| First Author | Kundu M | Year | 2005 |
| Journal | Blood | Volume | 106 |
| Issue | 10 | Pages | 3621-4 |
| PubMed ID | 16051740 | Mgi Jnum | J:106809 |
| Mgi Id | MGI:3619627 | Doi | 10.1182/blood-2005-04-1447 |
| Citation | Kundu M, et al. (2005) Runx1 deficiency predisposes mice to T-lymphoblastic lymphoma. Blood 106(10):3621-4 |
| abstractText | 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 (CBFbeta) 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 Runx1(lacZ/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 Runx1(lacZ/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. |
