BRCA1 induces DNA damage recognition factors and enhances nucleotide excision repair
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Updated: Sep 29, 2026

Assessment of Global DNA Double-Strand End Resection using BrdU-DNA Labeling coupled with Cell Cycle Discrimination Imaging
Published on: April 28, 2021
Anne-Renee Hartman1, James M Ford
1Department of Internal Medicine (Oncology), Stanford University Medical Center, Stanford, California 94305-5151, USA.
Abstract:
Inheritance of a mutation in the gene BRCA1 confers on women a 50-85% lifetime risk of developing breast cancer. Mutations in the TP53 tumor-suppressor gene are found in 70-80% of BRCA1-mutated breast cancer but only 30% of those with wildtype BRCA1 (ref. 3). The p53 protein regulates nucleotide excision repair (NER) through transcriptional regulation of genes involved in the recognition of adducts in genomic DNA. Loss of p53 function results in deficient global genomic repair (GGR), a subset of NER that targets and removes lesions from the whole genome. Here we show that BRCA1 specifically enhances the GGR pathway, independent of p53, and can induce p53-independent expression of the NER genes XPC, DDB2, and GADD45. Defects in the NER pathway in BRCA1-associated breast cancers may be causal in tumor development, suggesting a multistep model of carcinogenesis.
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