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Recent Research of DNA Repair and Damage in Human Health
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Recent Research of DNA Repair and Damage in Human Health

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (15 April 2024) | Viewed by 2149

Special Issue Editors

Dr. Pavel Vodička

E-Mail Website1 Website2
Guest Editor
1. Department of Molecular Biology of Cancer, Institute of Experimental Medicine of the Academy of Sciences of the Czech Republic, Prague, Czech Republic
2. Biomedical Center, Faculty of Medicine in Pilsen, Charles University, Pilsen, Czech Republic
3. First Faculty of Medicine, Charles University, Prague, Czech Republic
Interests: DNA and chromosomal damage; DNA repair; colorectal cancer; pancreatic cancer; cancer risk; cancer prognosis; therapy prediction
Special Issues, Collections and Topics in MDPI journals
Dr. Ezgi Eylül Bankoglu

E-Mail Website
Guest Editor
Institute of Pharmacology and Toxicology, University of Wuerzburg, Versbacher Straße 9, 97078 Wuerzburg, Germany
Interests: DNA damage; DNA repair; degenerative diseases; inflammation

Special Issue Information

Dear Colleagues,

The high-fidelity transfer of genetic information and the preservation of genomic integrity are fundamental preconditions of life. There are many pathways implicated in the maintenance of genomic integrity and the prevention of its instability; these mainly include DNA repair mechanisms, flawless DNA replication and mitosis, and telomere maintenance.

Due to the occurrence of abundant and versatile DNA damage, a complex biological system of DNA repair has evolved to ensure the fidelity of genetic information, genomic stability, and the integrity of cells.

DNA damage accumulation and an altered DNA damage response underlie several human pathologies, including various types of cancer. In addition, DNA damage and repair play a role in all inflammatory processes and in degenerative diseases. Furthermore, DNA damage accumulation and changes in DNA repair may occur in physiological aging. DNA repair and damage may be important players in telomeric and mitochondrial DNA; however, their role in human pathologies is not understood. Hence, several points must be addressed to improve the current understanding of DNA damage/DNA repair in humans and their potential implications in pathologies.

For this Special Issue, “Recent Research of DNA Repair and Damage in Human Health”, we welcome recent research and review articles on topics such as the effects of interindividual, intersex, and age differences on DNA damage repair, and differences in organs, together with the role of DNA damage repair, in the etiology of proliferative versus degenerative diseases. Moreover, we intend to address the topic of DNA repair in inflammation, as well as telomeric and mitochondrial DNA.

Dr. Pavel Vodička
Dr. Ezgi Eylül Bankoglu
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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.

Keywords

  • DNA damage
  • DNA repair
  • degenerative diseases
  • inflammation
  • aging
  • cancer

Published Papers (2 papers)

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Research

18 pages, 3007 KiB  
Article
Modelling the In Vivo and Ex Vivo DNA Damage Response after Internal Irradiation of Blood from Patients with Thyroid Cancer
by Sarah Schumann, Harry Scherthan, Philipp E. Hartrampf, Lukas Göring, Andreas K. Buck, Matthias Port, Michael Lassmann and Uta Eberlein
Int. J. Mol. Sci. 2024, 25(10), 5493; https://doi.org/10.3390/ijms25105493 - 17 May 2024
Viewed by 478
Abstract
This work reports on a model that describes patient-specific absorbed dose-dependent DNA damage response in peripheral blood mononuclear cells of thyroid cancer patients during radioiodine therapy and compares the results with the ex vivo DNA damage response in these patients. Blood samples of [...] Read more.
This work reports on a model that describes patient-specific absorbed dose-dependent DNA damage response in peripheral blood mononuclear cells of thyroid cancer patients during radioiodine therapy and compares the results with the ex vivo DNA damage response in these patients. Blood samples of 18 patients (nine time points up to 168 h post-administration) were analyzed for radiation-induced γ-H2AX + 53BP1 DNA double-strand break foci (RIF). A linear one-compartment model described the absorbed dose-dependent time course of RIF (Parameters: c characterizes DSB damage induction; k1 and k2 are rate constants describing fast and slow repair). The rate constants were compared to ex vivo repair rates. A total of 14 patient datasets could be analyzed; c ranged from 0.012 to 0.109 mGy−1, k2 from 0 to 0.04 h−1. On average, 96% of the damage is repaired quickly with k1 (range: 0.19–3.03 h−1). Two patient subgroups were distinguished by k1-values (n = 6, k1 > 1.1 h−1; n = 8, k1 < 0.6 h−1). A weak correlation with patient age was observed. While induction of RIF was similar among ex vivo and in vivo, the respective repair rates failed to correlate. The lack of correlation between in vivo and ex vivo repair rates and the applicability of the model to other therapies will be addressed in further studies. Full article
(This article belongs to the Special Issue Recent Research of DNA Repair and Damage in Human Health)
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14 pages, 2367 KiB  
Article
Optimizing the Comet Assay-Based In Vitro DNA Repair Assay for Placental Tissue: A Pilot Study with Pre-Eclamptic Patients
by Anastasiya Mircheva, Philippe Vangrieken, Salwan Al-Nasiry, Frederik-Jan van Schooten, Roger W. L. Godschalk and Sabine A. S. Langie
Int. J. Mol. Sci. 2024, 25(1), 187; https://doi.org/10.3390/ijms25010187 - 22 Dec 2023
Viewed by 1041
Abstract
The comet assay-based in vitro DNA repair assay has become a common tool for quantifying base excision repair (BER) activity in human lymphocytes or cultured cells. Here, we optimized the protocol for studying BER in human placental tissue because the placenta is a [...] Read more.
The comet assay-based in vitro DNA repair assay has become a common tool for quantifying base excision repair (BER) activity in human lymphocytes or cultured cells. Here, we optimized the protocol for studying BER in human placental tissue because the placenta is a non-invasive tissue for biomonitoring of early-life exposures, and it can be used to investigate molecular mechanisms associated with prenatal disorders. The optimal protein concentration of placental protein extracts for optimal damage recognition and incision was 2 mg protein/mL. The addition of aphidicolin did not lead to reduced non-specific incisions and was, therefore, not included in the optimized protocol. The interval between sample collection and analysis did not affect BER activity up to 70 min. Finally, this optimized protocol was tested on pre-eclamptic (PE) placental tissues (n = 11) and significantly lower BER activity in PE placentas compared to controls (n = 9) was observed. This was paralleled by a significant reduction in the expression of BER-related genes and increased DNA oxidation in PE placentas. Our study indicates that BER activity can be determined in placentas, and lower activity is present in PE compared with healthy. These findings should be followed up in prospective clinical investigations to examine BER’s role in the advancement of PE. Full article
(This article belongs to the Special Issue Recent Research of DNA Repair and Damage in Human Health)
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