Topical Collection "Genome Maintenance in Cancer Biology and Therapy"

Editor

Dr. Spencer Collis
E-Mail Website
Collection Editor
Weston Park Cancer Centre, Department of Oncology & Metabolism, University of Sheffield, Sheffield, S10 2RX, UK.
Interests: genome stability; DNA damage and repair; DNA replication; cell cycle checkpoints; cancer biology and therapy
Special Issues, Collections and Topics in MDPI journals

Topical Collection Information

Dear Colleagues,

Genome instability is a defined hallmark of cancer, and is an important mechanism in tumour development, progression, heterogeneity and drug resistance; the latter two being two common barriers to effective treatment. Genome instability in tumour cells often arises through heightened DNA damage and/or replication stress; a respective consequence of increased metabolic processes that produce DNA damaging by-products, and an increased proliferative state due to the action of activated oncogenes.

To preserve genomic integrity, human cells have developed interconnected genome maintenance mechanisms that facilitate an orchestration of DNA damage response pathways, DNA repair mechanisms, cell cycle checkpoints and cell division processes. The many cancer predisposing human diseases that are associated with underlying mutations in/dysregulation of key proteins within these pathways highlights the importance of genome stability mechanisms in the suppression of tumour development and progression.

In addition to a deeper understanding of cancer biology, the study of genome maintenance mechanisms and their co-ordinated regulation has revealed new therapeutic targets to improve the effectiveness of existing radio-/chemotherapy regimes, as well as identifying exploitable tumour-selective vulnerabilities around which both novel or repurposed therapeutic strategies can be developed. Furthering our understanding of genome maintenance mechanisms is therefore vital to help understand how such processes become dysfunctional in cancer development/progression, and to identify new targets and/or biomarkers to develop new therapeutic strategies to improve the clinical management of these disease and improve patient survival.

This new Topic section of Cancers therefore aims to publish new research articles and timely reviews on aspects of genome maintenance mechanisms that either play a role in cancer development and progression or reveal new therapeutic opportunities to better treat this disease.

Dr. Spencer Collis
Collection 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 papers will be peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the collection 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. 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 2200 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.

Published Papers (1 paper)

2021

Article
High Temperature Drives Topoisomerase Mediated Chromosomal Break Repair Pathway Choice
Cancers 2021, 13(10), 2315; https://doi.org/10.3390/cancers13102315 - 12 May 2021
Cited by 1 | Viewed by 1409
Abstract
Cancer-causing mutations often arise from inappropriate DNA repair, yet acute exposure to DNA damage is widely used to treat cancer. The challenge remains in how to specifically induce excessive DNA damage in cancer cells while minimizing the undesirable effects of genomic instability in [...] Read more.
Cancer-causing mutations often arise from inappropriate DNA repair, yet acute exposure to DNA damage is widely used to treat cancer. The challenge remains in how to specifically induce excessive DNA damage in cancer cells while minimizing the undesirable effects of genomic instability in noncancerous cells. One approach is the acute exposure to hyperthermia, which suppresses DNA repair and synergizes with radiotherapy and chemotherapy. An exception, however, is the protective effect of hyperthermia on topoisomerase targeting therapeutics. The molecular explanation for this conundrum remains unclear. Here, we show that hyperthermia suppresses the level of topoisomerase mediated single- and double-strand breaks induced by exposure to topoisomerase poisons. We further uncover that, hyperthermia suppresses hallmarks of genomic instability induced by topoisomerase targeting therapeutics by inhibiting nuclease activities, thereby channeling repair to error-free pathways driven by tyrosyl-DNA phosphodiesterases. These findings provide an explanation for the protective effect of hyperthermia from topoisomerase-induced DNA damage and may help to explain the inverse relationship between cancer incidence and temperature. They also pave the way for the use of controlled heat as a therapeutic adjunct to topoisomerase targeting therapeutics. Full article
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