In vivo activity of ABT-869, a multi-target kinase inhibitor, against acute myeloid leukemia with wild-type FLT3 receptor | ScholarBank@NUS

Please use this identifier to cite or link to this item: https://scholarbank.nus.edu.sg/handle/10635/25751

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.
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/10635/25751
ISSN:	01452126
Appears in Collections:	Staff Publications

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