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B‐cell translocation gene 2 ( BTG 2), a gene suppressed in a subset of aggressive breast cancer, is repressed by estrogen.  BTG 2 inhibits the expression of  HER  ligands and promotes  AKT  activation, which plays an essential role in the tamoxifen resistance of estrogen receptor ( ER )‐positive breast cancer. To determine if  BTG 2 expression modifies tamoxifen efficacy, a cohort of 60 patients treated with adjuvant tamoxifen monotherapy was analyzed. We found that increased  BTG 2 expression showed better clinical survival and was the only independent prognostic factor for disease‐free survival (hazard ratio, 0.691; 95% confidence interval, 0.495–0.963;  P  =   0.029). Tamoxifen suppressed the human epidermal growth factor receptor 2 ( HER 2)‐Akt signaling in  BTG 2 expressing  ER ‐positive breast cancer cells with a correlated increase in sensitivity, whereas  BTG 2 knockdown abrogated this sensitivity. Consistent with this observation, tamoxifen significantly suppressed the growth ratio, tumor weight and Ki‐67 expression in  BTG 2 expressing breast cancer xenografts in mice. These studies demonstrate that  BTG 2 is a significant factor in tamoxifen response, acting through modification of  AKT  activation in  ER ‐positive/ HER 2‐negative breast cancer.

Loss of B ‐cell translocation gene 2 expression in estrogen receptor‐positive breast cancer predicts tamoxifen resistance