Journal
CANCER CELL
Volume 12, Issue 4, Pages 367-380Publisher
CELL PRESS
DOI: 10.1016/j.ccr.2007.08.031
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Funding
- Howard Hughes Medical Institute Funding Source: Medline
- Medical Research Council [G116/187] Funding Source: Medline
- NCI NIH HHS [CA105423, P01 CA066996, P01 CA066996-100001, K08 CA113434-02, U01 CA105423, K08 CA113434-01A1, K08 CA113434, CA113434, CA66996] Funding Source: Medline
- PHS HHS [HHMI_GILLILAND_D] Funding Source: Medline
- MRC [G116/187] Funding Source: UKRI
- Medical Research Council [G116/187] Funding Source: researchfish
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Despite their known transforming properties, the effects of leukemogenic FLT3-ITD mutations on hematopoietic stem and multipotent progenitor cells and on hematopoietic differentiation are not well understood. We report a mouse model harboring an ITD in the murine Flt3 locus that develops myeloproliferative disease resembling CMML and further identified FLT3-ITD mutations in a subset of human CMML. These findings correlated with an increase in number, cell cycling, and survival of multipotent stem and progenitor cells in an ITD dose-dependent manner in animals that exhibited alterations within their myeloid progenitor compartments and a block in normal B cell development. This model provides insights into the consequences of constitutive signaling by an oncogenic tyrosine kinase on hematopoietic progenitor quiescence, function, and cell fate.
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