-3624. Prepublished online as a Blood First Edition Paper on July 28, 2005; DOI 10.1182/blood-2005-04-1447. This Article Full Text (PDF) All Versions of this Article: 2005-04-1447v1 106/10/3621    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Kundu, M. Articles by Liu, P. P Search for Related Content PubMed PubMed Citation Articles by Kundu, M. Articles by Liu, P. P Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted April 8, 2005 Accepted July 18, 2005 Runx1 deficiency predisposes mice to T-lymphoblastic lymphoma Mondira Kundu, Sheila Compton, Lisa Garrett-Beal, Terryl Stacy, Matthew Starost, Michael Eckhaus, Nancy A Speck, and Paul P Liu* Genetics and Molecular Biology Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD, USA Genetic Diseases Research Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD, USA Department of Biochemistry, Dartmouth Medical School, Hanover, NH, USA Division of Veterinary Resources, Office of Research Services, National Institutes of Health, Bethesda, MD, USA * Corresponding author; email: pliu{at}nhgri.nih.gov. Chromosomal rearrangements affecting RUNX1 and CBFB are common in acute leukemias. These mutations result in the expression of fusion proteins that act dominant-negatively to suppress the normal function of the CBF/RUNX complexes. In addition, loss-of-function mutations in RUNX1 have been identified in sporadic cases of acute myeloid leukemia (AML) and in association with the familial platelet disorder with propensity to develop AML (FPD/AML). In order to examine the hypothesis that decreased gene dosage of RUNX1 may be a critical event in the development of leukemia, we treated chimeric mice generated from Runx1lacZ/lacZ embryonic stem (ES) cells that have homozygous disruption of the Runx1 gene with N-ethyl-N-nitrosurea (ENU). We observed an increased incidence of T-lymphoblastic lymphoma in Runx1lacZ/lacZ compared to wild-type chimeras, and confirmed that the tumors were of ES cell origin. Our results therefore suggest that deficiency of Runx1 can indeed predispose mice to hematopoietic malignancies. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: P. Burda, N. Curik, J. Kokavec, P. Basova, D. Mikulenkova, A. I. Skoultchi, J. Zavadil, and T. Stopka PU.1 Activation Relieves GATA-1-Mediated Repression of Cebpa and Cbfb during Leukemia Differentiation Mol. Cancer Res., October 1, 2009; 7(10): 1693 - 1703. [Abstract] [Full Text] [PDF] H. Liu, L. Carlsson, and T. Grundstrom Identification of an N-terminal Transactivation Domain of Runx1 That Separates Molecular Function from Global Differentiation Function J. Biol. Chem., September 1, 2006; 281(35): 25659 - 25669. [Abstract] [Full Text] [PDF]

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