Abstract
Breast cancer (BC) is the most prevalent type worldwide, besides being one of the most common causes of death among women. It has been suggested that sporadic BC is most likely caused by low-penetrance genes, including those involved in DNA repair mechanisms. Furthermore, the accumulation of DNA damage may contribute to breast carcinogenesis. In the present study, the relationship between two DNA repair genes, viz., XRCC1 (Arg399Gln) and XRCC3 (Thr241Met) polymorphisms, and the levels of chromosome damage detected in 65 untreated BC women and 85 healthy controls, was investigated. Chromosome damage was evaluated through micronucleus assaying, and genotypes determined by PCR-RFLP methodology. The results showed no alteration in the risk of BC and DNA damage brought about by either XRCC1 (Arg399Gln) or XRCC3 (Thr241Met) action in either of the two groups. Nevertheless, on evaluating BC risk in women presenting levels of chromosome damage above the mean, the XRCC3Thr241Met polymorphism was found to be more frequent in the BC group than in the control, thereby leading to the conclusion that there is a slight association between XRCC3 (241 C/T) genotypes and BC risk in the subgroups with higher levels of chromosome damage.
Highlights
Breast cancer (BC) is one of the most common causes of death among women, with every indication of a slow and steady decrease in the age of onset
A large number of genetic variants associated with BC risk have been identified in genes involved in a wide variety of functions, including steroid hormone metabolism, detoxifica
The X-Ray Repair Cross Complementing 1 (XRCC1) gene involved in the Base Excision Repair (BER) pathway, is linked with a scaffolding protein that directly associates with other proteins, such as DNA polymerase ß, PARP (ADP-ribose polymerase) and DNA ligase III, in a complex that facilitates processes of BER DNA repair (Caldecott et al, 2003)
Summary
Breast cancer (BC) is one of the most common causes of death among women, with every indication of a slow and steady decrease in the age of onset. It is common knowledge that chromosome damage results from non- or misrepaired DSBs, with many polymorphisms, such as those of DNA repair genes, having been associated with increased cancer risk, and a possibly even higher level of chromosome damage (Norppa 2004).
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