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Cells
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DNA Damage and Repair for Targeted Cancer Therapy
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DNA Damage and Repair for Targeted Cancer Therapy

A special issue of Cells (ISSN 2073-4409).

Deadline for manuscript submissions: 31 August 2025 | Viewed by 3611

Special Issue Editors

Dr. Mohd Saleem Dar

E-Mail Website
Guest Editor
National Cancer Institute, NIH, Bethesda, MD 20892, USA
Interests: epigenetics; cancer biology and tumor immunology; histone and DNA; methyltransferases, long non-coding research; molecular biology and cell biology; drug discovery and PROTACS; protein purification and biochemistry
Dr. Mohsin Maqbool

E-Mail Website
Guest Editor
Sidney Kimmel Cancer Center, Jefferson Health, Philadelphia, PA, USA
Interests: cancer biology; molecular biology; cell signaling; DNA damage; leukemia; immunotherapy
Dr. Sajad Ahmad Bhat

E-Mail Website
Guest Editor
The Wistar Institute, 3601 Spruce St., Philadelphia, PA 19104, USA
Interests: tumor immunology and cancer biology; tumor microenvironment and gut microbiome; microbial metabolites; metabolomics; molecular and cell biology

Special Issue Information

Dear Colleagues,

DNA damage and repair mechanisms, including BER, NER, MMR, HR, and NHEJ, are crucial for genomic integrity. In cancer, these mechanisms are often dysregulated, making the cells vulnerable to targeted therapies. Inhibitors, e.g., PARP-I, kill cancer cells by accumulating DNA damage in HR-deficient cells, while ATR and ATM inhibitors target key regulators of the DNA damage response, sensitizing cells to these agents. Challenges such as resistance, toxicity, and the need for reliable biomarkers remain, but ongoing research seeks to overcome these obstacles.

In this Special Issue, we welcome research and review articles on DNA damage and repair, focusing on key repair pathways and their vulnerabilities in cancer cells. We also invite studies addressing resistance, toxicity, and biomarker identification. This issue aims to highlight how targeted therapies can enhance treatment efficacy and advance personalized cancer care.

Dr. Mohd Saleem Dar
Dr. Mohsin Maqbool
Dr. Sajad Ahmad Bhat
Guest Editor

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. Cells 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 2700 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

  • cancer cells
  • DNA damage and repair mechanism
  • genome organization
  • BER, NER, MMR, HR, and NHEJ
  • targeted therapy
  • inhibitors/PROATCS
  • drug resistance
  • drug toxicity
  • biomarkers
  • personalized medicine

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Published Papers (2 papers)

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17 pages, 3856 KiB  
Article
Poly (ADP-Ribose) Polymerase Inhibitor Olaparib-Resistant BRCA1-Mutant Ovarian Cancer Cells Demonstrate Differential Sensitivity to PARP Inhibitor Rechallenge
by Chi-Ting Shih, Tzu-Ting Huang, Jayakumar R. Nair, Kristen R. Ibanez and Jung-Min Lee
Cells 2024, 13(22), 1847; https://doi.org/10.3390/cells13221847 - 7 Nov 2024
Viewed by 1824
Abstract
Poly (ADP-ribose) polymerase inhibitors (PARPis) show cytotoxicity in homologous recombination deficiency (HRD) seen in BRCA-mutant ovarian cancer (OvCa). Despite initial responses, resistance often develops. The reintroduction of different PARPis, such as niraparib or rucaparib, has shown some clinical activity in BRCA mutation-associated [...] Read more.
Poly (ADP-ribose) polymerase inhibitors (PARPis) show cytotoxicity in homologous recombination deficiency (HRD) seen in BRCA-mutant ovarian cancer (OvCa). Despite initial responses, resistance often develops. The reintroduction of different PARPis, such as niraparib or rucaparib, has shown some clinical activity in BRCA mutation-associated OvCa patients with prior olaparib treatment, yet the underlying mechanisms remain unclear. To investigate the differential sensitivity to different PARPis, we established an olaparib-resistant BRCA1-mutant OvCa cell line (UWB-OlaJR) by exposing UWB1.289 cells to gradually increasing concentrations of olaparib. UWB-OlaJR exhibited restored HR capability without BRCA1 reversion mutation or increased drug efflux. We examined cell viability, DNA damage, and DNA replication fork dynamics in UWB-OlaJR treated with various PARPis. UWB-OlaJR exhibits varying sensitivity to PARPis, showing cross-resistance to veliparib and talazoparib, and sensitivity with increased cytotoxicity to niraparib and rucaparib. Indeed, DNA fiber assay reveals that niraparib and rucaparib cause higher replication stress than the others. Moreover, S1 nuclease fiber assay shows that niraparib and rucaparib induce greater DNA single-strand gaps than other PARPis, leading to increased DNA damage and cell death. Our study provides novel insights into differential PARPi sensitivity in olaparib-resistant BRCA-mutant OvCa, which requires further investigation of inter-agent differences in large prospective studies. Full article
(This article belongs to the Special Issue DNA Damage and Repair for Targeted Cancer Therapy)
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16 pages, 6880 KiB  
Review
Targeting the 8-oxodG Base Excision Repair Pathway for Cancer Therapy
by Anna Piscone, Francesca Gorini, Susanna Ambrosio, Anna Noviello, Giovanni Scala, Barbara Majello and Stefano Amente
Cells 2025, 14(2), 112; https://doi.org/10.3390/cells14020112 - 14 Jan 2025
Viewed by 1310
Abstract
Genomic integrity is critical for cellular homeostasis, preventing the accumulation of mutations that can drive diseases such as cancer. Among the mechanisms safeguarding genomic stability, the Base Excision Repair (BER) pathway plays a pivotal role in counteracting oxidative DNA damage caused by reactive [...] Read more.
Genomic integrity is critical for cellular homeostasis, preventing the accumulation of mutations that can drive diseases such as cancer. Among the mechanisms safeguarding genomic stability, the Base Excision Repair (BER) pathway plays a pivotal role in counteracting oxidative DNA damage caused by reactive oxygen species. Central to this pathway are enzymes like 8-oxoguanine glycosylase 1 (OGG1), which recognize and excise 8-oxo-7,8-dihydro-2′-deoxyguanosine (8-oxodG) lesions, thereby initiating a series of repair processes that restore DNA integrity. BER inhibitors have recently been identified as a promising approach in cancer therapy, increasing the sensitivity of cancer cells to radiotherapy and chemotherapy. By exploiting tumor-specific DNA repair dependencies and synthetic lethal interactions, these inhibitors could be used to selectively target cancer cells while sparing normal cells. This review provides a robust reference for scientific researchers, offering an updated perspective on small-molecule inhibitors targeting the 8-oxodG-BER pathway and highlighting their potential role in expanding cancer treatment strategies. Full article
(This article belongs to the Special Issue DNA Damage and Repair for Targeted Cancer Therapy)
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