What is it about?
Despite currently available concept, BRCA mutation is an imbalanced defect, crudely inhibiting the upregulation of estrogen receptor (ER) expression and liganded transcriptional activity, whereas ER-repressor functions become predominant. Compensatory high estrogen synthesis may upregulate the interplay between ERs and defective BRCA protein and restores the DNA repairing processes. BRCA-mutation carrier women may apparently be healthy or exhibit clinical signs of deficient estrogen signaling in spite of hyperestrogenism.
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Why is it important?
In BRCA-mutation carriers, defective estrogen signaling is associated with decreased genome stability and induces tumor development with conspicuous specificity for female organs having cyclic proliferative activity, such as the breast, endometrium and ovary.
Read the Original
This page is a summary of: DNA stabilization by the upregulation of estrogen signaling in BRCA gene mutation carriers, Drug Design Development and Therapy, May 2015, Taylor & Francis,
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BRCA1 and Estrogen Receptor α Expression Regulation in Breast Cancer Cells
The obtained results demonstrate a relationship between BRCA1 and steroid hormones signal transduction pathways in breast cancer cells and point out to the importance of complex BRCA1 and ERα expression regulation mechanisms studies including epigenetic gene expression regulation.
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