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Volume 36, Issue 9, Pages 1084-1090 (September 2008)


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AMD3100 synergizes with G-CSF to mobilize repopulating stem cells in Fanconi anemia knockout mice

Anna C. Pulliamab, M. Joe Hobsonbc, Samantha L. Cicconeab, Yan Libc, Shi Chenbc, Edward F. Srourac, Feng-Chun Yangbc, Hal E. Broxmeyerab, D. Wade ClappabcCorresponding Author Informationemail address

Received 30 January 2008; received in revised form 18 March 2008; accepted 21 March 2008. published online 21 May 2008.

Fanconi anemia (FA) is a heterogeneous inherited disorder characterized by a progressive bone marrow (BM) failure and susceptibility to myeloid leukemia. Genetic correction using gene-transfer technology is one potential therapy. A major hurdle in applying this technology in FA patients is the inability of granulocyte colony-stimulating factor (G-CSF) to mobilize sufficient numbers of hematopoietic stem (HSC)/progenitor cells (HPC) from the BM to the peripheral blood. Whether the low number of CD34+ cells is a result of BM hypoplasia or an inability of G-CSF to adequately mobilize FA HSC/HPC remains incompletely understood. Here we use competitive repopulation of lethally irradiated primary and secondary recipients to show that in two murine models of FA, AMD3100 synergizes with G-CSF resulting in a mobilization of HSC, whereas G-CSF alone fails to mobilize stem cells even in the absence of hypoplasia.

a Department of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, Ind., USA

b Indiana University Cancer Center, Indiana University School of Medicine, Indianapolis, Ind., USA

c Department of Pediatrics, Herman B. Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, Ind., USA

Corresponding Author InformationOffprint requests to: D. Wade Clapp, M.D., Cancer Research Center R4-402A, 1044 West Walnut Street, Indianapolis IN 46202

PII: S0301-472X(08)00130-6

doi:10.1016/j.exphem.2008.03.016


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