| First Author | Foley SB | Year | 2013 |
| Journal | Cell Rep | Volume | 5 |
| Issue | 1 | Pages | 51-60 |
| PubMed ID | 24095735 | Mgi Jnum | J:203111 |
| Mgi Id | MGI:5524981 | Doi | 10.1016/j.celrep.2013.08.037 |
| Citation | Foley SB, et al. (2013) Expression of BCR/ABL p210 from a knockin allele enhances bone marrow engraftment without inducing neoplasia. Cell Rep 5(1):51-60 |
| abstractText | Chronic myeloid leukemia (CML) and some acute lymphoblastic leukemias are characterized by the t(9;22) chromosome, which encodes the BCR/ABL oncogene. Multiple mouse models of CML express BCR/ABL at high levels from non-Bcr promoters, resulting in the development of leukemias. In contrast, a significant fraction of healthy humans have been found to have BCR/ABL-positive hematopoietic cells. To bridge the gap between the information derived from current mouse models and nonleukemic humans with the BCR/ABL oncogene, we generated a knockin model with BCR/ABL p210 expressed from the Bcr locus. Unlike previous models, expression of BCR/ABL from the knockin allele did not induce leukemia. BCR/ABL mutant cells did exhibit favorable bone marrow engraftment compared to control cells. These data suggest that BCR/ABL expression alone is insufficient to induce disease. This model allows for inducible spatial and temporal control of BCR/ABL expression for analysis of early steps in the pathogenesis of BCR/ABL-expressing leukemias. |
