TY - JOUR
T1 - Cellular responses to ionizing radiation damage
AU - Li, L.
AU - Story, M.
AU - Legerski, R. J.
N1 - Funding Information:
This meeting was supported in part by the Stringer Chair (James D. Cox, Division of Radiation Oncology, M. D. Anderson Cancer Center), United Energy Resources, Inc., Professorship of Cancer Research (Luka Milas, Department of Experimental Radiation Oncology, M .D. Anderson Cancer Center), and the Helen Buchanan and Stanley Joseph Seeger Research Professorship (Howard D. Thames, Department of Biomathematics, M. D. Anderson Cancer Center).
PY - 2001
Y1 - 2001
N2 - Purpose: 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 and Materials: 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. Conclusion: 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.
AB - Purpose: 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 and Materials: 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. Conclusion: 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.
KW - Cell cycle checkpoints
KW - DNA repair
KW - Ionizing radiation
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U2 - 10.1016/S0360-3016(00)01524-8
DO - 10.1016/S0360-3016(00)01524-8
M3 - Article
C2 - 11240259
AN - SCOPUS:0035869707
SN - 0360-3016
VL - 49
SP - 1157
EP - 1162
JO - International Journal of Radiation Oncology Biology Physics
JF - International Journal of Radiation Oncology Biology Physics
IS - 4
ER -