Future strategies for mitigation and treatment of chronic radiation-induced normal tissue injury. Semin Radiat Oncol 2007 Apr;17(2):141-8
Date
03/31/2007Pubmed ID
17395044DOI
10.1016/j.semradonc.2006.11.010Scopus ID
2-s2.0-33947512453 (requires institutional sign-in at Scopus site) 94 CitationsAbstract
Until the mid-1990s, radiation-induced normal-tissue injury was generally assumed to be solely caused by the delayed mitotic death of parenchymal or vascular cells, and these injuries were held to be progressive and untreatable. From this assumption, it followed that postirradiation interventions would be unlikely to reduce either the incidence or the severity of radiation-induced normal tissue injury. It is now clear that parenchymal and vascular cells are active participants in the response to radiation injury, an observation that allows for the possibility of pharmacologic mitigation and/or treatment of these injuries. Mitigation or treatment of chronic radiation injuries has now been experimentally shown in multiple organ systems (eg, lung, kidney, and brain), with different pharmacologic agents (eg, angiotensin-converting enzyme inhibitors, pentoxifylline, and superoxide dismutase mimetics) and with seemingly different mechanisms (eg, suppression of the renin-angiotensin system and suppression of chronic oxidative stress). Unfortunately, the mechanistic basis for most of the experimental successes has not been established, and assessment of the utility of these agents for clinical use has been slow. Clinical development of pharmacologic approaches to mitigation or treatment of chronic radiation injuries could lead to significant improvement in survival and quality of life for radiotherapy patients and for victims of radiation accidents or nuclear terrorism.
Author List
Moulder JE, Cohen EPMESH terms used to index this publication - Major topics in bold
HumansOxidative Stress
Radiation Injuries
Radiation Protection
Radiation-Protective Agents
Radioactive Hazard Release
Radiotherapy
Renin-Angiotensin System
