The DOI matches its Crossref record; 96 of the 97 references it cites were found in a registry or an index.
DNA double-strand break repair pathway choice and cancer
Open accessAbstract
Since DNA double-strand breaks (DSBs) contribute to the genomic instability that drives cancer development, DSB repair pathways serve as important mechanisms for tumor suppression. Thus, genetic lesions, such as BRCA1 and BRCA2 mutations, that disrupt DSB repair are often associated with cancer susceptibility. In addition, recent evidence suggests that DSB "mis-repair", in which DSBs are resolved by an inappropriate repair pathway, can also promote genomic instability and presumably tumorigenesis. This notion has gained currency from recent cancer genome sequencing studies which have uncovered numerous chromosomal rearrangements harboring pathological DNA repair signatures. In this perspective, we discuss the factors that regulate DSB repair pathway choice and their consequences for genome stability and cancer.
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“As a result, chromosomal rearrangements are accumulated in cancer cells, eventually leading to cell death [220].”
From Combination strategies with PD-1/PD-L1 blockade: current advances and future directions (2022) · cites this paper as [220]
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Repair Pathway Choices and Consequences at the Double-Strand Break
Ceccaldi, R., Rondinelli, B., & D’Andrea, A. D. (2016) · Trends in Cell Biology · doi:10.1016/j.tcb.2015.07.009 · Cited by 1,499
Combination strategies with PD-1/PD-L1 blockade: current advances and future directions
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Essential Roles for Polymerase θ-Mediated End Joining in the Repair of Chromosome Breaks
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Metadata
- Authors
- Aparicio, T., Baer, R., & Gautier, J.
- Affiliations
- Columbia University Irving Medical Center (US)
- Corresponding author
- Gautier, Jean
- ORCID
- Gautier, Jean
- Venue
- DNA Repair
- Publisher
- Elsevier BV
- Published
- 2014-07
- Volume
- 19
- Pages
- 169-175
- ISSN
- 1568-7856 (ISSN-L)
- 1568-7864
- PMC
- PMC4051845
- OpenAlex
- W2090854519
- Cited by
- 347
- References
- 97
- Citations by year
- 2026: 13 · 2025: 20 · 2024: 27 · 2023: 22 · 2022: 40 · 2021: 36 · 2020: 34 · 2019: 33 · 2018: 39 · 2017: 22 · 2016: 31 · 2015: 26 · 2014: 4
- FWCI
- 11.35
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- DNA repair (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Cancer Institute (P01CA174653, R01CA092245, R01CA167826)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Health Sciences › Medicine › Oncology › PARP inhibition in cancer therapy
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › BRCA gene mutations in cancer
- Keywords
- DNA double-strand break repair, repair pathway choice, genomic instability, cancer susceptibility, BRCA1, BRCA2, chromosomal rearrangements, tumor suppression, carcinogenesis
- MeSH terms
- Tumor Suppressor p53-Binding Protein 1, DNA Repair, Humans, Neoplasms, Recombination, Genetic, Signal Transduction, BRCA1 Protein, Genomic Instability, Intracellular Signaling Peptides and Proteins, DNA Breaks, Double-Stranded, DNA End-Joining Repair, Carcinogenesis
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