Assessing the likelihood of severe side effects in radiotherapy

被引:25
作者
Löbrich, M [1 ]
Kiefer, J
机构
[1] Univ Saarland, D-66421 Homburg, Germany
[2] Univ Giessen, Strahlenzentrum, Giessen, Germany
关键词
DNA double-strand breaks; ionizing radiation; gamma-H2AX analysis; radiosensitivity; radiotherapy;
D O I
10.1002/ijc.21782
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Ionizing radiation is a powerful tool to treat cancer. The curing effect is mainly based on the efficiency of ionizing radiation to kill the cancer cells and it is believed that DNA double-strand breaks (DSBs) represent the most significant genetic lesion introduced by radiation that causes cell killing. One limitation in radiotherapy is the unavoidable damage delivered to the normal, noncancer cells that can give rise to side effects. The ultimate goal in treatment planning is to maximize cell killing in the tumor by minimizing damage induction in the normal tissue surrounding the tumor. The biological response to the induction of DSBs is largely affected by DSB repair processes and it has, therefore, been a long-standing goal to determine a patient's DSB repair capacity to "individualize" treatment planning. A recently developed DSB repair assay that allows the assessment of patients' repair capacity under in vivo conditions may provide a new approach to predict individuals' responses to radiotherapy and may be able to contribute to improvements in treatment planning. (c) 2006 Wiley-Liss, Inc.
引用
收藏
页码:2652 / 2656
页数:5
相关论文
共 48 条
[1]  
Alapetite C, 1999, INT J CANCER, V83, P83, DOI 10.1002/(SICI)1097-0215(19990924)83:1<83::AID-IJC16>3.3.CO
[2]  
2-#
[3]  
Banáth JP, 2003, CANCER RES, V63, P4347
[4]   Relationship between in vitro chromosomal radiosensitivity of peripheral blood lymphocytes and the expression of normal tissue damage following radiotherapy for breast cancer [J].
Barber, JBP ;
Burrill, W ;
Spreadborough, AR ;
Levine, E ;
Warren, C ;
Kiltie, AE ;
Roberts, SA ;
Scott, D .
RADIOTHERAPY AND ONCOLOGY, 2000, 55 (02) :179-186
[5]   Increased ionizing radiation sensitivity and genomic instability in the absence of histone H2AX [J].
Bassing, CH ;
Chua, KF ;
Sekiguchi, J ;
Suh, H ;
Whitlow, SR ;
Fleming, JC ;
Monroe, BC ;
Ciccone, DN ;
Yan, C ;
Vlasakova, K ;
Livingston, DM ;
Ferguson, DO ;
Scully, R ;
Alt, FW .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2002, 99 (12) :8173-8178
[6]   Indicators of late normal tissue response after radiotherapy for head and neck cancer:: fibroblasts, lymphocytes, genetics, DNA repair, and chromosome aberrations [J].
Borgmann, K ;
Röper, B ;
Abd El-Awady, R ;
Brackrock, S ;
Bigalke, M ;
Dörk, T ;
Alberti, W ;
Dikomey, E ;
Dahm-Daphi, J .
RADIOTHERAPY AND ONCOLOGY, 2002, 64 (02) :141-152
[7]  
Burma S, 2001, J BIOL CHEM, V276, P42462, DOI 10.1074/jbc.C100466200
[8]  
Burnet NG, 1998, INT J CANCER, V79, P606, DOI 10.1002/(SICI)1097-0215(19981218)79:6<606::AID-IJC9>3.0.CO
[9]  
2-Y
[10]   Histone H2AX phosphorylation is dispensable for the initial recognition of DNA breaks [J].
Celeste, A ;
Fernandez-Capetillo, O ;
Kruhlak, MJ ;
Pilch, DR ;
Staudt, DW ;
Lee, A ;
Bonner, RF ;
Bonner, WM ;
Nussenzweig, A .
NATURE CELL BIOLOGY, 2003, 5 (07) :675-U51