| Autor: |
Yamauchi, Taylor, Danis, Etienne, Zhang, Xi, Riedel, Simone, Huang, Hua, Bernt, Kathrin M, Neff, Tobias |
| Zdroj: |
Blood; January 2016, Vol. 128 Issue: 22 p1516-1516, 1p |
| Abstrakt: |
The importance of stem cell and self-renewal programs in Acute Myeloid Leukemia (AML) is generally accepted, but the molecular details are incompletely understood. The master transcriptional regulator GATA2 is highly expressed in hematopoietic stem cells (HSCs) and has critically important roles in the hematopoietic system. Gata2is required for murine HSC development and maintenance, and heterozygous loss of Gata2compromises murine HSC- and progenitor cell-function. High levels of GATA2-expression have been correlated with adverse prognosis in human AML. GATA2is also overexpressed in human chronic myeloid leukemia. These data suggest an important role for GATA2in normal stem cells and in leukemia. However, genetic lesions resulting in compromised GATA2function can lead to MDS and in some cases AML. In a murine AML model driven by Flt3-ITDand inactivation of Tet2, Gata2is strongly downregulated. Furthermore, mouse models of leukemia suggest that high-level forced expression of Gata2can have a tumor suppressor role. To clarify the role of Gata2in AML we used homozygous genetic inactivation in established murine models of leukemia, using a a conditional allele. |
| Databáze: |
Supplemental Index |
| Externí odkaz: |
|
