ArticleNucleic acids research2015
Cells deficient in base-excision repair reveal cancer hallmarks originating from adjustments to genetic instability.
Article in Nucleic acids research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 42 citations in OpenAlex.
- The Cellular Response to Oxidatively Induced DNA Damage and Polymorphism of Some DNA Repair Genes Associated with Clinicopathological Features of Bladder Cancer.Oxidative medicine and cellular longevity · 2016Trial
- Genetic Variants in BER Pathway Genes Confer Wilms Tumor Susceptibility: New Insights from an Eight-Center Case-Control Study in Chinese Children.Annals of surgical oncology · 2026Article
- Silencing Uracil-DNA glycosylase inhibits colorectal cancer progression.Cancer cell international · 2026Article
- Base excision repair within structure-forming repeat sequences and its impact on cancer and other diseases.NAR cancer · 2025Review
- Initiation of base excision repair is modulated by nucleosome occupancy modifying sequences.DNA repair · 2025Article
- A Review of Numerical Models of Radiation Injury and Repair Considering Subcellular Targets and the Extracellular Microenvironment.International journal of molecular sciences · 2024Review
- Deciphering Stromal Changes between Metastatic and Non-metastatic Canine Mammary Carcinomas.Journal of mammary gland biology and neoplasia · 2023Article
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- The emerging relationship between metabolism and DNA repair.Cell cycle (Georgetown, Tex.) · 2021Review
- Review
- Review
- Molecular homology between canine spontaneous oral squamous cell carcinomas and human head-and-neck squamous cell carcinomas reveals disease drivers and therapeutic vulnerabilities.Neoplasia (New York, N.Y.) · 2020Article
- Persistent DNA damage triggers activation of the integrated stress response to promote cell survival under nutrient restriction.BMC biology · 2020Article
- Oxidative DNA-protein crosslinks formed in mammalian cells by abasic site lyases involved in DNA repair.DNA repair · 2020Article
- Impairment of Base Excision Repair in Dermal Fibroblasts Isolated From Nevoid Basal Cell Carcinoma Patients.Frontiers in oncology · 2020Article
- Chlamydia trachomatis and human herpesvirus 6 infections in ovarian cancer-Casual or causal?PLoS pathogens · 2019Review
- A rapid, safe, and quantitative in vitro assay for measurement of uracil-DNA glycosylase activity.Journal of molecular medicine (Berlin, Germany) · 2019Article
- Article
- Multiple Molecular Targets Associated with Genomic Instability in Lung Cancer.International journal of genomics · 2019Review
- Mechanisms of resistance to a PI3K inhibitor in gastrointestinal stromal tumors: anCancer management and research · 2019Article
Corrections and comments
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Authors and funding
5 authors at 4 institutions in 2 countries.
Funding
Abstract
Genetic instability, provoked by exogenous mutagens, is well linked to initiation of cancer. However, even in unstressed cells, DNA undergoes a plethora of spontaneous alterations provoked by its inherent chemical instability and the intracellular milieu. Base excision repair (BER) is the major cellular pathway responsible for repair of these lesions, and as deficiency in BER activity results in DNA damage it has been proposed that it may trigger the development of sporadic cancers. Nevertheless, experimental evidence for this model remains inconsistent and elusive. Here, we performed a proteomic analysis of BER deficient human cells using stable isotope labelling with amino acids in cell culture (SILAC), and demonstrate that BER deficiency, which induces genetic instability, results in dramatic changes in gene expression, resembling changes found in many cancers. We observed profound alterations in tissue homeostasis, serine biosynthesis, and one-carbon- and amino acid metabolism, all of which have been identified as cancer cell 'hallmarks'. For the first time, this study describes gene expression changes characteristic for cells deficient in repair of endogenous DNA lesions by BER. These expression changes resemble those observed in cancer cells, suggesting that genetically unstable BER deficient cells may be a source of pre-cancerous 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.