| First Author | Kirstetter P | Year | 2008 |
| Journal | Cancer Cell | Volume | 13 |
| Issue | 4 | Pages | 299-310 |
| PubMed ID | 18394553 | Mgi Jnum | J:136134 |
| Mgi Id | MGI:3795306 | Doi | 10.1016/j.ccr.2008.02.008 |
| Citation | Kirstetter P, et al. (2008) Modeling of C/EBPalpha mutant acute myeloid leukemia reveals a common expression signature of committed myeloid leukemia-initiating cells. Cancer Cell 13(4):299-310 |
| abstractText | Mutations in the CEBPA gene are present in 7%-10% of human patients with acute myeloid leukemia (AML). However, no genetic models exist that demonstrate their etiological relevance. To mimic the most common mutations affecting CEBPA-that is, those leading to loss of the 42 kDa C/EBPalpha isoform (p42) while retaining the 30kDa isoform (p30)-we modified the mouse Cebpa locus to express only p30. p30 supported the formation of granulocyte-macrophage progenitors. However, p42 was required for control of myeloid progenitor proliferation, and p42-deficient mice developed AML with complete penetrance. p42-deficient leukemia could be transferred by a Mac1+c-Kit+ population that gave rise only to myeloid cells in recipient mice. Expression profiling of this population against normal Mac1+c-Kit+ progenitors revealed a signature shared with MLL-AF9-transformed AML. |
