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Cancers
Special Issues
Genome Instability and Human Cancer
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Genome Instability and Human Cancer

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Tumor Microenvironment".

Deadline for manuscript submissions: 15 April 2025 | Viewed by 2497

Special Issue Editor

Dr. Jian Ouyang

E-Mail Website
Guest Editor
Department of Biochemistry and Molecular Biology, Medical University of South Carolina, Charleston, SC 29425, USA
Interests: DNA damage response; genomic instability

Special Issue Information

Dear Colleagues,

Genomic instability is not only a hallmark of cancer but also an enabling characteristic that fuels cancer progression. Genomic instability in cancer cells also contributes to the evolving intra-tumor heterogeneity and the rise of drug-resistant cancer cells after chemotherapy or targeted therapy. However, cancer cells still need to maintain their genomes in a delicate stability to avoid the cellular catastrophe, which could be triggered by excessive instability in the genome. Cancer cells depend on various mechanisms to suppress their genomic instability from reaching a catastrophic point, which constitutes a vulnerability that can be exploited for therapeutic interventions. Targeting cancer-cell-specific dependency on mechanisms that suppress the genomic instability may create a synthetic lethality scenario that could kill cancer cells specifically or boost tumor-targeted immunity by activating an innate immune response, enhancing the intrinsic immunogenicity of cancer cells, or modulating the tumor microenvironment.

Dr. Jian Ouyang
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 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. 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

  • genomic instability
  • cancer progression
  • drug resistance
  • tumor-targeted immunity

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Published Papers (2 papers)

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Review

18 pages, 969 KiB  
Review
A TRilogy of ATR’s Non-Canonical Roles Throughout the Cell Cycle and Its Relation to Cancer
by Yoon Ki Joo, Carlos Ramirez and Lilian Kabeche
Cancers 2024, 16(20), 3536; https://doi.org/10.3390/cancers16203536 - 19 Oct 2024
Viewed by 793
Abstract
Ataxia Telangiectasia and Rad3-related protein (ATR) is an apical kinase of the DNA Damage Response (DDR) pathway responsible for detecting and resolving damaged DNA. Because cancer cells depend heavily on the DNA damage checkpoint for their unchecked proliferation and propagation, ATR has gained [...] Read more.
Ataxia Telangiectasia and Rad3-related protein (ATR) is an apical kinase of the DNA Damage Response (DDR) pathway responsible for detecting and resolving damaged DNA. Because cancer cells depend heavily on the DNA damage checkpoint for their unchecked proliferation and propagation, ATR has gained enormous popularity as a cancer therapy target in recent decades. Yet, ATR inhibitors have not been the silver bullets as anticipated, with clinical trials demonstrating toxicity and mixed efficacy. To investigate whether the toxicity and mixed efficacy of ATR inhibitors arise from their off-target effects related to ATR’s multiple roles within and outside the DDR pathway, we have analyzed recently published studies on ATR’s non-canonical roles. Recent studies have elucidated that ATR plays a wide role throughout the cell cycle that is separate from its function in the DDR. This includes maintaining nuclear membrane integrity, detecting mechanical forces, and promoting faithful chromosome segregation during mitosis. In this review, we summarize the canonical, DDR-related roles of ATR and also focus on the non-canonical, multifaceted roles of ATR throughout the cell cycle and their clinical relevance. Through this summary, we also address the need for re-assessing clinical strategies targeting ATR as a cancer therapy based on these newly discovered roles for ATR. Full article
(This article belongs to the Special Issue Genome Instability and Human Cancer)
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16 pages, 1285 KiB  
Review
Tolerance of Oncogene-Induced Replication Stress: A Fuel for Genomic Instability
by Taichi Igarashi, Kimiyoshi Yano, Syoju Endo and Bunsyo Shiotani
Cancers 2024, 16(20), 3507; https://doi.org/10.3390/cancers16203507 - 17 Oct 2024
Viewed by 1299
Abstract
Activation of oncogenes disturbs a wide variety of cellular processes and induces physiological dysregulation of DNA replication, widely referred to as replication stress (RS). Oncogene-induced RS can cause replication forks to stall or collapse, thereby leading to DNA damage. While the DNA damage [...] Read more.
Activation of oncogenes disturbs a wide variety of cellular processes and induces physiological dysregulation of DNA replication, widely referred to as replication stress (RS). Oncogene-induced RS can cause replication forks to stall or collapse, thereby leading to DNA damage. While the DNA damage response (DDR) can provoke an anti-tumor barrier to prevent the development of cancer, a small subset of cells triggers replication stress tolerance (RST), allowing precancerous cells to survive, thereby promoting clonal expansion and genomic instability (GIN). Genomic instability (GIN) is a hallmark of cancer, driving genetic alterations ranging from nucleotide changes to aneuploidy. These alterations increase the probability of oncogenic events and create a heterogeneous cell population with an enhanced ability to evolve. This review explores how major oncogenes such as RAS, cyclin E, and MYC induce RS through diverse mechanisms. Additionally, we delve into the strategies employed by normal and cancer cells to tolerate RS and promote GIN. Understanding the intricate relationship between oncogene activation, RS, and GIN is crucial to better understand how cancer cells emerge and to develop potential cancer therapies that target these vulnerabilities. Full article
(This article belongs to the Special Issue Genome Instability and Human Cancer)
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