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Biomolecules 2016, 6(3), 32; doi:10.3390/biom6030032

Turning on the Radio: Epigenetic Inhibitors as Potential Radiopriming Agents

1
EpicentRx, Inc, Mountain View, CA 94040, USA
2
Department of Radiation Oncology, University of Michigan, Ann Arbor, MI 48109, USA
3
Department of Bioengineering UCSD, La Jolla, San Diego, CA 92093, USA
4
KU Medical Center, Kansas University, Kansas City, KS 66160, USA
5
Murtha Cancer Center, Walter Reed National Military Medical Center, Bethesda, MD 20889, USA
6
CFLS Data, Mountain View, CA 94040, USA
7
Department of Physiology, Helsinki University, 00100 Helsinki, Finland
8
Moores Cancer Center, UCSD, La Jolla, CA 92093, USA
9
InterWest Partners, Menlo Park, CA 94025, USA
*
Author to whom correspondence should be addressed.
Academic Editors: Gerda Egger and Melanie R. Hassler
Received: 29 April 2016 / Revised: 9 June 2016 / Accepted: 27 June 2016 / Published: 4 July 2016
(This article belongs to the Special Issue DNA Methylation and Cancer)
View Full-Text   |   Download PDF [1175 KB, uploaded 6 July 2016]   |  

Abstract

First introduced during the late 1800s, radiation therapy is fundamental to the treatment of cancer. In developed countries, approximately 60% of all patients receive radiation therapy (also known as the sixty percenters), which makes radioresistance in cancer an important and, to date, unsolved, clinical problem. Unfortunately, the therapeutic refractoriness of solid tumors is the rule not the exception, and the ubiquity of resistance also extends to standard chemotherapy, molecularly targeted therapy and immunotherapy. Based on extrapolation from recent clinical inroads with epigenetic agents to prime refractory tumors for maximum sensitivity to concurrent or subsequent therapies, the radioresistant phenotype is potentially reversible, since aberrant epigenetic mechanisms are critical contributors to the evolution of resistant subpopulations of malignant cells. Within the framework of a syllogism, this review explores the emerging link between epigenetics and the development of radioresistance and makes the case that a strategy of pre- or co-treatment with epigenetic agents has the potential to, not only derepress inappropriately silenced genes, but also increase reactive oxygen species production, resulting in the restoration of radiosensitivity. View Full-Text
Keywords: radiotherapy; radiosensitization; epigenetics; DNA methyltransferase inhibition; histone deacetylase inhibition; epigenetic priming; reactive oxygen species (ROS) radiotherapy; radiosensitization; epigenetics; DNA methyltransferase inhibition; histone deacetylase inhibition; epigenetic priming; reactive oxygen species (ROS)
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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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MDPI and ACS Style

Oronsky, B.; Scicinski, J.; Kim, M.M.; Cabrales, P.; Salacz, M.E.; Carter, C.A.; Oronsky, N.; Lybeck, H.; Lybeck, M.; Larson, C.; Reid, T.R.; Oronsky, A. Turning on the Radio: Epigenetic Inhibitors as Potential Radiopriming Agents. Biomolecules 2016, 6, 32.

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