期刊
CANCER CELL
卷 13, 期 4, 页码 299-310出版社
CELL PRESS
DOI: 10.1016/j.ccr.2008.02.008
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资金
- Associazione Italiana per la Ricerca sul Cancro Funding Source: Custom
- Lundbeck Foundation [R9-2007-978] Funding Source: researchfish
- Medical Research Council [G0700711B] Funding Source: researchfish
- NHLBI NIH HHS [R01 HL112719] Funding Source: Medline
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL112719] Funding Source: NIH RePORTER
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/EBP alpha 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.
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