期刊
CLINICAL ONCOLOGY
卷 26, 期 5, 页码 257-265出版社
ELSEVIER SCIENCE LONDON
DOI: 10.1016/j.clon.2014.01.009
关键词
ATR inhibition; checkpoint inhibition; Chk1 inhibition; radiosensitisation
类别
资金
- Head and Neck CR UK Programme Grant (CRUK) [A13407]
- NIHR RM/ICR Biomedical Research Centre
- Cancer Research UK [S_1458] Funding Source: researchfish
- National Institute for Health Research [ACF-2011-22-001] Funding Source: researchfish
Despite tremendous advances in radiotherapy techniques, allowing dose escalation to tumour tissues and sparing of organs at risk, cure rates from radiotherapy or chemoradiotherapy remain suboptimal for most cancers. In tandem with our growing understanding of tumour biology, we are beginning to appreciate that targeting the molecular response to radiation-induced DNA damage holds great promise for selective tumour radiosensitisation. In particular, approaches that inhibit cell cycle checkpoint controls offer a means of exploiting molecular differences between tumour and normal cells, thereby inducing so-called cancer-specific synthetic lethality. In this overview, we discuss cellular responses to radiation-induced damage and discuss the potential of using G2/M cell cycle checkpoint inhibitors as a means of enhancing tumour control rates. (C) 2014 The Royal College of Radiologists. Published by Elsevier Ltd. All rights reserved.
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