Abstract:
:The RUNX1/AML1 gene is the most frequently mutated gene in human leukemia. Conditional deletion of Runx1 in adult mice results in an increase of hematopoietic stem cells (HSCs), which serve as target cells for leukemia; however, Runx1(-/-) mice do not develop spontaneous leukemia. Here we show that maintenance of Runx1(-/-) HSCs is compromised, progressively resulting in HSC exhaustion. In leukemia development, the stem cell exhaustion was rescued by additional genetic changes. Retroviral insertional mutagenesis revealed Evi5 activation as a cooperating genetic alteration and EVI5 overexpression indeed prevented Runx1(-/-) HSC exhaustion in mice. Moreover, EVI5 was frequently overexpressed in human RUNX1-related leukemias. These results provide insights into the mechanism for maintenance of pre-leukemic stem cells and may provide a novel direction for therapeutic applications.
journal_name
Bloodjournal_title
Bloodauthors
Jacob B,Osato M,Yamashita N,Wang CQ,Taniuchi I,Littman DR,Asou N,Ito Ydoi
10.1182/blood-2009-07-232249subject
Has Abstractpub_date
2010-02-25 00:00:00pages
1610-20issue
8eissn
0006-4971issn
1528-0020pii
blood-2009-07-232249journal_volume
115pub_type
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