Use of the γ-H2AX assay to monitor DNA damage and repair in cancer research

被引:376
作者
Ivashkevich, Alesia [1 ]
Redon, Christophe E. [2 ]
Nakamura, Asako J. [3 ]
Martin, Roger F. [1 ]
Martin, Olga A. [1 ,4 ]
机构
[1] Peter MacCallum Canc Ctr, Lab Mol Radiat Biol, Melbourne, Vic, Australia
[2] NCI, Mol Pharmacol Lab, Ctr Canc Res, Bethesda, MD 20892 USA
[3] Osaka Med Coll, Dept Anat & Cell Biol, Osaka, Japan
[4] Peter MacCallum Canc Ctr, Dept Radiat Oncol, Melbourne, Vic, Australia
基金
美国国家卫生研究院;
关键词
gamma-H2AX; Double-strand breaks (DSBs); Translational research; Chemotherapy; Radiation therapy; Radiosensitivity; Biodosimetry; Imaging; DOUBLE-STRAND BREAKS; HISTONE H2AX PHOSPHORYLATION; MEASURE CHROMOSOMAL RADIOSENSITIVITY; PERIPHERAL-BLOOD LYMPHOCYTES; AUTOMATED BIODOSIMETRY TOOL; CORONARY CT ANGIOGRAPHY; IN-VIVO FORMATION; RADIATION SENSITIVITY; BIOLOGICAL DOSIMETRY; IONIZING-RADIATION;
D O I
10.1016/j.canlet.2011.12.025
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Formation of gamma-H2AX in response to DNA double stranded breaks (DSBs) provides the basis for a sensitive assay of DNA damage in human biopsies. The review focuses on the application of gamma-H2AX-based methods to translational studies to monitor the clinical response to DNA targeted therapies such as some forms of chemotherapy, external beam radiotherapy, radionuclide therapy or combinations thereof. The escalating attention on radiation biodosimetry has also highlighted the potential of the assay including renewed efforts to assess the radiosensitivity of prospective radiotherapy patients. Finally the gamma-H2AX response has been suggested as a basis for an in vivo imaging modality. (c) 2011 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:123 / 133
页数:11
相关论文
共 142 条
[81]   Radiation induced DNA damage and damage repair in human tumor and fibroblast cell lines assessed by histone H2AX phosphorylation [J].
Mahrhofer, H ;
Bürger, S ;
Oppitz, U ;
Flentje, M ;
Djuzenova, CS .
INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS, 2006, 64 (02) :573-580
[82]   Kinetics and dose-response of residual 53BP1/γ-H2AX foci:: Co-localization, relationship with DSB repair and clonogenic survival [J].
Markova, E. ;
Schultz, N. ;
Belyaev, I. Y. .
INTERNATIONAL JOURNAL OF RADIATION BIOLOGY, 2007, 83 (05) :319-329
[83]   INDUCTION OF DOUBLE-STRANDED BREAKS IN DNA BY BINDING WITH AN I-125-LABELED ACRIDINE [J].
MARTIN, RF .
INTERNATIONAL JOURNAL OF RADIATION BIOLOGY, 1977, 32 (05) :491-497
[84]   USE OF AN I-125-LABELED DNA LIGAND TO PROBE DNA-STRUCTURE [J].
MARTIN, RF ;
HOLMES, N .
NATURE, 1983, 302 (5907) :452-454
[85]   RANGE OF RADIOCHEMICAL DAMAGE TO DNA WITH DECAY OF I125 [J].
MARTIN, RF ;
HASELTINE, WA .
SCIENCE, 1981, 213 (4510) :896-898
[86]   Whole cell-ELISA to measure the γH2AX response of six aneugens and eight DNA-damaging chemicals [J].
Matsuzaki, Kaori ;
Harada, Asako ;
Takeiri, Akira ;
Tanaka, Kenji ;
Mishima, Masayuki .
MUTATION RESEARCH-GENETIC TOXICOLOGY AND ENVIRONMENTAL MUTAGENESIS, 2010, 700 (1-2) :71-79
[87]   Prediction of clonogenic cell survival curves based on the number of residual DNA double strand breaks measured by γH2AX staining [J].
Menegakis, Apostolos ;
Yaromina, Ala ;
Eicheler, Wolfgang ;
Doerfler, Annegret ;
Beuthien-Baumann, Bettina ;
Thames, Howard D. ;
Baumann, Michael ;
Krause, Mechthild .
INTERNATIONAL JOURNAL OF RADIATION BIOLOGY, 2009, 85 (11) :1032-1041
[88]   The complexity of phosphorylated H2AX foci formation and DNA repair assembly at DNA double-strand breaks [J].
Nakamura, Asako J. ;
Rao, V. Ashutosh ;
Pommier, Yves ;
Bonner, William M. .
CELL CYCLE, 2010, 9 (02) :389-397
[89]   DNA damage foci in mitosis are devoid of 53BP1 [J].
Nelson, Glyn ;
Buhmann, Matthias ;
von Zglinicki, Thomas .
CELL CYCLE, 2009, 8 (20) :3379-3383
[90]   Accumulation of oxidatively induced clustered DNA lesions in human tumor tissues [J].
Nowsheen, Somaira ;
Wukovich, Rebecca L. ;
Aziz, Khaled ;
Kalogerinis, Peter T. ;
Richardson, Christopher C. ;
Panayiotidis, Milialis I. ;
Bonner, William M. ;
Sedelnikova, Olga A. ;
Georgakilas, Alexandros G. .
MUTATION RESEARCH-GENETIC TOXICOLOGY AND ENVIRONMENTAL MUTAGENESIS, 2009, 674 (1-2) :131-136