Abstract
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.
| Original language | English |
|---|---|
| Pages (from-to) | 1084-1090 |
| Number of pages | 7 |
| Journal | Experimental Hematology |
| Volume | 36 |
| Issue number | 9 |
| DOIs | |
| State | Published - Sep 2008 |
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ASJC Scopus subject areas
- Cancer Research
- Cell Biology
- Genetics
- Hematology
- Oncology
- Transplantation
Cite this
AMD3100 synergizes with G-CSF to mobilize repopulating stem cells in Fanconi anemia knockout mice. / Pulliam, Anna C.; Hobson, M. Joe; Ciccone, Samantha L.; Li, Yan; Chen, Shi; Srour, Edward; Yang, Feng Chun; Broxmeyer, Hal; Clapp, D.
In: Experimental Hematology, Vol. 36, No. 9, 09.2008, p. 1084-1090.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - AMD3100 synergizes with G-CSF to mobilize repopulating stem cells in Fanconi anemia knockout mice
AU - Pulliam, Anna C.
AU - Hobson, M. Joe
AU - Ciccone, Samantha L.
AU - Li, Yan
AU - Chen, Shi
AU - Srour, Edward
AU - Yang, Feng Chun
AU - Broxmeyer, Hal
AU - Clapp, D.
PY - 2008/9
Y1 - 2008/9
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=49349095512&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=49349095512&partnerID=8YFLogxK
U2 - 10.1016/j.exphem.2008.03.016
DO - 10.1016/j.exphem.2008.03.016
M3 - Article
C2 - 18495331
AN - SCOPUS:49349095512
VL - 36
SP - 1084
EP - 1090
JO - Experimental Hematology
JF - Experimental Hematology
SN - 0301-472X
IS - 9
ER -