<b>Background:</b> Breast cancer bone metastasis (BCBM)-specific genes have been reported without considering biological differences based on estrogen receptor (ER) status.
<b>Background:</b> Smoking is a possible risk factor for breast cancer and has been linked to increased risk of estrogen receptor-positive (ER<sup>+</sup>) disease in some epidemiologic studies.
<b>Background:</b> Triple-negative breast cancer (TNBC) is a breast cancer that tests negative forestrogen receptor (ER), progesterone receptors, and human epidermal growth factor receptors 2 (HER2).
<b>Conclusion:</b><i>CYP2D6*10</i> pharmacogenetic-guided selective estrogen receptor modulator can be a cost-effective strategy in the Chinese patients with hormone receptor-positive breast cancer.
<b>Methods:</b> A Markov chain Monte Carlo simulation model estimated the costs and benefits of 3 extended endocrine strategies in a hypothetical cohort of premenopausal women with ER-positive early breast cancer: (1) no further treatment; (2) tamoxifen for 5 years (extended tamoxifen); or (3) OA/AI for 5 years.
<b>Principal conclusions:</b> Tumor-associated MUC1 is a very important biomarker for breast cancer next to the traditional markers estrogen receptor (ER), progesterone receptor (PR) and HER/2-neu.
<b>Purpose:</b> Although high glucocorticoid receptor (GR) expression in early-stage estrogen receptor (ER)-negative breast cancer is associated with shortened relapse-free survival (RFS), how associated GR transcriptional activity contributes to aggressive breast cancer behavior is not well understood.
<b>Purpose:</b> Antiendocrine therapy remains the most effective treatment for estrogen receptor-positive (ER<sup>+</sup>) breast cancer, but development of resistance is a major clinical complication.
<b>Purpose:</b> As estrogen receptor-positive (ER<sup>+</sup>) breast cancer in <i>BRCA1</i> mutation carriers arises at an older age with less aggressive tumor characteristics than ER-negative (ER<sup>-</sup>) <i>BRCA1</i>-mutated breast cancer, it has been suggested that these tumors are "sporadic" and not <i>BRCA1</i> driven.
<b>Purpose:</b> Hyperactivation of AKT is common and associated with endocrine resistance in estrogen receptor-positive (ER<sup>+</sup>) breast cancer.
<b>Purpose:</b> In breast cancer models, combination epigenetic therapy with a DNA methyltransferase inhibitor and a histone deacetylase inhibitor led to reexpression of genes encoding important therapeutic targets, including the estrogen receptor (ER).
<b>Purpose:</b> Steroidal androgens suppress androgen receptor and estrogen receptor positive (AR/ER<sup>+</sup>) breast cancer cells and were used to treat breast cancer, eliciting favorable response.
<sup>18</sup>F-alfatide II may have superiority to <sup>18</sup>F-FDG in detecting breast cancer with strongly positive estrogen receptor expression and negative HER-2 expression.
<sup>18</sup>F-FES and <sup>18</sup>F-FDG PET/CT imaging in vivo revealed that ERα expression in DIS-ZR751 treated with fulvestrant, and tumor activity in DIS-ZR751 treated with combination drugs decreased as early as 7 days after treatment.
(a) ERα(+) breast cancer cells dysfunctional for TP53 which proliferate irrespective of low estrogen and chemical MEK inhibition are likely to increase metabolic consumption becoming increasingly susceptible to 3-BrPA; (b) targeting the pyruvate pathway may improve response to endocrine therapy in ERα(+) breast cancer with p53 dysfunction.
-Mauro, L., Naimo, G. D., Gelsomino, L., Malivindi, R., Bruno, L., Pellegrino, M., Tarallo, R., Memoli, D., Weisz, A., Panno, M. L., Andò, S. Uncoupling effects of estrogen receptor α on LKB1/AMPK interaction upon adiponectin exposure in breast cancer.
1,25(OH)2D3 also induced amphiregulin mRNA in estrogen receptor-positive and -negative human breast cancer cell lines, but not in LNCaP human prostate cancer cells.