ArticleNucleic acids research2004
DNA double strand break repair in human bladder cancer is error prone and involves microhomology-associated end-joining.
Article in Nucleic acids research, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.
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Who cites it
69 citing papers in PubMed, 119 citations in OpenAlex.
- CRISPR/Cas9-Based Genome Editing: Understanding Differences in DNA Repair Pathways, Profiles, and Outcomes.International journal of molecular sciences · 2026Review
- Overexpression of the ERG oncogene in prostate cancer identifies candidates for PARP inhibitor-based radiosensitization.The Journal of clinical investigation · 2026Article
- Replication stress increases de novo CNVs across the malaria parasite genome.Nucleic acids research · 2026Article
- Replication stress increases de novo CNVs across the malaria parasite genome.bioRxiv : the preprint server for biology · 2025Article
- Contribution of MRE11, RAD50, and NBS1 Genotypes to Bladder Cancer Susceptibility.Cancer genomics & proteomics · 2025Article
- Combined inhibition of RAD51 and CHK1 causes synergistic toxicity in cisplatin resistant cancer cells by triggering replication fork collapse.International journal of cancer · 2025Article
- Pesticides and Bladder Cancer: Mechanisms Leading to Anti-Cancer Drug Chemoresistance and New Chemosensitization Strategies.International journal of molecular sciences · 2023Review
- DNA Polymerase Theta Plays a Critical Role in Pancreatic Cancer Development and Metastasis.Cancers · 2022Article
- Synthetic Lethality Targeting Polθ.Genes · 2022Review
- Does the Pachytene Checkpoint, a Feature of Meiosis, Filter Out Mistakes in Double-Strand DNA Break Repair and as a side-Effect Strongly Promote Adaptive Speciation?Integrative organismal biology (Oxford, England) · 2022Article
- A study of transposable element-associated structural variations (TASVs) using a de novo-assembled Korean genome.Experimental & molecular medicine · 2021Article
- Loss of TGFβ signaling increases alternative end-joining DNA repair that sensitizes to genotoxic therapies across cancer types.Science translational medicine · 2021Article
- Regulation of Error-Prone DNA Double-Strand Break Repair and Its Impact on Genome Evolution.Cells · 2020Review
- Establishment of a Transformation CoupledFrontiers in oncology · 2020Article
- What Does the History of Research on the Repair of DNA Double-Strand Breaks Tell Us?-A Comprehensive Review of Human Radiosensitivity.International journal of molecular sciences · 2019Review
- Human papillomavirus 16 promotes microhomology-mediated end-joining.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Rewiring E2F1 with classical NHEJ via APLF suppression promotes bladder cancer invasiveness.Journal of experimental & clinical cancer research : CR · 2019Article
- Microhomology-mediated end joining: Good, bad and ugly.Mutation research · 2018Review
- Loss of PTEN-assisted G2/M checkpoint impedes homologous recombination repair and enhances radio-curability and PARP inhibitor treatment response in prostate cancer.Scientific reports · 2018Article
- RadiosensitizationMolecular cancer therapeutics · 2018Article
9 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In human cells DNA double strand breaks (DSBs) can be repaired by the non-homologous end-joining (NHEJ) pathway. In a background of NHEJ deficiency, DSBs with mismatched ends can be joined by an error-prone mechanism involving joining between regions of nucleotide microhomology. The majority of joins formed from a DSB with partially incompatible 3' overhangs by cell-free extracts from human glioblastoma (MO59K) and urothelial (NHU) cell lines were accurate and produced by the overlap/fill-in of mismatched termini by NHEJ. However, repair of DSBs by extracts using tissue from four high-grade bladder carcinomas resulted in no accurate join formation. Junctions were formed by the non-random deletion of terminal nucleotides and showed a preference for annealing at a microhomology of 8 nt buried within the DNA substrate; this process was not dependent on functional Ku70, DNA-PK or XRCC4. Junctions were repaired in the same manner in MO59K extracts in which accurate NHEJ was inactivated by inhibition of Ku70 or DNA-PK(cs). These data indicate that bladder tumour extracts are unable to perform accurate NHEJ such that error-prone joining predominates. Therefore, in high-grade tumours mismatched DSBs are repaired by a highly mutagenic, microhomology-mediated, alternative end-joining pathway, a process that may contribute to genomic instability observed in bladder cancer.
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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.