ReviewClinical and translational medicine2016
Choices have consequences: the nexus between DNA repair pathways and genomic instability in cancer.
Review in Clinical and translational medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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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.
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Who cites it
47 citing papers in PubMed, 96 citations in OpenAlex.
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- Genetic analysis of PALB2 gene WD40 domain in canine mammary tumour patients.Veterinary medicine and science · 2024Article
- BCL11B promotes T-cell acute lymphoblastic leukaemia cell survival via the XRCC5/C11ORF21 axis.Clinical and translational medicine · 2024Article
- Real-world TRAE association between niraparib and platinum-based chemotherapy.Frontiers in oncology · 2024Article
- RAD51 is a poor prognostic marker and a potential therapeutic target for oral squamous cell carcinoma.Cancer cell international · 2023Article
- The mechanism and clinical application of DNA damage repair inhibitors combined with immune checkpoint inhibitors in the treatment of urologic cancer.Frontiers in cell and developmental biology · 2023Review
- Roles of DNA damage repair and precise targeted therapy in renal cancer (Review).Oncology reports · 2022Article
- Review
- STAT3-induced NCK1 elevation promotes migration of triple-negative breast cancer cells via regulating ERK1/2 signaling.Molecular biology reports · 2022Article
- Pak2 reduction induces a failure of early embryonic development in mice.Reproductive biology and endocrinology : RB&E · 2021Article
- Therapeutic potential of targeting membrane-spanning proteoglycan SDC4 in hepatocellular carcinoma.Cell death & disease · 2021Article
- FZD2 promotes TGF-β-induced epithelial-to-mesenchymal transition in breast cancer via activating notch signaling pathway.Cancer cell international · 2021Article
- RPA-mediated recruitment of Bre1 couples histone H2B ubiquitination to DNA replication and repair.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Suppression of Tumorigenicity 5 Ameliorates Tumor Characteristics of Invasive Breast Cancer CellsFrontiers in oncology · 2021Article
- Prediction of the VeriStrat test in first-line therapy of pemetrexed-based regimens for advanced lung adenocarcinoma patients.Cancer cell international · 2020Article
- PARP inhibitors and epithelial ovarian cancer: Molecular mechanisms, clinical development and future prospective.Oncology letters · 2020Review
- Aberrant methylation of WD-repeat protein 41 contributes to tumour progression in triple-negative breast cancer.Journal of cellular and molecular medicine · 2020Article
- Hallmarks of Splicing Defects in Cancer: Clinical Applications in the Era of Personalized Medicine.Cancers · 2020Review
- Prognostic impact of glioblastoma stem cell markers OLIG2 and CCND2.Cancer medicine · 2020Article
- Observational
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe genome is under constant assault from a multitude of sources that can lead to the formation of DNA double-stand breaks (DSBs). DSBs are cytotoxic lesions, which if left unrepaired could lead to genomic instability, cancer and even cell death. However, erroneous repair of DSBs can lead to chromosomal rearrangements and loss of heterozygosity, which in turn can also cause cancer and cell death. Hence, although the repair of DSBs is crucial for the maintenance of genome integrity the process of repair need to be well regulated and closely monitored. MAIN BODY: The two most commonly used pathways to repair DSBs in higher eukaryotes include non-homologous end joining (NHEJ) and homologous recombination (HR). NHEJ is considered to be error-prone, intrinsically mutagenic quick fix remedy to seal together the broken DNA ends and restart replication. In contrast, HR is a high-fidelity process that has been very well conserved from phage to humans. Here we review HR and its sub-pathways. We discuss what factors determine the sub pathway choice including etiology of the DSB, chromatin structure at the break site, processing of the DSBs and the mechanisms regulating the sub-pathway choice. We also elaborate on the potential of targeting HR genes for cancer therapy and anticancer strategies.
conclusionThe DNA repair field is a vibrant one, and the stage is ripe for scrutinizing the potential treatment efficacy and future clinical applications of the pharmacological inhibitors of HR enzymes as mono- or combinatorial therapy regimes.
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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.