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DNA Replication/Repair, and the DNA Damage Response in Human Disease...
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DNA Replication/Repair, and the DNA Damage Response in Human Disease 2023

A special issue of Genes (ISSN 2073-4425). This special issue belongs to the section "Molecular Genetics and Genomics".

Deadline for manuscript submissions: closed (10 October 2023) | Viewed by 7632

Special Issue Editors

Dr. Dong Zhang

E-Mail Website
Guest Editor
Department of Biomedical Sciences, College of Osteopathic Medicine, New York Institute of Technology, Old Westbury, NY 11568, USA
Interests: DNA damage response; DNA repair; telomere biology and alternative lengthening of telomeres (ALT); ALT cancers
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Marietta Lee

E-Mail Website
Guest Editor
Department Biochemistry and Molecular Biology, New York Medical College, Valhalla, NY 10595, USA
Interests: DNA replication; DNA polymerases; DNA repair; cell cycle regulation
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The faithful duplication of the genome is vital for human fitness and health. The high-fidelity DNA polymerases for DNA replication, DNA damage response, and DNA repair all play essential roles in maintaining the stability of our genome. Mutations in genes involved in DNA replication, DNA damage response, and DNA repair can cause genome instability and affect the normal physiology of various cell types, tissues, and organs, leading to a variety of genetic diseases, including familial breast cancers, Fanconi anemia, and many others. In recent years, great advances have been achieved in understanding how DNA replication, DNA damage response, and DNA repair contribute to the clinical manifestations of various genetic diseases. Most importantly, tremendous strides have been made in developing precision medicine in treating these genetic diseases.

This Special Issue entitled “DNA Replication/Repair, and the DNA Damage Response in Human Disease 2023” is the second Special Issue in a series that studies DNA Replication/Repair, and the DNA Damage Response in Human Disease. The first Special Issue, published in 2022, comprised eleven manuscripts and can be found at https://www.mdpi.com/journal/genes/special_issues/DNA_Response_Disease. We welcome the submission of reviews, original research articles, and short communications that focus on identification, molecular mechanisms, and novel therapies of these genetic diseases.

Dr. Dong Zhang
Prof. Dr. Marietta Lee
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. Genes is an international peer-reviewed open access monthly 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 2600 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.

Keywords

  • DNA replication
  • DNA repair
  • DNA damage response
  • genetic diseases
  • cancers

Published Papers (3 papers)

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Research

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15 pages, 1160 KiB  
Article
Single-Molecule Telomere Assay via Optical Mapping (SMTA-OM) Can Potentially Define the ALT Positivity of Cancer
by Kaitlin Raseley, Zeal Jinwala, Dong Zhang and Ming Xiao
Genes 2023, 14(6), 1278; https://doi.org/10.3390/genes14061278 - 16 Jun 2023
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Abstract
Telomeres play an essential role in protecting the ends of linear chromosomes and maintaining the integrity of the human genome. One of the key hallmarks of cancers is their replicative immortality. As many as 85–90% of cancers activate the expression of telomerase (TEL+) [...] Read more.
Telomeres play an essential role in protecting the ends of linear chromosomes and maintaining the integrity of the human genome. One of the key hallmarks of cancers is their replicative immortality. As many as 85–90% of cancers activate the expression of telomerase (TEL+) as the telomere maintenance mechanism (TMM), and 10–15% of cancers utilize the homology-dependent repair (HDR)-based Alternative Lengthening of Telomere (ALT+) pathway. Here, we performed statistical analysis of our previously reported telomere profiling results from Single Molecule Telomere Assay via Optical Mapping (SMTA-OM), which is capable of quantifying individual telomeres from single molecules across all chromosomes. By comparing the telomeric features from SMTA-OM in TEL+ and ALT+ cancer cells, we demonstrated that ALT+ cancer cells display certain unique telomeric profiles, including increased fusions/internal telomere-like sequence (ITS+), fusions/internal telomere-like sequence loss (ITS−), telomere-free ends (TFE), super-long telomeres, and telomere length heterogeneity, compared to TEL+ cancer cells. Therefore, we propose that ALT+ cancer cells can be differentiated from TEL+ cancer cells using the SMTA-OM readouts as biomarkers. In addition, we observed variations in SMTA-OM readouts between different ALT+ cell lines that may potentially be used as biomarkers for discerning subtypes of ALT+ cancer and monitoring the response to cancer therapy. Full article
(This article belongs to the Special Issue DNA Replication/Repair, and the DNA Damage Response in Human Disease 2023)
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Review

