Recent Advances in Biomolecular Radiation Research

A special issue of Biology (ISSN 2079-7737). This special issue belongs to the section "Medical Biology".

Deadline for manuscript submissions: closed (30 November 2021) | Viewed by 2372

Special Issue Editors


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Guest Editor
West German Cancer Center, Department of Medical Oncology, University Hospital Essen, University of Duisburg-Essen, 45147 Essen, Germany
Interests: DNA repair; immune response; cancer therapy; software tools; molecular biology
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Guest Editor
Department of Anesthesiology, Intensive Care Medicine and Pain Management, Medical Faculty of Ruhr-University Bochum, Bochum, Germany
Interests: critically ill; intensive care therapy; pain pathways; software solutions

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Guest Editor
Department of Therapeutic Radiology, Yale University, New Haven, CT, USA
Interests: radiation response; DNA repair; molecular biology; cancer biology; pharmacology

Special Issue Information

Dear colleagues,

Together with surgery and chemotherapy, radiotherapy is part of the standard treatment options for cancer patients. So far, photon radiation is the most frequently used radiotherapy in the clinical setting.

During the last few decades, major advances have been made in our understanding of the mechanisms driving the development of radiotherapy, radiosensitization, and normal tissue protection. A major progress is represented by the further development of particle radiation, especially proton therapy. However, further knowledge is needed to understand how different types of radiation, combination with chemotherapy, and also approaches combining radiotherapy with immunotherapy lead to possible benefits for patients.

This Special Issue addresses these emerging questions. We would like to focus on clinical advances of radiation research but also in particular on studies revealing biomolecular mechanisms which underlie the cellular response to radiation. Here, topics of our SI range from DNA damage response and DNA repair over protein and organelle damage to tissue- and system-wide radiation effects. In particular, we welcome studies focusing on immune response altering effects of radiation.

Gathering more detailed knowledge of the experts in our exciting research field addressing the relationships of molecular alterations, cellular response, and clinic-related outcome offers a great opportunity to promote a better understanding and development of new radiotherapeutic approaches.

Dr. Sebastian Oeck
Dr. Nathalie M. Malewicz
Dr. Adam J. Krysztofiak
Guest Editors

Manuscript Submission Information

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Keywords

  • radiation
  • DNA damage
  • DNA repair
  • molecular stress response
  • genotoxicity
  • dosimetry
  • radiotherapy
  • combination treatment
  • molecular biology

Published Papers (1 paper)

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Research

11 pages, 1758 KiB  
Article
Zinc Supplementation Enhances the Pro-Death Function of UPR in Lymphoma Cells Exposed to Radiation
by Roberta Gonnella, Luisa Guttieri, Maria Saveria Gilardini Montani, Roberta Santarelli, Erica Bassetti, Gabriella D’Orazi and Mara Cirone
Biology 2022, 11(1), 132; https://doi.org/10.3390/biology11010132 - 13 Jan 2022
Cited by 7 | Viewed by 1841
Abstract
We have previously shown that Zinc supplementation triggered ER stress/UPR in cancer cells undergoing treatment by genotoxic agents, reactivated wtp53 in cancer cells harboring mutant p53 (mutp53) and potentiated the activity of wtp53 in those carrying wtp53. In this study, we used Zinc [...] Read more.
We have previously shown that Zinc supplementation triggered ER stress/UPR in cancer cells undergoing treatment by genotoxic agents, reactivated wtp53 in cancer cells harboring mutant p53 (mutp53) and potentiated the activity of wtp53 in those carrying wtp53. In this study, we used Zinc chloride alone or in combination with 2 Gy radiation to treat Primary Effusion Lymphoma (PEL) cells, an aggressive B-cell lymphoma associated with KSHV that harbors wt or partially functioning p53. We found that Zinc triggered a mild ER stress/UPR in these lymphoma cells and activated ERK1/2, molecule known to sustain cell survival in the course of UPR activation. In combination with radiations, Zinc triggered a stronger p53 activation that counteracted its mediated ERK1/2 phosphorylation, further upregulating the UPR molecule CHOP and promoting cell death. These data suggest that Zinc supplementation could be a promising strategy to reduce the doses of radiation and possibly of other DNA-damaging agents to obtain an efficient capacity to induce lymphoma cell death. Full article
(This article belongs to the Special Issue Recent Advances in Biomolecular Radiation Research)
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