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ROS and the DNA damage response in cancer
Open accessAbstract
Reactive oxygen species (ROS) are a group of short-lived, highly reactive, oxygen-containing molecules that can induce DNA damage and affect the DNA damage response (DDR). There is unequivocal pre-clinical and clinical evidence that ROS influence the genotoxic stress caused by chemotherapeutics agents and ionizing radiation. Recent studies have provided mechanistic insight into how ROS can also influence the cellular response to DNA damage caused by genotoxic therapy, especially in the context of Double Strand Breaks (DSBs). This has led to the clinical evaluation of agents modulating ROS in combination with genotoxic therapy for cancer, with mixed success so far. These studies point to context dependent outcomes with ROS modulator combinations with Chemotherapy and radiotherapy, indicating a need for additional pre-clinical research in the field. In this review, we discuss the current knowledge on the effect of ROS in the DNA damage response, and its clinical relevance.
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“The most frequently occurring mutations in the tumor suppressor gene TP53 in lung cancer are Guanine → Thymine and Guanine → Adenine transversions (Srinivas et al. 2019; Gibbons et al. 2014).”
From Reactive Oxygen Species, Toxicity, Oxidative Stress, and Antioxidants: Chronic Diseases and Aging (2023) · cites this paper as Srinivas et al. 2019
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“Consistent with these findings, chronically elevated ROS, which often occurs in SLE, affects several aspects of DNA damage response and may lead to accumulation of such genomic changes (57,58).”
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Ammonia detoxification promotes CD8+ T cell memory development by urea and citrulline cycles
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Metadata
- Authors
- Srinivas, U. S., Tan, B. W. Q., Vellayappan, B. A., & Jeyasekharan, A. D.
- Affiliations
- National University of Singapore (SG)
- National University Hospital (SG)
- Corresponding author
- Jeyasekharan, Anand D.
- Venue
- Redox Biology
- Publisher
- Elsevier BV
- Published
- 2019-07
- Volume
- 25
- Pages
- 101084
- ISSN
- 2213-2317 (ISSN-L)
- PMC
- PMC6859528
- OpenAlex
- W2906120852
- Cited by
- 2,144
- References
- 153
- Citations by year
- 2026: 217 · 2025: 396 · 2024: 392 · 2023: 381 · 2022: 335 · 2021: 262 · 2020: 132 · 2019: 26
- FWCI
- 10.28
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Redox Biology (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- National University of Singapore (submittedVersion, cc-by-nc-nd)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Medical Research Council (NMRC/TA/0052/2016)
- AstraZeneca
- Ministry of Health -Singapore
- Meso Scale Diagnostics
- National Research Foundation Singapore
- Ministry of Education - Singapore
- Janssen Pharmaceuticals
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Health Sciences › Medicine › Radiology, Nuclear Medicine and Imaging › Effects of Radiation Exposure
- Keywords
- reactive oxygen species, DNA damage response, cancer, DNA double-strand breaks, genotoxic stress, anticancer agents, ionizing radiation, radiosensitizers, combination therapy, oxidative DNA damage
- MeSH terms
- Animals, DNA Damage, DNA Repair, Humans, Neoplasms, Tumor Suppressor Protein p53, Apoptosis, Reactive Oxygen Species
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