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- W4361239314 abstract "<div>Abstract<p>Germline mutations in <i>BRCA1</i> predispose carriers to a high incidence of breast and ovarian cancers. BRCA1 functions to maintain genomic stability through critical roles in DNA repair, cell-cycle arrest, and transcriptional control. A major question has been why BRCA1 loss or mutation leads to tumors mainly in estrogen-regulated tissues, given that BRCA1 has essential functions in all cell types. Here, we report that estrogen and estrogen metabolites can cause DNA double-strand breaks (DSB) in estrogen receptor-α–negative breast cells and that BRCA1 is required to repair these DSBs to prevent metabolite-induced genomic instability. We found that BRCA1 also regulates estrogen metabolism and metabolite-mediated DNA damage by repressing the transcription of estrogen-metabolizing enzymes, such as CYP1A1, in breast cells. Finally, we used a knock-in human cell model with a heterozygous <i>BRCA1</i> pathogenic mutation to show how BRCA1 haploinsufficiency affects these processes. Our findings provide pivotal new insights into why <i>BRCA1</i> mutation drives the formation of tumors in estrogen-regulated tissues, despite the general role of BRCA1 in DNA repair in all cell types. <i>Cancer Res; 74(10); 2773–84. ©2014 AACR</i>.</p></div>" @default.
- W4361239314 created "2023-03-31" @default.
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- W4361239314 date "2023-03-30" @default.
- W4361239314 modified "2023-09-25" @default.
- W4361239314 title "Data from BRCA1 Deficiency Exacerbates Estrogen-Induced DNA Damage and Genomic Instability" @default.
- W4361239314 doi "https://doi.org/10.1158/0008-5472.c.6505080" @default.
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