We studied the effects of AZD1152, an Aurora B kinase inhibitor, on Burkitt's 
lymphoma (BL) and Hodgkin's lymphoma (HL) in human tissues and cell cultures and 
in a murine xenograft model of lymphoma. Aurora kinase A and B levels were 
assessed by RT-PCR and immunohistochemistry. They were aberrantly expressed in 
BL and HL cell lines, and in lymph nodes from patients with BL and HL. Next, 
activation of the Aurora B promoter was detected by reporter gene assays. The 
promoter activity of Aurora B kinase was high in BL cell lines and the Aurora B 
promoter contained a positive regulatory region between -74 and -104 from the 
transcription initiation site. AZD1152-hQPA had antiproliferative effects in the 
BL and HL cell lines studied; inhibited the phosphorylation of histone H3 and 
retinoblastoma proteins, and resulted in cells with > 4N DNA content. 
AZD1152-hQPA induced caspase-dependent apoptosis of some cell lines, 
demonstrated by loss of mitochondrial membrane potential, activation of 
caspase-9, followed by activation of caspase-3. This effect was accompanied by 
the inhibition of survivin expression. In vivo efficacy was determined in 
NOD/SCID/γc(null) mice implanted with the Ramos human BL cell line. AZD1152 had 
anti-tumour effects in this murine xenograft model. There preclinical data 
suggest that the inhibition of Aurora B kinase is a potentially useful 
therapeutic strategy in BL and HL.