Recent progress in defining mechanisms and potential targets for prevention of normal tissue injury after radiation therapy.
The ability to optimize treatments for cancer on the basis of relative risks for normal tissue injury has important implications in oncology, because higher doses of radiation might, in some diseases, improve both local control and survival. To achieve this goal, a thorough understanding of the molecular mechanisms responsible for radiation-induced toxicity will be essential. Recent research has demonstrated that ionizing radiation triggers a series of genetic and molecular events, which might lead to chronic persistent alterations in the microenvironment and an aberrant wound-healing response. Disrupted epithelial-stromal cell communication might also be important. With the application of a better understanding of fundamental biology to clinical practice, new approaches to treating and preventing normal tissue injury can focus on correcting these disturbed molecular processes.
Anscher
Mitchell S
MS
Department of Radiation Oncology, Duke University Medical Center, Durham, NC 27710, USA. anscher@radonc.duke.edu
Chen
Liguang
L
Rabbani
Zahid
Z
Kang
Song
S
Larrier
Nicole
N
Huang
Hong
H
Samulski
Thaddeus V
TV
Dewhirst
Mark W
MW
Brizel
David M
DM
Folz
Rodney J
RJ
Vujaskovic
Zeljko
Z
D015687:Cell Hypoxia; D016207:Cytokines / Q000378:metabolism; D004730:Endothelium, Vascular / Q000528:radiation effects; D006801:Humans; D009369:Neoplasms / Q000532:radiotherapy*; D011832:Radiation Injuries / Q000378:metabolism / Q000517:prevention & control*; D011836:Radiation Tolerance; D017382:Reactive Oxygen Species / Q000378:metabolism; D013482:Superoxide Dismutase / Q000378:metabolism; D016212:Transforming Growth Factor beta / Q000378:metabolism
D016207:Cytokines; D017382:Reactive Oxygen Species; D016212:Transforming Growth Factor beta; D013482:Superoxide Dismutase