Please use this identifier to cite or link to this item: https://doi.org/10.1016/j.leukres.2007.11.025
Title: In vivo activity of ABT-869, a multi-target kinase inhibitor, against acute myeloid leukemia with wild-type FLT3 receptor
Authors: Zhou, J. 
Khng, J.
Jasinghe, V.J. 
Bi, C.
Poon, L.F. 
Xie, Z. 
Chen, C.-S. 
Neo, C.H.S.
Pan, M.
Yu, H. 
Yeoh, A.E.-J. 
Lu, Y. 
Glaser, K.B.
Albert, D.H.
Davidsen, S.K.
Keywords: Acute myeloid leukemia
In vivo
Tyrosine kinase inhibitor
Whole-body imaging technology
Wild-type FLT3 receptor
Issue Date: 2008
Citation: Zhou, J., Khng, J., Jasinghe, V.J., Bi, C., Poon, L.F., Xie, Z., Chen, C.-S., Neo, C.H.S., Pan, M., Yu, H., Yeoh, A.E.-J., Lu, Y., Glaser, K.B., Albert, D.H., Davidsen, S.K. (2008). In vivo activity of ABT-869, a multi-target kinase inhibitor, against acute myeloid leukemia with wild-type FLT3 receptor. Leukemia Research 32 (7) : 1091-1100. ScholarBank@NUS Repository. https://doi.org/10.1016/j.leukres.2007.11.025
Abstract: Neoangiogenesis plays an important role in leukemogenesis. We investigated the in vivo anti-leukemic effect of ABT-869 against AML with wild-type FLT3 using RFP transfected HL60 cells with in vivo imaging technology on both the subcutaneous and systemic leukemia xenograft models. ABT-869 showed a five-fold inhibition of tumor growth in comparison with vehicle control. IHC analysis revealed that ABT-869 decreased p-VEGFR1, Ki-67 labeling index, VEGF and remarkably increased apoptotic cells in the xenograft models. ABT-869 also reduced the leukemia burden and prolonged survival. Our study supports the rationale for clinically testing an anti-angiogenesis agent in AML with wild-type FLT3. © 2007 Elsevier Ltd. All rights reserved.
Source Title: Leukemia Research
URI: http://scholarbank.nus.edu.sg/handle/10635/26977
ISSN: 01452126
DOI: 10.1016/j.leukres.2007.11.025
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