ArticlePloS one2019
Defective base excision repair in the response to DNA damaging agents in triple negative breast cancer.
Article in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
25 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.
- DNA Repair Genes as Drug Candidates for Early Breast Cancer Onset in Latin America: A Systematic Review.International journal of molecular sciences · 2021Pooled it
- DNA damage response pathway alterations in urothelial carcinoma: a road to precision oncology or a dead-end street?The oncologist · 2026Review
- Short-term consumption of the modified standard American diet perturbed the metabolic balance and altered DNA damage in MMTV-PyMT transgenic mice.Breast cancer research : BCR · 2025Article
- Signaling pathway dysregulation in breast cancer.Oncotarget · 2025Review
- XRCC1 Polymorphisms p.Arg194Trp, p.Arg280His, and p.Arg399Gln, Polycyclic Aromatic Hydrocarbons, and Infertility: A Case-Control and In Silico Study.Biochemical genetics · 2025Article
- Review
- Article
- Novel Techniques for Mapping DNA Damage and Repair in the Brain.International journal of molecular sciences · 2024Review
- MANCR lncRNA Modulates Cell-Cycle Progression and Metastasis by Cis-Regulation of NuclearMolecular and cellular biology · 2024Article
- Article
- XMR: an explainable multimodal neural network for drug response prediction.Frontiers in bioinformatics · 2023Article
- Hypoxia: syndicating triple negative breast cancer against various therapeutic regimens.Frontiers in oncology · 2023Review
- Simultaneous Short- and Long-Patch Base Excision Repair (BER) Assay in Live Mammalian Cells.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Unboxing the molecular modalities of mutagens in cancer.Environmental science and pollution research international · 2022Review
- Glucose Increases STAT3 Activation, Promoting Sustained XRCC1 Expression and Increasing DNA Repair.International journal of molecular sciences · 2022Article
- Article
- Human Variation in DNA Repair, Immune Function, and Cancer Risk.Frontiers in immunology · 2022Review
- Investigation of the Effects and Mechanisms of Anticancer Action of a Ru(II)-Arene Iminophosphorane Compound in Triple Negative Breast Cancer Cells.ChemMedChem · 2021Article
- Large-scale preparation of fluorescence multiplex host cell reactivation (FM-HCR) reporters.Nature protocols · 2021Article
- Cytoprotective Effect of Vitamin D on Doxorubicin-Induced Cardiac Toxicity in Triple Negative Breast Cancer.International journal of molecular sciences · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
DNA repair defects have been increasingly focused on as therapeutic targets. In hormone-positive breast cancer, XRCC1-deficient tumors have been identified and proposed as targets for combination therapies that damage DNA and inhibit DNA repair pathways. XRCC1 is a scaffold protein that functions in base excision repair (BER) by mediating essential interactions between DNA glycosylases, AP endonuclease, poly(ADP-ribose) polymerase 1, DNA polymerase β (POL β), and DNA ligases. Loss of XRCC1 confers BER defects and hypersensitivity to DNA damaging agents. BER defects have not been evaluated in triple negative breast cancers (TNBC), for which new therapeutic targets and therapies are needed. To evaluate the potential of XRCC1 as an indicator of BER defects in TNBC, we examined XRCC1 expression in the TCGA database and its expression and localization in TNBC cell lines. The TCGA database revealed high XRCC1 expression in TNBC tumors and TNBC cell lines show variable, but mostly high expression of XRCC1. XRCC1 localized outside of the nucleus in some TNBC cell lines, altering their ability to repair base lesions and single-strand breaks. Subcellular localization of POL β also varied and did not correlate with XRCC1 localization. Basal levels of DNA damage correlated with observed changes in XRCC1 expression, localization, and measure repair capacity. The results confirmed that XRCC1 expression changes indicate DNA repair capacity changes but emphasize that basal DNA damage levels along with protein localization are better indicators of DNA repair defects. Given the observed over-expression of XRCC1 in TNBC preclinical models and tumors, XRCC1 expression levels should be assessed when evaluating treatment responses of TNBC preclinical model cells.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.