Journal
CANCER CELL
Volume 25, Issue 4, Pages 415-427Publisher
CELL PRESS
DOI: 10.1016/j.ccr.2014.02.008
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Funding
- National Institutes of Health [R01AI094642, R21HL114368, R37DK50107, R01DK68634]
- Japan Society for the Promotion of Science (JSPS) [KAKENHI 22118001, 24249015, 22790269, 24790957]
- Midwest Athletes Against Childhood Cancer
- Core Research for Evolutionary Science and Technology research program of the Japan Science and Technology Agency
- Naito Foundation
- Mitsubishi Foundation
- Takeda Science Foundation
- Grants-in-Aid for Scientific Research [22790269, 24591404, 24659456, 24790957] Funding Source: KAKEN
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Chromosomal inversion between 3q21 and 3q26 results in high-risk acute myeloid leukemia (AML). In this study, we identified a mechanism whereby a GATA2 distal hematopoietic enhancer (G2DHE or 77-kb enhancer) is brought into close proximity to the EVI1 gene in inv(3)(q21;q26) inversions, leading to leukemogenesis. We examined the contribution of G2DHE to leukemogenesis by creating a bacterial artificial chromosome (BAC) transgenic model that recapitulates the inv(3)(q21;q26) allele. Transgenic mice harboring a linked BAG developed leukemia accompanied by EVI1 overexpression neoplasia that was not detected in mice bearing the same transgene but that was missing the GATA2 enhancer. These results establish the mechanistic basis underlying the pathogenesis of a severe form of leukemia through aberrant expression of the EVI1 proto-oncogene.
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