DNA Damage Repair and Cancer Therapeutics

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Biophysics: Structure, Dynamics, and Function".

Deadline for manuscript submissions: 31 May 2026 | Viewed by 1868

Special Issue Editor

Biochemistry & Structure Biology, University of Texas Health San Antonio, San Antonio, TX, USA
Interests: BRCAs; DNA damage repair; homologous recombination; tumorigenesis

Special Issue Information

Dear Colleagues,

We would like to invite you to contribute to a Special Issue on "DNA Damage Repair and Cancer Therapeutics" in the journal Biomolecules. DNA damage and its repair mechanisms are critical areas of research as they play a fundamental role in maintaining genomic stability and preventing cancer. Defects in these processes, particularly in genes such as BRCA1 and BRCA2, can lead to the development and progression of cancers. Understanding the role of these mechanisms in cancer is essential for developing novel therapies that address the significant need for effective cancer treatments.

This Special Issue aims to bring together cutting-edge research and reviews that explore the intricate relationship between DNA repair mechanisms and cancer treatment strategies. By focusing on this critical intersection, we seek to highlight innovative therapeutic approaches and deepen our understanding of how targeting DNA repair pathways can enhance cancer treatment outcomes, which is of great interest to the field at large. In this Special Issue, original research articles and reviews are welcome.

Research areas may include (but are not limited to) the following:

  • Mechanisms of DNA damage and repair;
  • The role of DNA repair pathways in cancer development;
  • Targeting DNA repair mechanisms in cancer therapy;
  • PARP inhibitors and other DNA repair inhibitors;
  • Combination therapies involving DNA repair inhibitors;
  • Biomarkers for DNA repair defects in cancer;
  • Personalized medicine approaches based on DNA repair profiles;
  • Immunotherapy and DNA damage response.

We look forward to receiving your contributions. We believe that this Special Issue will significantly advance our understanding of DNA damage repair and its potential in cancer therapy. Please do not hesitate to reach out regarding your interest or any questions relating to this Special Issue. If you are unable to contribute, we would greatly appreciate you sharing the details of this Special Issue with peers who may be interested.

Dr. Wenjing Li
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 250 words) can be sent to the Editorial Office for assessment.

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

  • DNA damage repair
  • cancer therapy
  • genomic stability
  • targeted therapy
  • biomarkers

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Published Papers (2 papers)

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Research

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25 pages, 70058 KB  
Article
Mechanisms of DNA Damage Recognition by UDG and PARP1 in the Nucleosome
by Safwen Ghediri, Parvathy A. P. Sarma, Vinnarasi Saravanan, Corinne Abbadie, Ralf Blossey and Fabrizio Cleri
Biomolecules 2025, 15(5), 649; https://doi.org/10.3390/biom15050649 - 30 Apr 2025
Viewed by 1329
Abstract
The DNA base-excision repair (BER) pathway shares the second part of its enzymatic chain with the single-strand break (SSB) repair pathway. BER is initiated by a glycosylase, such as UDG, while SSBR is initiated by the multifunctional enzyme PARP1. The very early steps [...] Read more.
The DNA base-excision repair (BER) pathway shares the second part of its enzymatic chain with the single-strand break (SSB) repair pathway. BER is initiated by a glycosylase, such as UDG, while SSBR is initiated by the multifunctional enzyme PARP1. The very early steps in the identification of the DNA damage are crucial to the correct initiation of the repair chains, and become even more complex when considering the realistic environment of damage to the DNA in the nucleosome. We performed molecular dynamics computer simulations of the interaction between the glycosylase UDG and a mutated uracil (as could result from oxidative deamination of cytosine), and between the Zn1-Zn2 fragment of PARP1 and a simulated SSB. The model system is a whole nucleosome in which DNA damage is inserted at various typical positions along the 145-bp sequence. It is shown that damage recognition by the enzymes requires very strict conditions, unlikely to be matched by pure random search along the DNA. We propose that mechanical deformation of the DNA around the defective sites may help signaling the presence of the defect, accelerating the search process. Full article
(This article belongs to the Special Issue DNA Damage Repair and Cancer Therapeutics)
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Review

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21 pages, 1845 KB  
Review
The PELP1 Pathway and Its Importance in Cancer Treatment
by Khaled Mohamed Nassar, Panneerdoss Subbarayalu, Suryavathi Viswanadhapalli and Ratna K. Vadlamudi
Biomolecules 2025, 15(12), 1729; https://doi.org/10.3390/biom15121729 - 12 Dec 2025
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Abstract
Proline-, glutamic acid-, and leucine-rich protein 1 (PELP1) is a proto-oncogene that serves as a nuclear and cytoplasmic scaffolding protein. PELP1 plays a critical role in nuclear receptor signaling, ribosome biogenesis, chromatin modifications, cell cycle progression, non-genomic signaling, and DNA damage response. PELP1 [...] Read more.
Proline-, glutamic acid-, and leucine-rich protein 1 (PELP1) is a proto-oncogene that serves as a nuclear and cytoplasmic scaffolding protein. PELP1 plays a critical role in nuclear receptor signaling, ribosome biogenesis, chromatin modifications, cell cycle progression, non-genomic signaling, and DNA damage response. PELP1 expression is upregulated in a variety of cancers, including breast, ovarian, endometrial, prostate, and liver cancers and serves as a prognostic factor for poor survival. PELP1’s structural motifs, unique scaffolding function, and oncogenic activity make it a potential target for a range of therapeutic approaches. This review summarizes the most recent advancements in PELP1 biology, with a particular focus on the emergent oncogenic functions of PELP1 and its inhibitors for the treatment of cancer. Full article
(This article belongs to the Special Issue DNA Damage Repair and Cancer Therapeutics)
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