Abstract
AimsXRCC3 and RAD51 are two important members in homologous recombination repair pathway. This study was performed to detect the expressions of these two molecules in breast cancer and explore their correlations with clinicopathological factors.Methods and ResultsImmunohistochemistry was used to detect protein expressions of XRCC3 and RAD51 in 248 cases of breast cancer tissue and 78 cases of adjacent non-cancerous tissue. Data showed that expressions for both XRCC3 and RAD51 were significantly increased in breast cancer. High XRCC3 expression was associated with large tumor size and positive PR and HER2 status, while high RAD51 expression was associated with axillary lymph node metastasis and positive PR and HER2 status. The result of multivariate analysis demonstrated that HER2, PR and RAD51 were significantly association with XRCC3. And besides XRCC3, axillary lymph node metastasis and PR were significantly correlated with RAD51.ConclusionsXRCC3 and RAD51 were significantly associated with clinicopathological factors and they might play important roles in the development and progress of breast cancer.
Highlights
Breast cancer is one of the most common cancers and the leading cause of tumor-related death among women worldwide.Though the exact etiology remains unknown, increasing evidence indicates that breast cancer pathogenesis is tightly linked with double-strand break (DSB) repair dysfunction [1,2].RAD51, which catalyses strand transfer between a broken sequence and its undamaged homologue to allow re-synthesis of the damaged region, represents the central recombinase of homologous recombination repair (HRR)
The result of multivariate analysis demonstrated that HER2, PR and RAD51 were significantly association with XRCC3
Besides XRCC3, axillary lymph node metastasis and PR were significantly correlated with RAD51
Summary
Breast cancer is one of the most common cancers and the leading cause of tumor-related death among women worldwide.Though the exact etiology remains unknown, increasing evidence indicates that breast cancer pathogenesis is tightly linked with double-strand break (DSB) repair dysfunction [1,2].RAD51, which catalyses strand transfer between a broken sequence and its undamaged homologue to allow re-synthesis of the damaged region, represents the central recombinase of homologous recombination repair (HRR). Though the exact etiology remains unknown, increasing evidence indicates that breast cancer pathogenesis is tightly linked with double-strand break (DSB) repair dysfunction [1,2]. It is known that RAD51 expression is significantly increased in breast cancer [4,5]. The research conducted by Maacke et al suggested a correlation between wild-type RAD51 expression and histological grading invasive ductal breast cancer [4]. Though later study performed by Barbano et al didn’t confirm this association, they found that high RAD51 mRNA expression was associated with breast cancer patient’s outcome [5]. Epidemiological studies have demonstrated a correlation between gene polymorphisms of XRCC3 and breast cancer risk [6,7,8].
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