title: Modifying normal tissue damage postirradiation. Report of a workshop sponsored by the Radiation Research Program, National Cancer Institute, Bethesda, Maryland, September 6-8, 2000.
abstract: Late effects that develop in normal tissues adjacent to the tumor site in the months to years after radiotherapy can reduce the quality of life of cancer survivors. They can be dose-limiting and debilitating or life-threatening. There is now evidence that some late effects may be preventable or partially reversible. A workshop, "Modifying Normal Tissue Damage Postirradiation", was sponsored by the Radiation Research Program of the National Cancer Institute to identify the current status of and research needs and opportunities in this area. Mechanistic, genetic and physiological studies of the development of late effects are needed and will provide a rational basis for development of treatments. Interdisciplinary teams will be needed to carry out this research, including pathologists, physiologists, geneticists, molecular biologists, experts in functional imaging, wound healing, burn injury, molecular biology, and medical oncology, in addition to radiation biologists, physicists and oncologists. The participants emphasized the need for developing and choosing appropriate models, and for radiation dose-response studies to determine whether interventions remain effective at the radiation doses used clinically. Both preclinical and clinical studies require long-term follow-up, and easier-to-use, more objective clinical scoring systems must be developed and standardized. New developments in biomedical imaging should provide useful tools in all these endeavors. The ultimate goals are to improve the quality of life and efficacy of treatment for cancer patients treated with radiotherapy.
authors.affiliation: Radiation Research Program, National Cancer Institute, 6130 Executive Boulevard, 6010, Bethesda, Maryland 20892-7440, USA. stoneh@exchange.nih.gov
authors.forename: Helen B
authors.initials: HB
authors.lastname: Stone
authors.forename: William H
authors.initials: WH
authors.lastname: McBride
authors.forename: C Norman
authors.initials: CN
authors.lastname: Coleman
mesh_terms: D000818:Animals; D015687:Cell Hypoxia; D018925:Chemokines / Q000378:metabolism; D016207:Cytokines / Q000378:metabolism / Q000627:therapeutic use; D003952:Diagnostic Imaging; D010450:Endopeptidases / Q000502:physiology; D005109:Extracellular Matrix / Q000502:physiology; D006133:Growth Substances / Q000502:physiology / Q000627:therapeutic use; D006801:Humans; D006931:Hyperbaric Oxygenation; D051379:Mice; D008809:Mice, Inbred C3H; D008810:Mice, Inbred C57BL; D023421:Models, Animal; D009369:Neoplasms / Q000150:complications / Q000532:radiotherapy; D011323:Primates; D011519:Proto-Oncogenes / Q000528:radiation effects; D011788:Quality of Life; D011832:Radiation Injuries / Q000473:pathology / Q000503:physiopathology / Q000517:prevention & control* / Q000628:therapy; D011833:Radiation Injuries, Experimental / Q000209:etiology / Q000473:pathology / Q000628:therapy; D011836:Radiation Tolerance; D011878:Radiotherapy / Q000009:adverse effects*; D051381:Rats; D017978:Receptors, Growth Factor / Q000502:physiology; D012084:Renin-Angiotensin System / Q000187:drug effects / Q000502:physiology; D012720:Severity of Illness Index; D013552:Swine; D013997:Time Factors; D016212:Transforming Growth Factor beta / Q000502:physiology
chemical_list: D018925:Chemokines; D016207:Cytokines; D006133:Growth Substances; D017978:Receptors, Growth Factor; D016212:Transforming Growth Factor beta; D010450:Endopeptidases