Variation in the manganese superoxide dismutase gene (SOD2) is not a major cause of radiotherapy complications in breast cancer patients.

Abstract

Small proportions of patients receiving radiotherapy develop marked long-term radiation damage. It is thought that this is due, at least in part, to intrinsic differences in cellular radiosensitivity, but the underlying mechanism is unknown. Reactive oxygen species are involved in cellular radiation damage, hence inter-individual differences in free radical detoxification may be related to radiosensitivity. Within mitochondria manganese superoxide dismutase (MnSOD) provides a major defence against oxidative damage by reactive oxygen species. MnSOD has been linked to expression of malignant phenotype and apoptosis and polymorphic variation in the gene, SOD2 to risk of breast cancer. Forty-one breast cancer patients developing marked changes in breast appearance after radiotherapy and 39 patients who showed no clinically detectable reaction after radiotherapy were analyzed for germline sequence variation in SOD2. The Ala-9Val polymorphism was detected, but no other sequence variants were detected in SOD2. Both alleles of the Ala-9Val polymorphism were equally distributed between the two patient groups. Sequence variation in SOD2 is not the major cause of radiotherapy complications in women with breast cancer.