ReviewCancer letters2012
Pathways for repairing and tolerating the spectrum of oxidative DNA lesions.
Review in Cancer letters, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
76 citing papers in PubMed, 135 citations in OpenAlex.
- Radiotherapy and cytokines: A systems view of immunotherapy and toxicity (Review).International journal of molecular medicine · 2026Review
- Saline-Alkaline Stress Suppresses Soybean Germination and Early Seedling Growth via Induction of DNA Damage in Roots.Plants (Basel, Switzerland) · 2026Article
- Mutagenic Potentials of DNA Interstrand Cross-Links Induced by 7,8-Dihydro-8-Oxoadenine.Molecules (Basel, Switzerland) · 2026Article
- Fyn inhibition by TAE684: A synergistic strategy to suppress melanoma and reverse vemurafenib resistance.Cell death & disease · 2025Article
- Oxidative Stress, Parity History, and Remnant Follicles in the Aged Ovary: Insights on Ovarian Cancer Risk and Protection.Antioxidants (Basel, Switzerland) · 2025Review
- Piezoelectric sterilization techniques: from innovations to applications.Frontiers in chemistry · 2025Review
- Transcription-coupled DNA repair protects genome stability upon oxidative stress-derived DNA strand breaks.FEBS letters · 2025Review
- SMAD4 Limits PARP1 dependent DNA Repair to Render Pancreatic Cancer Cells Sensitive to Radiotherapy.Cell death & disease · 2024Article
- SARS-CoV-2 and the DNA damage response.The Journal of general virology · 2023Review
- A Dietary Antioxidant Formulation Ameliorates DNA Damage Caused by γ-Irradiation in Normal Human Bronchial Epithelial Cells In Vitro.Antioxidants (Basel, Switzerland) · 2022Article
- Mitochondrial DNA Instability in Mammalian Cells.Antioxidants & redox signaling · 2022Review
- AOP report: Development of an adverse outcome pathway for oxidative DNA damage leading to mutations and chromosomal aberrations.Environmental and molecular mutagenesis · 2022Article
- Colon fibroblasts from Pirc rats (F344/NTac-ApcInternational journal of cancer · 2022Article
- A matter of delicate balance: Loss and gain of Cockayne syndrome proteins in premature aging and cancer.Frontiers in aging · 2022Review
- Estimation of the Level of Abasic Sites in Plant mRNA Using Aldehyde Reactive Probe.Methods in molecular biology (Clifton, N.J.) · 2022Article
- Review
- Activation of DNA Damage Tolerance Pathways May Improve Immunotherapy of Mesothelioma.Cancers · 2021Article
- Review
- The Cockayne syndrome group A and B proteins are part of a ubiquitin-proteasome degradation complex regulating cell division.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- The Key Characteristics of Carcinogens: Relationship to the Hallmarks of Cancer, Relevant Biomarkers, and Assays to Measure Them.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2020Article
16 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Reactive oxygen species (ROS) arise from both endogenous and exogenous sources. These reactive molecules possess the ability to damage both the DNA nucleobases and the sugar phosphate backbone, leading to a wide spectrum of lesions, including non-bulky (8-oxoguanine and formamidopyrimidine) and bulky (cyclopurine and etheno adducts) base modifications, abasic sites, non-conventional single-strand breaks, protein-DNA adducts, and intra/interstrand DNA crosslinks. Unrepaired oxidative DNA damage can result in bypass mutagenesis during genome copying or gene expression, or blockage of the essential cellular processes of DNA replication or transcription. Such outcomes underlie numerous pathologies, including, but not limited to, carcinogenesis and neurodegeneration, as well as the aging process. Cells have adapted and evolved defense systems against the deleterious effects of ROS, and specifically devote a number of cellular DNA repair and tolerance pathways to combat oxidative DNA damage. Defects in these protective pathways trigger hereditary human diseases that exhibit increased cancer incidence, developmental defects, neurological abnormalities, and/or premature aging. We review herein classic and atypical oxidative DNA lesions, outcomes of encountering these damages during DNA replication and transcription, and the consequences of losing the ability to repair the different forms of oxidative DNA damage. We particularly focus on the hereditary human diseases Xeroderma Pigmentosum, Cockayne Syndrome and Fanconi Anemia, which may involve defects in the efficient repair of oxidative modifications to chromosomal DNA.
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What OpenQuestion holds
Registered trials
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.