Genome Instability, Ubiquitin Signaling and Cancer Therapy
A special issue of Cancers (ISSN 2072-6694).
Deadline for manuscript submissions: 30 March 2027 | Viewed by 257
Editors
Interests: genome instability; E3 ubiquitin ligases; targeted protein degradation; PROTACs; cell cycle regulation; cancer therapy
Interests: cancer research; immunity; microbiome; immunology; chromatin biology
Special Issues, Collections and Topics in MDPI journals
Special Issue Information
Dear Colleagues,
Genome instability is a defining hallmark of cancer and a central driver of tumor initiation, progression, and therapeutic response. The accumulation of DNA damage, defects in DNA repair pathways, and dysregulated cell cycle control collectively promote chromosomal instability and an increased mutational burden, thereby fueling tumor heterogeneity and evolution. While these processes facilitate oncogenesis, they also create vulnerabilities that can be therapeutically exploited, exemplified by the use of PARP inhibitors in BRCA-mutated cancers.
Central to the maintenance of genomic integrity is the ubiquitin–proteasome system (UPS), a highly coordinated network that regulates protein turnover and cellular signaling. Ubiquitination is mediated through a cascade involving E1 activating enzymes, E2 conjugating enzymes, and E3 ubiquitin ligases, the latter conferring substrate specificity by recognizing and targeting diverse proteins for degradation or functional modulation. Through these mechanisms, ubiquitin signaling governs essential processes such as DNA damage response, replication stress resolution, checkpoint activation, and apoptosis. The dysregulation of these pathways is increasingly recognized as a major contributor to genome instability and cancer development.
This Special Issue brings together cutting-edge research articles and comprehensive reviews that explore the mechanistic and translational interplay between genome instability, ubiquitin signaling, and cancer therapy. Topics of interest include the roles of E3 ligases in DNA repair and replication fidelity, ubiquitin-mediated checkpoint regulation, non-canonical ubiquitin and ubiquitin-like modifications, and emerging therapeutic strategies targeting the UPS and targeted protein degradation.
By bridging molecular mechanisms with clinical applications, this Special Issue will advance precision oncology and highlight innovative strategies to exploit genome instability for improved cancer treatment outcomes.
Dr. Sehbanul Islam
Guest Editor
Dr. Aftab Alam
Co-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 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-anonymized peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cancers 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 2900 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 response
- DNA repair
- replication stress
- ubiquitin–proteasome system
- E3 ubiquitin ligases
- targeted protein degradation
- cell cycle checkpoints
- drug resistance
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