Systems biology perspectives on the carcinogenic potential of radiation [electronic resource]

• Ngôn ngữ: eng
• Ký hiệu phân loại: 576.8 Evolution
• Thông tin xuất bản: Washington, D.C. : Oak Ridge, Tenn. : United States. Dept. of Energy. Office of Science ; Distributed by the Office of Scientific and Technical Information, U.S. Dept. of Energy, 2014
• Mô tả vật lý: Size: p. i145-i154 : , digital, PDF file.
• Bộ sưu tập: Metadata
• ID: 261415
• Chủ đề: 1. 59 basic biological sciences; 2. 60 applied life sciences; 3. 63 radiation, thermal, and other environ. pollutant effects on living orgs. and biol. mat; 4. Breast cancer; 5. Et al; 6. Heavy ion radiation; 7. Ionizing radiation; 8. Life sciences & biomedicine - other topics; 9. Modeling; 10. Oncology; 11. Radiology, nuclear medicine & medical imaging

Tóm tắt

 This review focuses on recent experimental and modeling studies that attempt to define the physiological context in which high linear energy transfer (LET) radiation increases epithelial cancer risk and the efficiency with which it does so. Radiation carcinogenesis is a two-compartment problem: ionizing radiation can alter genomic sequence as a result of damage due to targeted effects (TE) from the interaction of energy and DNA
  it can also alter phenotype and multicellular interactions that contribute to cancer by poorly understood nontargeted effects (NTE). Rather than being secondary to DNA damage and mutations that can initiate cancer, radiation NTE create the critical context in which to promote cancer. Systems biology modeling using comprehensive experimental data that integrates different levels of biological organization and time-scales is a means of identifying the key processes underlying the carcinogenic potential of high-LET radiation. We hypothesize that inflammation is a key process, and thus cancer susceptibility will depend on specific genetic predisposition to the type and duration of this response. Systems genetics using novel mouse models can be used to identify such determinants of susceptibility to cancer in radiation sensitive tissues following high-LET radiation. Improved understanding of radiation carcinogenesis achieved by defining the relative contribution of NTE carcinogenic effects and identifying the genetic determinants of the high-LET cancer susceptibility will help reduce uncertainties in radiation risk assessment.