Journal article
Utilizing Superoxide Dismutase Mimetics to Enhance Radiation Therapy Response While Protecting Normal Tissues
Seminars in radiation oncology, Vol.29(1), pp.72-80
01/2019
DOI: 10.1016/j.semradonc.2018.10.005
PMCID: PMC6310053
PMID: 30573187
Abstract
Symptomatic normal tissue injury is a common side effect following definitive therapeutic radiation and chemotherapy treatment for a variety of malignancies. These cancer therapy related toxicities may occur acutely during treatment resulting in reduced or missed therapy agent administration or after the completion of therapy resulting in significant chronic morbidities that significantly diminish patient quality of life. Radiation and chemotherapy induce the formation of reactive oxygen species (ROS) both in normal tissues and tumor cells. One type of ROS common to both chemotherapy and radiation therapy is the formation of superoxide (O
). Fortunately, due to metabolic differences between cancer and normal cell metabolism, as well as improved targeting techniques, ROS generation following radiation and chemotherapy is generally greater in cancer cells compared to normal tissues. However, the levels of ROS generated in normal tissues are capable of inducing significant toxicity. Thus, several groups are focusing on metabolism-based approaches to mitigate normal tissue effects occurring both during and following cancer therapy. This review will summarize the most current preclinical and clinical data available demonstrating the efficacy of small molecule, superoxide dismutase mimetics in minimizing radiation and chemotherapy-induced normal tissue injury, resulting in enhanced patient outcomes.
Details
- Title: Subtitle
- Utilizing Superoxide Dismutase Mimetics to Enhance Radiation Therapy Response While Protecting Normal Tissues
- Creators
- Kranti A Mapuskar - From the Free Radical and Radiation Biology Program, Holden Comprehensive Cancer Center, University of Iowa Carver College of Medicine, Iowa City, IA.; Department of Radiation Oncology, Holden Comprehensive Cancer Center, University of Iowa Carver College of Medicine, Iowa City, IACarryn M Anderson - Department of Radiation Oncology, Holden Comprehensive Cancer Center, University of Iowa Carver College of Medicine, Iowa City, IADouglas R Spitz - From the Free Radical and Radiation Biology Program, Holden Comprehensive Cancer Center, University of Iowa Carver College of Medicine, Iowa City, IA.; Department of Radiation Oncology, Holden Comprehensive Cancer Center, University of Iowa Carver College of Medicine, Iowa City, IAInes Batinic-Haberle - Department of Radiation Oncology, Duke University School of Medicine, Durham, NCBryan G Allen - From the Free Radical and Radiation Biology Program, Holden Comprehensive Cancer Center, University of Iowa Carver College of Medicine, Iowa City, IA.; Department of Radiation Oncology, Holden Comprehensive Cancer Center, University of Iowa Carver College of Medicine, Iowa City, IA.. Electronic address: bryan-allen@uiowa.eduRebecca E Oberley-Deegan - Department of Biochemistry and Molecular Biology, College of Medicine, Nebraska Medical Center, Omaha, NE.. Electronic address: Becky.Deegan@UNMC.edu
- Resource Type
- Journal article
- Publication Details
- Seminars in radiation oncology, Vol.29(1), pp.72-80
- DOI
- 10.1016/j.semradonc.2018.10.005
- PMID
- 30573187
- PMCID
- PMC6310053
- NLM abbreviation
- Semin Radiat Oncol
- ISSN
- 1053-4296
- eISSN
- 1532-9461
- Publisher
- United States
- Grant note
- P30 CA014236 / NCI NIH HHS P01 CA217797 / NCI NIH HHS T32 GM007337 / NIGMS NIH HHS R01 CA178888 / NCI NIH HHS R01 CA182804 / NCI NIH HHS P20 GM103480 / NIGMS NIH HHS P30 CA036727 / NCI NIH HHS P30 CA086862 / NCI NIH HHS
- Language
- English
- Date published
- 01/2019
- Academic Unit
- Pathology; Radiation Oncology
- Record Identifier
- 9984047621602771
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