Redox Biology· 2018Q1· Review
ROS and the DNA damage response in cancer
- 2,113citations
- Q1SCImago
- 2018year
Short summary
Reactive oxygen species (ROS) influence the cellular response to DNA damage, particularly double-strand breaks (DSBs), with implications for cancer therapy.
AI-generated from the title and abstract; the full text is not read.
Key points
- ROS can induce DNA damage and influence the DNA damage response (DDR).
- ROS affect the cellular response to DNA damage caused by genotoxic therapies, including chemotherapy and ionizing radiation.
- Mechanistic insights reveal ROS's role in cellular responses to double-strand breaks (DSBs).
- Clinical trials combining ROS modulators with genotoxic therapy show mixed results, suggesting context-dependent outcomes.
AI-generated from the title and abstract; the full text is not read.
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.
The authors' abstract, as published at the source. Redox Biology, 2018 · DOI ↗
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Field: Radiology, Nuclear Medicine and Imaging
Radiology, Nuclear Medicine and ImagingMedicine