Cellular responses to ionizing radiation damage.
OBJECTIVE
The purpose of this report is to provide current perspectives on studies of DNA damage and cell cycle response after ionizing radiation, and their applications in radiation oncology.


METHODS
Presentations at the Seventh Annual Radiation Oncology Workshop, held at the International Festival Institute at Round Top, TX, were summarized.


RESULTS
Eighteen speakers presented their current work covering a wide range of studies on cellular responses to ionizing radiation. These presentations and discussions form the framework of our report.


CONCLUSIONS
In response to ionizing radiation, cells immediately activate a series of biochemical pathways that promote cell survival while maintaining genetic integrity. The main cellular defense system against ionizing radiation exposure is composed of two distinct types of biochemical pathways, that is, the DNA damage cell cycle checkpoint pathways and the DNA repair pathways. The DNA damage checkpoint pathways are activated directly by DNA damage, while the repair pathways are constitutively active and are likely modulated by checkpoint signals. Discussions here emphasize that the ATM protein is a central component of the ionizing radiation-responsive pyramid and is essential for activating divergent molecular responses that involve transcriptional regulation, cell cycle arrest, and modulation of DNA repair. The relationship between homologous recombinational repair and nonhomologous end joining of double-strand breaks is also discussed.
Li
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Department of Experimental Radiation Oncology, The University of Texas M. D. Anderson Cancer Center, Houston, TX 77030, USA.
Story
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Legerski
R J
RJ
D000818:Animals; D064007:Ataxia Telangiectasia Mutated Proteins; D002453:Cell Cycle / Q000528:radiation effects*; D018797:Cell Cycle Proteins / Q000378:metabolism / Q000528:radiation effects; D002470:Cell Survival / Q000528:radiation effects; D004247:DNA / Q000528:radiation effects; D004249:DNA Damage; D004260:DNA Repair; D004268:DNA-Binding Proteins; D020022:Genetic Predisposition to Disease; D006801:Humans; D009369:Neoplasms / Q000378:metabolism / Q000532:radiotherapy; D017346:Protein Serine-Threonine Kinases / Q000378:metabolism / Q000528:radiation effects; D011832:Radiation Injuries / Q000378:metabolism / Q000503:physiopathology*; D011853:Radiobiology; D025521:Tumor Suppressor Proteins
D018797:Cell Cycle Proteins; D004268:DNA-Binding Proteins; D025521:Tumor Suppressor Proteins; D004247:DNA; C576324:ATM protein, human; D064007:Ataxia Telangiectasia Mutated Proteins; D017346:Protein Serine-Threonine Kinases