And epidemiological studies have demonstrated a correlation between gene polymorphisms of XRCC3 and breast cancer risk. But the expression of XRCC3 in breast cancer was not well studied. In this study, immunohistochemistry was used to explore the prevalence of XRCC3 and RAD51 expression and their possible roles in breast cancer. As a major defense against environmental damage to cells, DNA repair is vital to the integrity of genome. Abnormality in this AbMole Povidone iodine process is believed to implicate in tumorigenesis. Theoretically, decreased or loss of expression of DNA repair proteins could damage the DNA repair capacity and lead to genomic instability, thus increase susceptibility to cancer. However, a series of studies suggested that changes in the expression of DNA repair protein were quite complicated during tumorigenesis, as some were downregulated but others were up-regulated. XRCC3 is a human homolog of RAD51 and participate in the HRR pathway. It plays an important role in the assembly or stabilization of a multimeric form of RAD51 during DNA repair. While few studies on XRCC3 expression in breast cancer were reported. Our results showed that the expression levels of both XRCC3 and RAD51 were significantly increased in breast cancer, which was consistent with their high mRNA expressions. How to explain this phenomenon? Is it a result of cells responding to DNA damage but not sufficient to maintain the genome stability? Or the overexpression of these proteins promotes genome instability and tumorigenesis? Richardson et al. used a genetic system to examine the potential for multiple DSBs to lead to genome rearrangements in the presence of increased RAD51 expression, and found a connection between elevated RAD51 protein levels and genome instability as well as tumor progression. Studies on XRCC3 function revealed that XRCC3 was required for the proliferation of MCF7 cells and the decrease in its expression leaded to the accumulation of DNA breaks and the induction of p53-dependent cell death. And on the other hand, cells over-expressing XRCC3 were more invasive and showed a higher tumorigenesis in vivo. What’s more, our study suggested significant associations existed between the expression of these two markers and HER2 level, which was a strong poor prognostic factor in breast cancer. And high expression of XRCC3 and RAD51 were associated with large tumor size and axillary lymph node metastasis respectively. Base on these results, we are disposed to agree that overexpression of XRCC3 and RAD51 may play an important role in the pathogenesis of breast cancer. Accumulated evidence indicated that activation of erbB family of receptors could promote chemo and radiotherapy resistance when mutated or over-expressed. And recent studies demonstrated a role of erbB-signaling in regulating DSB repair.