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 Blood, 1 December 2006, Vol. 108, No. 12, pp. 3916-3918.
Prepublished online as a Blood First Edition Paper on August 10, 2006; DOI 10.1182/blood-2006-05-022921.

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Submitted May 16, 2006
Accepted July 19, 2006

Polymorphisms in human homeobox HLX1 and DNA repair RAD51 genes increase the risk of therapy-related acute myeloid leukemia

Mays Jawad, Claire Helen Seedhouse*, Nigel Russell, and Mark Plumb

Department of Genetics, University of Leicester, Leicester, UK
Academic Haematology, Clinical Sciences Building, University Of Nottingham, Nottingham, UK

* Corresponding author; email: claire.seedhouse{at}nottingham.ac.uk.

Studies of mouse radiation-induced AML suggest that the number of target stem cells is a risk factor, and the HLX1 homeobox gene, which is important for hemopoietic development, a candidate gene. The distribution of the C/T-3’ UTR polymorphism in HLX1 in AML and therapy-related AML (t-AML) patients compared to controls was therefore determined. The presence of the variant HLX1 allele significantly increases the risk of t-AML (OR= 3.36, 95% CI 1.65-6.84). The DNA repair gene RAD51 (135G/C-5’ UTR) polymorphism also increases t-AML risk, and when combined analysis was performed on both RAD51 and HLX1 variant alleles, a synergistic 9.5-fold increase (95% CI 2.22-40.64) in the risk of t-AML was observed. We suggest that the HLX1 polymorphism has an effect on stem cell numbers, whereas an increased DNA repair capacity (RAD51) will suppress apoptosis, a genetic interaction that may increase the number of genomes at risk during cancer therapy.


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