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Targeting DNA Repair in Cancer

Submission Deadline: 30 April 2026 (closed) View: 1893 Submit to Special Issue

Guest Editor(s)

Assist. Prof. Panagiotis J. Vlachostergios

Email: pjv9003@med.cornell.edu

Affiliation: Division of Hematology and Medical Oncology, Weill Cornell Medicine, New York, 10065, USA; Department of Medical Oncology, IASO Thessalias General Hospital, Larissa, 41500, Greece

Homepage:

Research Interests: DNA repair, homologous recombination, genitourinary malignancies, cancer genetics, cancer genomics, precision oncology, immunooncology, biomarker research

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Assoc. Prof. Stergios Boussios

Email: stergiosboussios@gmail.com

Affiliation: Faculty of Medicine, School of Health Sciences, University of Ioannina, Ioannina, 45110, Greece; Department of Medical Oncology, University Hospital of Ioannina, Ioannina, 45500, Greece

Homepage:

Research Interests: homologous recombination of DNA, biomarkers, PARP inhibitors

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Summary

DNA repair mechanisms are critical for preserving genomic integrity, but are frequently defective in cancer, providing opportunities for therapeutic targeting. Targeting DNA repair pathways (e.g., homologous recombination, base excision repair, and mismatch repair) has advanced as an effective cancer therapeutic approach, with PARP inhibitors providing the prototype for the use in BRCA mutant cancers. Current studies are revealing novel synthetic lethal interactions, resistance mechanisms, and combination regimens that could expand the applicability of DNA repair-targeted therapies. Knowledge of the crosslinking repair pathway, cancer microenvironment, and immune response also raises the prospect of new routes in precision medicine.

Original research articles, reviews, opinions, etc., are welcome for our coming special issue "Targeting DNA Repair in Cancer." This collection will discuss new discoveries in DNA repair. This series will describe the development of therapeutic strategies for DNA repair pathways, mechanisms of resistance to DNA repair inhibitors, new biomarkers for patient stratification, and novel combination strategies. We especially encourage manuscripts that connect fundamental mechanistic work with clinical applications, discuss translational prospects, or propose new avenues in using synthetic lethality. Contributions from academia as well as industry are solicited. Come work with us in the frontiers of precision oncology.


Keywords

DNA repair, cancer therapeutics, synthetic lethality, PARP inhibitors, homologous recombination, genomic instability, tumor microenvironment, resistance mechanisms, precision oncology, DNA damage response (DDR), biomarkers, combination therapy, targeted therapy, BRCA mutations, translational research

Published Papers


  • Open Access

    REVIEW

    Cancer Stem Cell Biology: DNA Repair Mechanisms, Therapeutic Resistance, and Emerging Treatment Strategies

    Mateusz Kciuk, Julia Gałęziewska, Weronika Kruczkowska, Katarzyna Wanke, Damian Kołat, Beata Marciniak, Renata Kontek
    Oncology Research, DOI:10.32604/or.2026.083197
    (This article belongs to the Special Issue: Targeting DNA Repair in Cancer)
    Abstract DNA is continuously challenged by endogenous and exogenous insults, generating lesions that threaten genomic stability. Normal stem cells preserve genome integrity through highly coordinated DNA damage response (DDR) networks involving efficient base excision repair (BER), homologous recombination (HR), cell-cycle checkpoints, and TP53-mediated quality control. Cancer stem cells (CSCs), a rare tumor subpopulation responsible for tumor initiation, metastasis, relapse, and therapeutic resistance, exploit these protective mechanisms while acquiring distinct DNA repair adaptations. This review examines how stemness-associated signaling pathways, including Hedgehog, Notch, and Wnt/β-catenin, interact with DDR programs to promote CSC survival under genotoxic stress. CSCs… More >

  • Open Access

    REVIEW

    Overcoming the Shield: Mechanisms of Resistance to DNA Repair Inhibitors and Strategies to Restore Synthetic Lethality

    Kannan Sridharan, Ondrej Fiala, Gowri Sivaramakrishnan, Mimma Rizzo, Matteo Santoni
    Oncology Research, DOI:10.32604/or.2026.081879
    (This article belongs to the Special Issue: Targeting DNA Repair in Cancer)
    Abstract The emergence of resistance to poly (ADP-ribose) polymerase (PARP) inhibitors poses a significant obstacle in treating cancers characterized by BReast CAncer gene (BRCA) mutations or homologous recombination deficiency. Despite the substantial clinical benefits brought by drugs such as olaparib, niraparib, and talazoparib, a substantial proportion of tumors ultimately develop resistance. The underlying mechanisms are diverse and include the reconstitution of homologous recombination via secondary BRCA reversion mutations, stabilization of replication forks, enhanced drug efflux mediated by p-glycoproteins, and structural or functional alterations in PARP1 itself. A thorough grasp of these resistance pathways is critical for the… More >

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