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      Effects of hyperthermia on DNA repair pathways: one treatment to inhibit them all

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          Abstract

          The currently available arsenal of anticancer modalities includes many DNA damaging agents that can kill malignant cells. However, efficient DNA repair mechanisms protect both healthy and cancer cells against the effects of treatment and contribute to the development of drug resistance. Therefore, anti-cancer treatments based on inflicting DNA damage can benefit from inhibition of DNA repair. Hyperthermia – treatment at elevated temperature – considerably affects DNA repair, among other cellular processes, and can thus sensitize (cancer) cells to DNA damaging agents. This effect has been known and clinically applied for many decades, but how heat inhibits DNA repair and which pathways are targeted has not been fully elucidated. In this review we attempt to summarize the known effects of hyperthermia on DNA repair pathways relevant in clinical treatment of cancer. Furthermore, we outline the relationships between the effects of heat on DNA repair and sensitization of cells to various DNA damaging agents.

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          The cellular and molecular basis of hyperthermia.

          B Hildebrandt (2002)
          In oncology, the term 'hyperthermia' refers to the treatment of malignant diseases by administering heat in various ways. Hyperthermia is usually applied as an adjunct to an already established treatment modality (especially radiotherapy and chemotherapy), where tumor temperatures in the range of 40-43 degrees C are aspired. In several clinical phase-III trials, an improvement of both local control and survival rates have been demonstrated by adding local/regional hyperthermia to radiotherapy in patients with locally advanced or recurrent superficial and pelvic tumors. In addition, interstitial hyperthermia, hyperthermic chemoperfusion, and whole-body hyperthermia (WBH) are under clinical investigation, and some positive comparative trials have already been completed. In parallel to clinical research, several aspects of heat action have been examined in numerous pre-clinical studies since the 1970s. However, an unequivocal identification of the mechanisms leading to favorable clinical results of hyperthermia have not yet been identified for various reasons. This manuscript deals with discussions concerning the direct cytotoxic effect of heat, heat-induced alterations of the tumor microenvironment, synergism of heat in conjunction with radiation and drugs, as well as, the presumed cellular effects of hyperthermia including the expression of heat-shock proteins (HSP), induction and regulation of apoptosis, signal transduction, and modulation of drug resistance by hyperthermia.
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            Repair of strand breaks by homologous recombination.

            Maria Jasin, Rodney Rothstein (2013)
            In this review, we discuss the repair of DNA double-strand breaks (DSBs) using a homologous DNA sequence (i.e., homologous recombination [HR]), focusing mainly on yeast and mammals. We provide a historical context for the current view of HR and describe how DSBs are processed during HR as well as interactions with other DSB repair pathways. We discuss the enzymology of the process, followed by studies on DSB repair in living cells. Whenever possible, we cite both original articles and reviews to aid the reader for further studies.
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              53BP1 nuclear bodies form around DNA lesions generated by mitotic transmission of chromosomes under replication stress.

              Claudia Lukas, Velibor Savic, Simon Bekker-Jensen … (2011)
              Completion of genome duplication is challenged by structural and topological barriers that impede progression of replication forks. Although this can seriously undermine genome integrity, the fate of DNA with unresolved replication intermediates is not known. Here, we show that mild replication stress increases the frequency of chromosomal lesions that are transmitted to daughter cells. Throughout G1, these lesions are sequestered in nuclear compartments marked by p53-binding protein 1 (53BP1) and other chromatin-associated genome caretakers. We show that the number of such 53BP1 nuclear bodies increases after genetic ablation of BLM, a DNA helicase associated with dissolution of entangled DNA. Conversely, 53BP1 nuclear bodies are partially suppressed by knocking down SMC2, a condensin subunit required for mechanical stability of mitotic chromosomes. Finally, we provide evidence that 53BP1 nuclear bodies shield chromosomal fragile sites sequestered in these compartments against erosion. Together, these data indicate that restoration of DNA or chromatin integrity at loci prone to replication problems requires mitotic transmission to the next cell generations. © 2011 Macmillan Publishers Limited. All rights reserved.
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                Author and article information

                Contributors
                Arlene L. Oei: a.l.oei@amc.uva.nl
                Lianne E. M. Vriend: l.e.vriend@amc.uva.nl
                Johannes Crezee: h.crezee@amc.uva.nl
                Nicolaas A. P. Franken: n.a.franken@amc.uva.nl
                Przemek M. Krawczyk: +31 20 5668746 , p.krawczyk@amc.uva.nl
                Journal
                Journal ID (nlm-ta): Radiat Oncol
                Journal ID (iso-abbrev): Radiat Oncol
                Title: Radiation Oncology (London, England)
                Publisher: BioMed Central (London )
                ISSN (Electronic): 1748-717X
                Publication date (Electronic): 7 August 2015
                Publication date PMC-release: 7 August 2015
                Publication date Collection: 2015
                Volume: 10
                Electronic Location Identifier: 165
                Affiliations
                [ ]Laboratory for Experimental Oncology and Radiobiology (LEXOR), Center for Experimental and Molecular Medicine, Academic Medical Center, University of Amsterdam, 1105 AZ Amsterdam, The Netherlands
                [ ]Van Leeuwenhoek Centre for Advanced Microscopy (LCAM)-AMC, Department of Cell Biology and Histology, Academic Medical Center, University of Amsterdam, Meibergdreef 15, 1105 AZ Amsterdam, The Netherlands
                [ ]Department of Radiotherapy, Academic Medical Center, University of Amsterdam, 1105 AZ Amsterdam, The Netherlands
                Article
                Publisher ID: 462
                DOI: 10.1186/s13014-015-0462-0
                PMC ID: 4554295
                PubMed ID: 26245485
                SO-VID: aba536bc-1406-4248-81c2-a76afa491f0d
                Copyright © © Oei et al. 2015
                License:

                Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                History
                Date received : 8 May 2015
                Date accepted : 13 July 2015
                Categories
                Subject: Research
                Custom metadata
                issue-copyright-statement © The Author(s) 2015

                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: hyperthermia,dna damage,dna repair,chemotherapy
                Data availability:
                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: hyperthermia, dna damage, dna repair, chemotherapy

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