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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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NEOPLASIA
Brief report

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

From the Department of Genetics, University of Leicester; and Academic Haematology, Clinical Sciences Building, Nottingham University Hospitals, United Kingdom.

Studies of radiation-induced acute myeloid leukemia (AML) in mice suggest that the number of target stem cells is a risk factor, and the HLX1 homeobox gene, which is important for hematopoietic development, is a candidate gene. The distribution of the C/T-3' untranslated region (UTR) polymorphism in HLX1 in patients with AML and therapy-related AML (t-AML) compared with 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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