Journal article
Inhibition of apoptosis by BCL2 prevents leukemic transformation of a murine myelodysplastic syndrome
CI Slape, J Saw, JBM Jowett, PD Aplan, A Strasser, SM Jane, DJ Curtis
Blood | AMER SOC HEMATOLOGY | Published : 2012
Abstract
Programmed cell death or apoptosis is a prominent feature of low-risk myelodysplastic syndromes (MDS), although the underlying mechanism remains controversial. High-risk MDS have less apoptosis associated with increased expression of the prosurvival BCL2-related proteins. To address the mechanism and pathogenic role of apoptosis and BCL2 expression in MDS, we used a mouse model resembling human MDS, in which the fusion protein NUP98-HOXD13 (NHD13) of the chromosomal translocation t(2;11)(q31;p15) is expressed in hematopoietic cells. Hematopoietic stem and progenitor cells from 3-month-old mice had increased rates of apoptosis associated with increased cell cycling and DNA damage. Gene expres..
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Awarded by National Cancer Institute
Funding Acknowledgements
This work was supported by the National Health and Medical Research Council of Australia (Project Grant 628367, Program Grant 461221, NHMRC Australia Fellowship), the Cancer Council of Victoria, the Leukemia & Lymphoma Society (SCOR grant no. 7413), the National Institutes of Health (CA43540), and operational infrastructure grants through the Australian Government IRISS and the Victorian State Government OIS. This research was supported by the Intramural Research Program of the National Institutes of Health, National Cancer Institute.C.I.S. and P.D.A. receive royalties from the National Institutes of Health Technology Transfer office for the invention of NUP98-HOXD13 mice. The remaining authors declare no competing financial interests.