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9.2
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Journals
Biomolecules
Special Issues
DNA Damage and Repair in Cancer Treatment
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DNA Damage and Repair in Cancer Treatment

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: 30 September 2025 | Viewed by 343

Special Issue Editors

Prof. Dr. Alexandros Georgakilas

E-Mail Website
Guest Editor
DNA Damage Laboratory, Department of Physics, School of Applied Mathematical and Physical Sciences, Zografou Campus, National Technical University of Athens (NTUA), 15780 Athens, Greece
Interests: DNA damage; DNA repair; cancer; radiation therapy; bioinformatics
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Lorenzo Manti

E-Mail Website
Guest Editor
Department of Mathematics and Physics, Università della Campania “L. Vanvitelli”, Viale Lincoln, 5, 81100 Caserta, Italy
Interests: radiation-induced chromosome aberrations; DNA repair; hadrontherapy; radiosensitization and radioprotection
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue intends to showcase the most recent research on the importance of mitigation of DNA damage and maintenance of genome integrity in cancer therapy. Normal-tissue response is the limiting factor for curative radiotherapy. Hence, strategies to mitigate radiation-induced DNA damage in normal cells are crucial to abate unwanted sequelae. In fact, failure in maintaining DNA integrity is a key factor in radiation-induced carcinogenesis and poor radiotherapy outcome. Thus, radiotherapy strives to achieve normal-tissue protection while impairing cancer cell repair ability. Therefore, in this Special Issue, we welcome original fundamental research carried out by pre-clinical in vitro and/or in vivo approaches, as well as up-to-date reviews on these topics, with special emphasis on the novel frontiers in the fields of anticancer molecular targets.

Prof. Dr. Alexandros Georgakilas
Prof. Dr. Lorenzo Manti
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. Biomolecules 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 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

  • ionizing radiation
  • DNA damage
  • DNA repair
  • genomic instability
  • patient radioprotection
  • tumour radiosensitization
  • radiation-induced carcinogenesis

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Published Papers (1 paper)

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Review

39 pages, 5612 KiB  
Review
The Multifaceted Role of p53 in Cancer Molecular Biology: Insights for Precision Diagnosis and Therapeutic Breakthroughs
by Bolong Xu, Ayitila Maimaitijiang, Dawuti Nuerbiyamu, Zhengding Su and Wenfang Li
Biomolecules 2025, 15(8), 1088; https://doi.org/10.3390/biom15081088 - 27 Jul 2025
Abstract
The protein p53, often referred to as the “guardian of the genome,” is essential for preserving cellular balance and preventing cancerous transformations. As one of the most commonly altered genes in human cancers, its impaired function is associated with tumor initiation, development, and [...] Read more.
The protein p53, often referred to as the “guardian of the genome,” is essential for preserving cellular balance and preventing cancerous transformations. As one of the most commonly altered genes in human cancers, its impaired function is associated with tumor initiation, development, and resistance to treatment. Exploring the diverse roles of p53, which include regulating the cell cycle, repairing DNA, inducing apoptosis, reprogramming metabolism, and modulating immunity, provides valuable insights into cancer mechanisms and potential treatments. This review integrates recent findings on p53′s dual nature, functioning as both a tumor suppressor and an oncogenic promoter, depending on the context. Wild-type p53 suppresses tumors by inducing cell cycle arrest or apoptosis in response to genotoxic stress, while mutated variants often lose these functions or gain novel pro-oncogenic activities. Emerging evidence highlights p53′s involvement in non-canonical pathways, such as regulating tumor microenvironment interactions, metabolic flexibility, and immune evasion mechanisms. For instance, p53 modulates immune checkpoint expression and influences the efficacy of immunotherapies, including PD-1/PD-L1 blockade. Furthermore, advancements in precision diagnostics, such as liquid biopsy-based detection of p53 mutations and AI-driven bioinformatics tools, enable early cancer identification and stratification of patients likely to benefit from targeted therapies. Therapeutic strategies targeting p53 pathways are rapidly evolving. Small molecules restoring wild-type p53 activity or disrupting mutant p53 interactions, such as APR-246 and MDM2 inhibitors, show promise in clinical trials. Combination approaches integrating gene editing with synthetic lethal strategies aim to exploit p53-dependent vulnerabilities. Additionally, leveraging p53′s immunomodulatory effects through vaccine development or adjuvants may enhance immunotherapy responses. In conclusion, deciphering p53′s complex biology underscores its unparalleled potential as a biomarker and therapeutic target. Integrating multi-omics analyses, functional genomic screens, and real-world clinical data will accelerate the translation of p53-focused research into precision oncology breakthroughs, ultimately improving patient outcomes. Full article
(This article belongs to the Special Issue DNA Damage and Repair in Cancer Treatment)
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