Conflict of interest: Nothing to declare.
Targeting the wee1 kinase for treatment of pediatric Down syndrome acute myeloid leukemia
Version of Record online: 24 JUN 2014
© 2014 Wiley Periodicals, Inc.
Pediatric Blood & Cancer
Volume 61, Issue 10, pages 1767–1773, October 2014
How to Cite
Caldwell, J. T., Edwards, H., Buck, S. A., Ge, Y. and Taub, J. W. (2014), Targeting the wee1 kinase for treatment of pediatric Down syndrome acute myeloid leukemia. Pediatr. Blood Cancer, 61: 1767–1773. doi: 10.1002/pbc.25081
- Issue online: 19 AUG 2014
- Version of Record online: 24 JUN 2014
- Manuscript Accepted: 2 APR 2014
- Manuscript Received: 22 JAN 2014
- National Cancer Institute. Grant Numbers: R01 CA120772, T32 CA009531
- Karmanos Cancer Institute
- Children's Research Center of Michigan
- Kids Without Cancer, Children's Leukemia Foundation of Michigan
- Elana Fund
- Herrick Foundation
- Justin's Gift Charity
- The Buric Family
- Leukemia and Lymphoma Society
- Sehn Family Foundation
- Dale Meyer Memorial Endowment for Leukemia Research
- Ring Screw Textron Endowed Chair for Pediatric Cancer Research
Additional Supporting Information may be found in the online version of this article.
|pbc25081-sm-0001-SuppFigLeg-S1.docx||14K||Supplemental Figure Legends.|
|pbc25081-sm-0001-SuppFig-S1.tif||4179K||Fig. S1 MK-1775 effects on cell cycle, mitosis, and DNA damage.|
|pbc25081-sm-0001-SuppFig-S2.tif||4973K||Fig. S2 MK-1775 can decrease G2/M fraction of viable CMY cells, especially at higher doses.|
|pbc25081-sm-0001-SuppFig-S3.tif||6679K||Fig. S3 CMK cells treated with the combination of AraC and lower doses of MK-1775 appear to die out of S-phase.|
|pbc25081-sm-0001-SuppTab-S1.docx||14K||Table S1 3-Day IC50s in CMK and CMY|
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