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Annals of Oncology 2007 18(9):1523-1528; doi:10.1093/annonc/mdm191
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© 2007 European Society for Medical Oncology

hematologic malignancies

Increased risk of acute myeloid leukaemia due to polymorphisms in detoxification and DNA repair enzymes

MT Voso*, E Fabiani, F D'Alo', F Guidi, A Di Ruscio, S Sica, L Pagano, M Greco, S Hohaus and G Leone

Istituto di Ematologia, Universita’ Cattolica del Sacro Cuore, Roma, Italy

* Correspondence to: Dr M. Teresa Voso, Istituto di Ematologia, Universita’ Cattolica del Sacro Cuore, L.go A. Gemelli, 1, 00168 Roma, Italy. Tel: +39-0630154180; Fax: +39-0635503777; E-mail: mtvoso{at}rm.unicatt.it

Background: Polymorphisms in genes involved in detoxification and DNA-repair pathways may modify the individual's risk for genomic damage, and, as a consequence, the risk of developing malignant diseases.

Patients and methods: We performed a case-control study including 160 cases of acute myeloid leukaemia (AML) and 162 matched controls to test the impact of six genomic polymorphisms on the risk to develop AML and/or therapy-related AML.

Results: We found a significantly higher prevalence of the polymorphic variants RAD51-G135C and CYP3A4-A-290G genes in AML cases, when compared with controls (P = 0.02 and P = 0.04), increasing the risk of AML 2.1-folds (95% CI: 1.1–4.0) and 3.2-fold (95% CI: 1.1–11.5), respectively. Carriers of both the RAD51-G135C and CYP3A4-A-290G variants were at highest AML risk (P = 0.003; OR:13,6; 95% CI: 2.0–585.5), suggesting a synergistic effect between these polymorphisms.

Conclusions: These results suggest that polymorphic variants in DNA-repair and detoxification enzymes may co-operate in modulating the individual's risk of AML.

Key words: acute myeloid leukaemia, detoxification, DNA-repair, polymorphisms

Received for publication January 17, 2007. Revision received April 3, 2007. Accepted for publication April 11, 2007.


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Ann Oncol 2007 18: 1427. [Extract] [Full Text]  





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