Cited by 2,144Redox biology and oxidative stressDNA Repair MechanismsEffects of Radiation Exposure

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ROS and the DNA damage response in cancer

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Srinivas, Upadhyayula Sai, Tan, Bryce W.Q., Vellayappan, Balamurugan A., Jeyasekharan, Anand D.·2019·Redox Biology

DOI 10.1016/j.redox.2018.101084PMC PMC6859528

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Abstract

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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“It has been observed Ionizing radiation from radiation therapy induces DNA damage through both ionization breaks, and, notably, DBSs, with the latter being of utmost importance [141,142].”
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“The role of ROS in normal and cancer-associated signalling have been studied extensively over the last couple of decades [27], revealing multiple mechanisms underpinning their cancer associated effects, including the modulation of cell signalling [28], oxidative DNA damage [29], promoting genomic instability [30], and…”
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“High concentrations of ROS directly induce deoxyribonucleic acid (DNA) damage, contributing to aging[14].”
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Catalase Overexpression Drives an Aggressive Phenotype in Glioblastoma
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“There is unequivocal pre-clinical and clinical evidence that ROS influence the genotoxic stress caused by ionizing radiation [40].”
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“As the main cause of cellular oxidative stress, ROS can damage DNA and cause accumulation of carcinogenic alterations, eventually initiating tumor pathogenesis (Srinivas et al., 2019).”
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“ROS contributes a dual role to the development of disease that function in cells as signaling molecules and unavoidable toxic byproducts of aerobic metabolism (14, 15).”
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“In the present study, AFB1-induced DNA damage resulted from the elevation of ROS which can directly oxidize nucleoside bases, leading to G-T or G-A transversions as Srinivas et al. reported [56].”
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“Unrepaired oxidative DNA damage, such as DNA base lesions and single strand breaks (SSBs), may collide with replication forks during DNA repair and/or transcription leading to DNA replication stress and the formation of lethal DNA double-strand breaks (DSBs) to compromise cell survival (Markkanen, 2017; Srinivas et al…”
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“Moreover, ROS are well known as DDR inducers (Srinivas et al. 2019).”
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BackgroundInfluential
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Background
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“According to some studies, ROS has a certain therapeutic effect on TNBC [17].”
Background

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.
ORCID: Vellayappan, Balamurugan A.
Jeyasekharan, Anand D.
Venue: Redox Biology
Publisher: Elsevier BV
Published: 2019-07
Volume: 25
Pages: 101084
ISSN: 2213-2317 (ISSN-L)
DOI: 10.1016/j.redox.2018.101084
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: cc-by
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/legal/tdmrep-license (tdm)
creativecommons.org/licenses/by/4.0/ (vor)
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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