ReviewNucleic acids research2021
Shaping the BRCAness mutational landscape by alternative double-strand break repair, replication stress and mitotic aberrancies.
Review in Nucleic acids research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
What it found
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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.
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Who cites it
40 citing papers in PubMed, 65 citations in OpenAlex.
- 53BP1-independent Shieldin-BRCA1 antagonism at replication-coupled double-strand breaks.Nature communications · 2026Article
- The role of Alu elements in causing BRCA1 structural variation and breast cancer susceptibility.Genes & genomics · 2026Review
- Dissecting the RAD51-BRC4 Interaction Landscape through Integrative Molecular Simulations and Experimental Biophysics.Journal of chemical information and modeling · 2025Article
- Mechanisms and genomic implications of break-induced replication.Nature structural & molecular biology · 2025Review
- Preserving centromere identity: right amounts of CENP-A at the right place and time.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2025Review
- Krüppel-like Factor 4-Deficient Cells Are Sensitive to Etoposide-Induced DNA Damage.Current issues in molecular biology · 2025Article
- The cardio-oncologic burden of breast cancer: molecular mechanisms and importance of preclinical models.Basic research in cardiology · 2025Review
- Translational and clinical comparison of whole genome and transcriptome to panel sequencing in precision oncology.NPJ precision oncology · 2025Article
- HDAC4 influences the DNA damage response and counteracts senescence by assembling with HDAC1/HDAC2 to control H2BK120 acetylation and homology-directed repair.Nucleic acids research · 2024Article
- The splicing factor CCAR1 regulates the Fanconi anemia/BRCA pathway.Molecular cell · 2024Article
- Microhomology-mediated repair machinery and its relationship with HPV-mediated oncogenesis.Journal of medical virology · 2024Review
- Inherited BRCA1 and RNF43 pathogenic variants in a familial colorectal cancer type X family.Familial cancer · 2024Article
- Human RAD52 stimulates the RAD51-mediated homology search.Life science alliance · 2024Article
- Low microsatellite instability: A distinct instability type in gastric cancer?Journal of cancer research and clinical oncology · 2023Article
- Mcl-1 deficiency in murine livers leads to nuclear polyploidisation and mitotic errors: Implications for hepatocellular carcinoma.JHEP reports : innovation in hepatology · 2023Article
- Mutational signature assignment heterogeneity is widespread and can be addressed by ensemble approaches.Briefings in bioinformatics · 2023Article
- CSB Regulates Pathway Choice in Response to DNA Replication Stress Induced by Camptothecin.International journal of molecular sciences · 2023Article
- Altered cytoplasmic and nuclear ADP-ribosylation levels analyzed with an improved ADP-ribose binder are a prognostic factor in renal cell carcinoma.The journal of pathology. Clinical research · 2023Article
- USP51/PD-L1/ITGB1-deployed juxtacrine interaction plays a cell-intrinsic role in promoting chemoresistant phenotypes in non-small cell lung cancer.Cancer communications (London, England) · 2023Article
- Transcriptionally regulated miR-26a-5p may act as BRCAness in Triple-Negative Breast Cancer.Breast cancer research : BCR · 2023Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tumours with mutations in the BRCA1/BRCA2 genes have impaired double-stranded DNA break repair, compromised replication fork protection and increased sensitivity to replication blocking agents, a phenotype collectively known as 'BRCAness'. Tumours with a BRCAness phenotype become dependent on alternative repair pathways that are error-prone and introduce specific patterns of somatic mutations across the genome. The increasing availability of next-generation sequencing data of tumour samples has enabled identification of distinct mutational signatures associated with BRCAness. These signatures reveal that alternative repair pathways, including Polymerase θ-mediated alternative end-joining and RAD52-mediated single strand annealing are active in BRCA1/2-deficient tumours, pointing towards potential therapeutic targets in these tumours. Additionally, insight into the mutations and consequences of unrepaired DNA lesions may also aid in the identification of BRCA-like tumours lacking BRCA1/BRCA2 gene inactivation. This is clinically relevant, as these tumours respond favourably to treatment with DNA-damaging agents, including PARP inhibitors or cisplatin, which have been successfully used to treat patients with BRCA1/2-defective tumours. In this review, we aim to provide insight in the origins of the mutational landscape associated with BRCAness by exploring the molecular biology of alternative DNA repair pathways, which may represent actionable therapeutic targets in in these cells.
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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.