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18 pages, 1229 KiB  
Review
Therapeutic Targeting of DNA Replication Stress in Cancer
by Long Gu, Robert J. Hickey and Linda H. Malkas
Genes 2023, 14(7), 1346; https://doi.org/10.3390/genes14071346 - 26 Jun 2023
Cited by 2 | Viewed by 3806
Abstract
This article reviews the currently used therapeutic strategies to target DNA replication stress for cancer treatment in the clinic, highlighting their effectiveness and limitations due to toxicity and drug resistance. Cancer cells experience enhanced spontaneous DNA damage due to compromised DNA replication machinery, [...] Read more.
This article reviews the currently used therapeutic strategies to target DNA replication stress for cancer treatment in the clinic, highlighting their effectiveness and limitations due to toxicity and drug resistance. Cancer cells experience enhanced spontaneous DNA damage due to compromised DNA replication machinery, elevated levels of reactive oxygen species, loss of tumor suppressor genes, and/or constitutive activation of oncogenes. Consequently, these cells are addicted to DNA damage response signaling pathways and repair machinery to maintain genome stability and support survival and proliferation. Chemotherapeutic drugs exploit this genetic instability by inducing additional DNA damage to overwhelm the repair system in cancer cells. However, the clinical use of DNA-damaging agents is limited by their toxicity and drug resistance often arises. To address these issues, the article discusses a potential strategy to target the cancer-associated isoform of proliferating cell nuclear antigen (caPCNA), which plays a central role in the DNA replication and damage response network. Small molecule and peptide agents that specifically target caPCNA can selectively target cancer cells without significant toxicity to normal cells or experimental animals. Full article
(This article belongs to the Special Issue DNA Replication/Repair, and the DNA Damage Response in Human Disease 2023)
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21 pages, 2405 KiB  
Review
Lagging Strand Initiation Processes in DNA Replication of Eukaryotes—Strings of Highly Coordinated Reactions Governed by Multiprotein Complexes
by Heinz Peter Nasheuer and Nichodemus O. Onwubiko
Genes 2023, 14(5), 1012; https://doi.org/10.3390/genes14051012 - 29 Apr 2023
Cited by 2 | Viewed by 1913
Abstract
In their influential reviews, Hanahan and Weinberg coined the term ‘Hallmarks of Cancer’ and described genome instability as a property of cells enabling cancer development. Accurate DNA replication of genomes is central to diminishing genome instability. Here, the understanding of the initiation of [...] Read more.
In their influential reviews, Hanahan and Weinberg coined the term ‘Hallmarks of Cancer’ and described genome instability as a property of cells enabling cancer development. Accurate DNA replication of genomes is central to diminishing genome instability. Here, the understanding of the initiation of DNA synthesis in origins of DNA replication to start leading strand synthesis and the initiation of Okazaki fragment on the lagging strand are crucial to control genome instability. Recent findings have provided new insights into the mechanism of the remodelling of the prime initiation enzyme, DNA polymerase α-primase (Pol-prim), during primer synthesis, how the enzyme complex achieves lagging strand synthesis, and how it is linked to replication forks to achieve optimal initiation of Okazaki fragments. Moreover, the central roles of RNA primer synthesis by Pol-prim in multiple genome stability pathways such as replication fork restart and protection of DNA against degradation by exonucleases during double-strand break repair are discussed. Full article
(This article belongs to the Special Issue DNA Replication/Repair, and the DNA Damage Response in Human Disease 2023)
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