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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.

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NEOPLASIA
Brief report

Runx1 deficiency predisposes mice to T-lymphoblastic lymphoma

Mondira Kundu, Sheila Compton, Lisa Garrett-Beal, Terryl Stacy, Matthew F. Starost, Michael Eckhaus, Nancy A. Speck, and P. Paul Liu

From the Genetics and Molecular Biology Branch and Genetic Diseases Research Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD; Department of Biochemistry, Dartmouth Medical School, Hanover, NH; and Division of Veterinary Resources, Office of Research Services, National Institutes of Health, Bethesda, MD.

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 Runt-related transcription factor 1 (RUNX)/core binding factor {beta} (CBF{beta}) complexes. In addition, loss-of-function mutations in Runt-related transcription factor 1 (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-nitrosourea (ENU). We observed an increased incidence of T-lymphoblastic lymphoma in Runx1lacZ/lacZ compared with 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.


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