We investigated the effects of targeting the mitotic regulators aurora kinase A 
and B in pediatric acute lymphoblastic leukemia (ALL) and acute myeloid leukemia 
(AML). Aurora protein expression levels in pediatric ALL and AML patient samples 
were determined by western blot and reverse phase protein array. Both kinases 
were overexpressed in ALL and AML patients (P<0.0002), especially in 
E2A-PBX1-translocated ALL cases (P<0.002), compared with normal bone-marrow 
mononuclear cells. Aurora kinase expression was silenced in leukemic cell lines 
using short hairpin RNAs and locked nucleic acid-based mRNA antagonists. Aurora 
B knockdown resulted in proliferation arrest and apoptosis, whereas aurora A 
knockdown caused no or only minor growth delay. Most tested cell lines were 
highly sensitive to the AURKB-selective inhibitor 
barasertib-hydroxyquinazoline-pyrazol-anilide (AZD1152-HQPA) in the nanomolar 
range, as tested with an MTS 
(3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium) 
assay. But most importantly, primary ALL cells with a high aurora B protein 
expression, especially E2A-PBX1-positive cases, were sensitive as well. In adult 
AML early clinical trials, clear responses are observed with barasertib. Here we 
show that inhibition of aurora B, more than aurora A, has an antiproliferative 
and pro-apoptotic effect on acute leukemia cells, indicating that particularly 
targeting aurora B may offer a new strategy to treat pediatric ALL and AML.