Advances in the biological responses to radiation-induced DNA damage: A selection of papers from the Joint 43rd European Radiation Research Society (ERRS) and 20th German Society for Biological Radiation Research (GBS) Annual Meetings

A special issue of Cancers (ISSN 2072-6694).

Deadline for manuscript submissions: closed (31 December 2017) | Viewed by 19231

Special Issue Editors

Institute of Medical Radiation Biology, University of Duisburg-Essen, Medical School, Hufeland Str. 55, 45122 Essen, Germany
Interests: DNA double-strand breaks and their processing in the development of cancer and cellular responses to ionizing radiation
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Experimental Biophysics, Kirchhoff-Institute for Physics, University of Heidelberg, Im Neuenheimer Feld 227, 69120 Heidelberg, Germany
Interests: genom-architecture on the micro- and nano-scale during tumor genesis and after ionizing radiation exposure; nano-probes for DNA; DNA patterning; protein arrangements on the nano-scale in cell membranes
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Institute of Cell Biology (Cancer Research), University Hospital Essen, Virchowstrasse 173, 45122 Essen, Germany
Interests: intrinsic and microenvironment-mediated radiation resistance; cell and tissue responses to ionizing radiation; stress-induced metabolic reprogramming; biomarkers for radiosensitivity; combinatorial treatments for tumor radiosensitization and normal tissue protection
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Radiation Biophysics Laboratory, Department of Physics, University of Naples Federico II, Complesso Universitario di Monte Sant’Angelo, Via Cinthia, 80126 Naples, Italy
Interests: radiation-induced chromosome aberrations; DNA repair; hadrontherapy; radiosensitization and radioprotection
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The Special Issue of Cancers will consist of selected papers from the “Joint 43rd European Radiation Research Society (ERRS) and 20th German Society for Biological Radiation Research (GBS) Annual Meetings”, taking place in Essen (Germany), on 17–21 September 2017. This international conference represents one of the major European events for the scientific community working on the biological effects of radiation exposures at the molecular, cellular and systemic levels. It encompasses several complementary fields including radiation biology, chemistry, physics and medicine. The meeting represents a unique opportunity for scientists from all over the world to gather and share their most recent results. Particular attention is devoted to translational aspects and novel strategies for clinical applications, together with a particular focus on fundamental mechanisms of radiation action. The selected papers will cover relevant and novel advances in the field, as they will emerge at the conference. This Special Issue aims to serve as a state-of-the-art overview of recent progress in the field.

Prof. Dr. George Iliakis
Dr. Alexandros G. Georgakilas
Dr. Lorenzo Manti
Prof. Dr. Michael Hausmann
Prof. Dr. Verena Jendrossek
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cancers is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Published Papers (2 papers)

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Research

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15 pages, 3764 KiB  
Article
Localization Microscopy Analyses of MRE11 Clusters in 3D-Conserved Cell Nuclei of Different Cell Lines
by Marion Eryilmaz, Eberhard Schmitt, Matthias Krufczik, Franziska Theda, Jin-Ho Lee, Christoph Cremer, Felix Bestvater, Wladimir Schaufler, Michael Hausmann and Georg Hildenbrand
Cancers 2018, 10(1), 25; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers10010025 - 22 Jan 2018
Cited by 21 | Viewed by 5932
Abstract
In radiation biophysics, it is a subject of nowadays research to investigate DNA strand break repair in detail after damage induction by ionizing radiation. It is a subject of debate as to what makes up the cell’s decision to use a certain repair [...] Read more.
In radiation biophysics, it is a subject of nowadays research to investigate DNA strand break repair in detail after damage induction by ionizing radiation. It is a subject of debate as to what makes up the cell’s decision to use a certain repair pathway and how the repair machinery recruited in repair foci is spatially and temporarily organized. Single-molecule localization microscopy (SMLM) allows super-resolution analysis by precise localization of single fluorescent molecule tags, resulting in nuclear structure analysis with a spatial resolution in the 10 nm regime. Here, we used SMLM to study MRE11 foci. MRE11 is one of three proteins involved in the MRN-complex (MRE11-RAD50-NBS1 complex), a prominent DNA strand resection and broken end bridging component involved in homologous recombination repair (HRR) and alternative non-homologous end joining (a-NHEJ). We analyzed the spatial arrangements of antibody-labelled MRE11 proteins in the nuclei of a breast cancer and a skin fibroblast cell line along a time-course of repair (up to 48 h) after irradiation with a dose of 2 Gy. Different kinetics for cluster formation and relaxation were determined. Changes in the internal nano-scaled structure of the clusters were quantified and compared between the two cell types. The results indicate a cell type-dependent DNA damage response concerning MRE11 recruitment and cluster formation. The MRE11 data were compared to H2AX phosphorylation detected by γH2AX molecule distribution. These data suggested modulations of MRE11 signal frequencies that were not directly correlated to DNA damage induction. The application of SMLM in radiation biophysics offers new possibilities to investigate spatial foci organization after DNA damaging and during subsequent repair. Full article
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Review

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33 pages, 1685 KiB  
Review
New Insights into Protein Kinase B/Akt Signaling: Role of Localized Akt Activation and Compartment-Specific Target Proteins for the Cellular Radiation Response
by Klaudia Szymonowicz, Sebastian Oeck, Nathalie M. Malewicz and Verena Jendrossek
Cancers 2018, 10(3), 78; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers10030078 - 18 Mar 2018
Cited by 77 | Viewed by 12252
Abstract
Genetic alterations driving aberrant activation of the survival kinase Protein Kinase B (Akt) are observed with high frequency during malignant transformation and cancer progression. Oncogenic gene mutations coding for the upstream regulators or Akt, e.g., growth factor receptors, RAS and phosphatidylinositol-3-kinase (PI3K), or [...] Read more.
Genetic alterations driving aberrant activation of the survival kinase Protein Kinase B (Akt) are observed with high frequency during malignant transformation and cancer progression. Oncogenic gene mutations coding for the upstream regulators or Akt, e.g., growth factor receptors, RAS and phosphatidylinositol-3-kinase (PI3K), or for one of the three Akt isoforms as well as loss of the tumor suppressor Phosphatase and Tensin Homolog on Chromosome Ten (PTEN) lead to constitutive activation of Akt. By activating Akt, these genetic alterations not only promote growth, proliferation and malignant behavior of cancer cells by phosphorylation of various downstream signaling molecules and signaling nodes but can also contribute to chemo- and radioresistance in many types of tumors. Here we review current knowledge on the mechanisms dictating Akt’s activation and target selection including the involvement of miRNAs and with focus on compartmentalization of the signaling network. Moreover, we discuss recent advances in the cross-talk with DNA damage response highlighting nuclear Akt target proteins with potential involvement in the regulation of DNA double strand break repair. Full article
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