Abstract
AMD3100 sensitizes acute lymphoblastic leukemia cells to chemotherapy in vivo
Highlights
Despite substantial advances in the treatment of acute lymphoblastic leukemia (ALL) during the past four decades, long-term survival remains at approximately 80% for children and 40% for adults
The CXCL12–CXCR4 interaction was shown to be essential for the earliest stages of B-cell development and is involved in retaining pre-B cells in the bone marrow
We previously showed that AMD3100 is able to block protection provided by a stromal layer to mouse transgenic Bcr/Abl P190 ALL cells treated with Imatinib.[4]
Summary
Blood Cancer Journal (2011) 1, e14; doi:10.1038/bcj.2011.13; published online 1 April 2011. We previously showed that AMD3100 is able to block protection provided by a stromal layer to mouse transgenic Bcr/Abl P190 ALL cells treated with Imatinib.[4] To test whether these results can be extended in vivo, we performed fluorescence-activated cell sorting analysis on the peripheral blood of leukemic P190 Bcr/Abl ALL (8093)-transplanted mice before and 2 h after intraperitoneal injection with saline or AMD3100, as it has been shown that a single bolus of AMD3100 can mobilize progenitor cells.[1] Interestingly, there was a marked increase in circulating leukemic CD45.2 þ (8093 ALL) cells after injection of AMD3100 (Figure 1a) but not in mobilized CD45.1 þ C57BL/6 cells This lack of effect on endogenous CD45 þ cells may be caused by the suppression of normal hematopoiesis by the presence of large numbers of malignant lymphoblasts in the bone marrow at this stage.
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