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DNA Repair in Cancers 2.0
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DNA Repair in Cancers 2.0

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Oncology".

Deadline for manuscript submissions: closed (31 July 2022) | Viewed by 4963

Special Issue Editor

Dr. Igor Belyaev

E-Mail Website
Guest Editor
Cancer Research Institute, Biomedical Research Center, Slovak Academy of Sciences, Dúbravska cesta 9, 845 05 Bratislava, Slovakia
Interests: DNA damage and repair; apoptosis; stem cells; ionizing and non-ionizing radiation; electromagnetic fields
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

DNA damage and repair are essential factors which underlie different aspects of cancer, such as induction, promotion, treatment, and risk assessment. DNA double-strand breaks (DSB) represent a most important type of DNA damage, resulting in the formation of chromosomal aberrations, which represent one of the major causes for cancer origination. Thus, the focus of this Special Issue will be DSB. However, other types of DNA damage and related issues dealing with mutations, apoptosis, cell cycle, senescence, DNA damage checkpoints, and DNA repair defects in cancer may also be covered in this Special Issue. There are multiple agents, including various chemicals and ionizing radiations, which induce DNA damage and are efficiently used in treatment of cancer through chemo- and radiotherapy. All these topics are to be covered including challenging issues, such as new aspects in mechanisms of DNA repair; induction of DNA damage by non-ionizing radiation and electromagnetic fields; relationship of DNA damage response with individual radiosensitivity of cancer patients; DNA damage response in normal and cancer stem cells; evaluation of DNA damage and repair for predicting normal and tumor tissue radiosensitivity, assessment of predisposition to cancer and cancer risk, cancer diagnostics and treatment.

We would like to invite you to contribute to the Special Issue “DNA Repair in Cancers” of the International Journal of Molecular Sciences (IJMS, https://www.mdpi.com/journal/ijms). This journal has a good impact factor (latest Impact Factor 5.923) and is indexed in Pubmed. Both original studies and reviews are welcome for this Special Issue. If you would like to contribute a review article or original research, it would be greatly appreciated if you could provide a tentative title and a very short abstract of several lines.

Dr. Igor Belyaev
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 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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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
  • DNA double stand breaks
  • DNA repair
  • Cancer
  • Mutation
  • Apoptosis
  • Chromosomal aberrations
  • Radiation
  • Electromagnetic fields

Published Papers (2 papers)

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Research

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14 pages, 2942 KiB  
Article
Inhibition of E. coli RecQ Helicase Activity by Structurally Distinct DNA Lesions: Structure—Function Relationships
by Ana H. Sales, Vincent Zheng, Maya A. Kenawy, Mark Kakembo, Lu Zhang, Vladimir Shafirovich, Suse Broyde and Nicholas E. Geacintov
Int. J. Mol. Sci. 2022, 23(24), 15654; https://doi.org/10.3390/ijms232415654 - 09 Dec 2022
Viewed by 1348
Abstract
DNA helicase unwinding activity can be inhibited by small molecules and by covalently bound DNA lesions. Little is known about the relationships between the structural features of DNA lesions and their impact on unwinding rates and processivities. Employing E.coli RecQ helicase as a [...] Read more.
DNA helicase unwinding activity can be inhibited by small molecules and by covalently bound DNA lesions. Little is known about the relationships between the structural features of DNA lesions and their impact on unwinding rates and processivities. Employing E.coli RecQ helicase as a model system, and various conformationally defined DNA lesions, the unwinding rate constants kobs = kU + kD, and processivities P = (kU/(kU + kD) were determined (kU, unwinding rate constant; kD, helicase-DNA dissociation rate constant). The highest kobs values were observed in the case of intercalated benzo[a]pyrene (BP)-derived adenine adducts, while kobs values of guanine adducts with minor groove or base-displaced intercalated adduct conformations were ~10–20 times smaller. Full unwinding was observed in each case with the processivity P = 1.0 (100% unwinding). The kobs values of the non-bulky lesions T(6−4)T, CPD cyclobutane thymine dimers, and a guanine oxidation product, spiroiminodihydantoin (Sp), are up to 20 times greater than some of the bulky adduct values; their unwinding efficiencies are strongly inhibited with processivities P = 0.11 (CPD), 0.062 (T(6−4)T), and 0.63 (Sp). These latter observations can be accounted for by correlated decreases in unwinding rate constants and enhancements in the helicase DNA complex dissociation rate constants. Full article
(This article belongs to the Special Issue DNA Repair in Cancers 2.0)
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Review

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12 pages, 658 KiB  
Review
The Chromatin Remodeler HELLS: A New Regulator in DNA Repair, Genome Maintenance, and Cancer
by Estanislao Peixoto, Asad Khan, Zachary A. Lewis, Rafael Contreras-Galindo and Wioletta Czaja
Int. J. Mol. Sci. 2022, 23(16), 9313; https://doi.org/10.3390/ijms23169313 - 18 Aug 2022
Cited by 5 | Viewed by 2977
Abstract
Robust, tightly regulated DNA repair is critical to maintaining genome stability and preventing cancer. Eukaryotic DNA is packaged into chromatin, which has a profound, yet incompletely understood, regulatory influence on DNA repair and genome stability. The chromatin remodeler HELLS (helicase, lymphoid specific) has [...] Read more.
Robust, tightly regulated DNA repair is critical to maintaining genome stability and preventing cancer. Eukaryotic DNA is packaged into chromatin, which has a profound, yet incompletely understood, regulatory influence on DNA repair and genome stability. The chromatin remodeler HELLS (helicase, lymphoid specific) has emerged as an important epigenetic regulator of DNA repair, genome stability, and multiple cancer-associated pathways. HELLS belongs to a subfamily of the conserved SNF2 ATP-dependent chromatin-remodeling complexes, which use energy from ATP hydrolysis to alter nucleosome structure and packaging of chromatin during the processes of DNA replication, transcription, and repair. The mouse homologue, LSH (lymphoid-specific helicase), plays an important role in the maintenance of heterochromatin and genome-wide DNA methylation, and is crucial in embryonic development, gametogenesis, and maturation of the immune system. Human HELLS is abundantly expressed in highly proliferating cells of the lymphoid tissue, skin, germ cells, and embryonic stem cells. Mutations in HELLS cause the human immunodeficiency syndrome ICF (Immunodeficiency, Centromeric instability, Facial anomalies). HELLS has been implicated in many types of cancer, including retinoblastoma, colorectal cancer, hepatocellular carcinoma, and glioblastoma. Here, we review and summarize accumulating evidence highlighting important roles for HELLS in DNA repair, genome maintenance, and key pathways relevant to cancer development, progression, and treatment. Full article
(This article belongs to the Special Issue DNA Repair in Cancers 2.0)
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