Abstract
Abstract To evaluate whether deficient DNA repair contributes to elevated DNA damage and breast carcinogenesis, we used a newly developed flow-cytometry assay for rapid assessment of H2AX phosphorylation (gamma-H2AX) in response to double strand breaks (DSBs) in peripheral lymphocytes from 64 breast cancer cases and 71 controls. Basal or ionizing radiation (IR)-induced gamma-H2AX was not influenced by age, smoking status, family history (FH), age at menarche, age at first birth or parity and body mass index (BMI). With limited sample size, basal or IR-induced gamma-H2AX level did not differ between breast cancer cases (mean+SD, 6.65+1.18; 29.23+6.88) and controls (6.48+0.95; 27.19+7.26). In subgroup analysis of women with younger age at first live birth (<24), breast cancer cases have a significantly higher IR-induced gamma-H2AX level (29.87+6.45) than that in controls (26.60+7.19). In cases, African Americans (AA) had a significantly higher IR-induced gamma-H2AX level (32.17+6.76) than that in Caucasians (28.08+6.65), particularly in the younger age group (<50), never smokers, negative FH, and higher BMI (>25 kg/m2). In younger cases, a higher gamma-H2AX was observed in AA (p=0.042) compared to Caucasians (32.71+5.43 vs. 27.32+5.33). In never smokers, AA cases had a significantly higher level of IR-induced gamma-H2AX than Caucasians (32.70+5.77 vs. 27.58+6.41, p=0.03). In cases without FH, AA had a significantly higher level of IR-induced gamma-H2AX than Caucasians (32.38+6.90 vs. 28.02+7.09, p=0.044). In cases with a higher BMI, AA had a significantly higher level of IR-induced gamma-H2AX than Caucasians (33.36+5.94 vs. 26.93+6.00, p=0.001). Our results, although based on a relatively small group of subjects, indicate that DSBs response is significantly higher in AA breast cancer cases. Future larger studies are warranted to test whether this racial/ethnic difference in IR-induced gamma-H2AX levels contribute to breast cancer risk, tumor phenotypes, treatment response, and/or clinical outcome. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 4704.
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