Autor: |
Samantha B. Foley, Zacariah L. Hildenbrand, Abigail A. Soyombo, Jeffery A. Magee, Yipin Wu, Katherine I. Oravecz-Wilson, Theodora S. Ross |
Jazyk: |
angličtina |
Rok vydání: |
2013 |
Předmět: |
|
Zdroj: |
Cell Reports, Vol 5, Iss 1, Pp 51-60 (2013) |
Druh dokumentu: |
article |
ISSN: |
2211-1247 |
DOI: |
10.1016/j.celrep.2013.08.037 |
Popis: |
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. |
Databáze: |
Directory of Open Access Journals |
Externí odkaz: |
|