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- W2485344984 abstract "PR-12 Women of African ancestry are more likely to develop ER-negative, PR-negative and HER2-negative basal-like breast cancers, with worse prognoses and lack of therapeutic targets (Polite and Olopade, 2005). The underlying biological mechanisms are still largely unknown. ER and its ligand estrogen play vital roles in the development, progression and treatment of breast cancer. A potential mechanism for hormone resistance is the acquired loss of ER gene expression at the transcriptional level during disease progression. Methylation of the CpG islands in the 59 regulatory region of the ER gene has been associated with loss of ER gene expression in ER-negative breast cancers (Lapidus RG et al., 1998). An increasing number of studies have also provided evidence linking disruption of the Fanconi anemia/BRCA cascade to breast cancer. BRCA1-mutated and promoter-methylated cancers are often of high grade and are ER-negative, suggesting that alterations of the BRCA1 or related pathways might contribute to some sporadic breast cancers (Wei M et al., 2005). Our objectives were to examine the methylation status and expression profiles of ER, correlate the findings with BRCA1 and FANCF methylation and map the critical CpGs for ER expression. In analyzing a subset of domestic samples, we found that the CpG islands in the 59 region of the ER gene are methylated in 59 of 120 (49.2%) primary breast cancers, including 45 of 59 ER-negative tumors (76.3%, P" @default.
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- W2485344984 date "2007-11-01" @default.
- W2485344984 modified "2023-09-22" @default.
- W2485344984 title "Estrogen receptor α (ER), BRCA1 and FANCF promoter methylation occur in distinct subsets of sporadic breast cancers" @default.
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