| Radiation induced non-targeted response: mechanism and potential clinical implications. | |
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MedLine Citation:
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PMID: 21143185 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Generations of students in radiation biology have been taught that heritable biological effects require direct damage to DNA. Radiation-induced non-targeted/bystander effects represent a paradigm shift in our understanding of the radiobiological effects of ionizing radiation in that extranuclear and extracellular effects may also contribute to the biological consequences of exposure to low doses of radiation. Although radiation induced bystander effects have been well documented in a variety of biological systems, including 3D human tissue samples and whole organisms, the mechanism is not known. There is recent evidence that the NF-κB-dependent gene expression of interleukin 8, interleukin 6, cyclooxygenase-2, tumor necrosis factor and interleukin 33 in directly irradiated cells produced the cytokines and prostaglandin E2 with autocrine/paracrine functions, which further activated signaling pathways and induced NF-κB-dependent gene expression in bystander cells. The observations that heritable DNA alterations can be propagated to cells many generations after radiation exposure and that bystander cells exhibit genomic instability in ways similar to directly hit cells indicate that the low dose radiation response is a complex interplay of various modulating factors. The potential implication of the non-targeted response in radiation induced secondary cancer is discussed. A better understanding of the mechanism of the non-targeted effects will be invaluable to assess its clinical relevance and ways in which the bystander phenomenon can be manipulated to increase therapeutic gain in radiotherapy. |
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Authors:
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Tom K Hei; Hongning Zhou; Yunfei Chai; Brian Ponnaiya; Vladimir N Ivanov |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Review |
Journal Detail:
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Title: Current molecular pharmacology Volume: 4 ISSN: 1874-4702 ISO Abbreviation: Curr Mol Pharmacol Publication Date: 2011 Jun |
Date Detail:
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Created Date: 2011-06-15 Completed Date: 2011-09-30 Revised Date: 2012-05-22 |
Medline Journal Info:
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Nlm Unique ID: 101467997 Medline TA: Curr Mol Pharmacol Country: United Arab Emirates |
Other Details:
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Languages: eng Pagination: 96-105 Citation Subset: IM |
Affiliation:
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Center for Radiological Research, Department of Radiation Oncology, Columbia University Medical Center, Vanderbilt Clinic, New York, USA. tkh1@columbia.edu |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Apoptosis / radiation effects Bystander Effect / radiation effects* DNA / radiation effects DNA Damage Gap Junctions / metabolism Gene Expression / radiation effects Humans Intercellular Signaling Peptides and Proteins / metabolism MAP Kinase Signaling System / radiation effects NF-kappa B / metabolism Radiation, Ionizing* Radiobiology Receptors, Growth Factor / metabolism |
| Grant Support | |
ID/Acronym/Agency:
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EB-002033/EB/NIBIB NIH HHS; ES09089/ES/NIEHS NIH HHS; P01-CA 49062/CA/NCI NIH HHS; P41 EB002033/EB/NIBIB NIH HHS; R01-ES 012888/ES/NIEHS NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Intercellular Signaling Peptides and Proteins; 0/NF-kappa B; 0/Receptors, Growth Factor; 9007-49-2/DNA |
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