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FLT3 mutations confer enhanced proliferation and survival properties to multipotent progenitors in a murine model of chronic myelomonocytic leukemia.

Authors: Lee, BH  Tothova, Z  Levine, RL  Anderson, K  Buza-Vidas, N  Cullen, DE  McDowell, EP  Adelsperger, J  Frohling, S  Huntly, BJ  Beran, M  Jacobsen, SE  Gilliland, DG 
Citation: Lee BH, etal., Cancer Cell. 2007 Oct;12(4):367-80.
Pubmed: (View Article at PubMed) PMID:17936561
DOI: Full-text: DOI:10.1016/j.ccr.2007.08.031

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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CRRD Object Information
CRRD ID: 11049465
Created: 2016-04-06
Species: All species
Last Modified: 2016-04-06
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.