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J Neurooncol. 2017 Sep;134(3):513-521. doi: 10.1007/s11060-017-2427-7. Epub 2017 Jul 31.

GBM radiosensitizers: dead in the water…or just the beginning?

Author information

1
Department of Therapeutic Radiology, Yale School of Medicine, New Haven, CT, 06520, USA. ranjit.bindra@yale.edu.
2
Institute of Cancer Sciences & Beatson West of Scotland Cancer Centre, University of Glasgow, Glasgow, UK.
3
Department of Radiation Oncology, University of Pennsylvania, School of Medicine, Philadelphia, PA, 19081, USA.
4
Radiation Oncology Department, Duke University School of Medicine, Durham, NC, USA.

Abstract

The finding that most GBMs recur either near or within the primary site after radiotherapy has fueled great interest in the development of radiosensitizers to enhance local control. Unfortunately, decades of clinical trials testing a wide range of novel therapeutic approaches have failed to yield any clinically viable radiosensitizers. However, many of  the previous radiosensitizing strategies were not based on clear pre-clinical evidence, and in many cases blood-barrier penetration was not considered. Furthermore, DNA repair inhibitors have only recenly arrived in the clinic, and likely represent potent agents for glioma radiosensitization. Here, we present recent progress in the use of small molecule DNA damage response inhibitors as GBM radiosensitizers. In addition, we discuss the latest progress in targeting hypoxia and oxidative stress for GBM radiosensitization.

KEYWORDS:

DNA damage response; DNA repair; Hypoxia; Radiosensitizer

PMID:
28762004
DOI:
10.1007/s11060-017-2427-7
[Indexed for MEDLINE]

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