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Dear Colleagues,

We are seeking to gauge interest in submitting articles to a Special Issue curated by the International Journal of Molecular Sciences on “New Findings and Insights in Inflammation-Induced DNA Damage, Mutations and Cancer”.

Inflammation and mutagenesis are well-known hallmarks of cancer, and while the mechanisms linking inflammation or mutagenesis to cancer are frequently interrogated, the interrelationships between inflammation and mutagenesis and subsequent influences on cancer are less well studied. DNA damage is a key node in the network that connects inflammation and mutagenesis—inflammation both causes and is caused by DNA damage, and DNA damage is the dominant cause of mutagenesis (aside from spontaneous replication errors). Additionally, increases in cellular proliferation (a result of inflammation and a feature of carcinogenesis) sensitize cells to DNA damage-induced mutations. Environmental exposures and endogenous processes can increase inflammation, DNA damage, and/or proliferation, in turn provoking the progressive accumulation of mutations that leads to carcinogenesis. Interrogation of the cellular signaling mechanisms underlying inflammation, DNA damage, and proliferation will also provide insight into key events in the pathway, from inflammation and/or exposure to the adverse outcome of cancer. As such, integrated studies of inflammation, DNA damage, cellular proliferation, and mutagenesis are needed to elucidate the mechanisms of cancer development, to evaluate chemicals for carcinogenic potential, and to identify potential opportunities for intervention.

This Special Issue of the International Journal of Molecular Sciences is dedicated to recent advances in understanding the complex relationships between inflammation, DNA damage, and mutagenesis that govern cancer development.

Dr. Jennifer Kay
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

Inflammation
DNA damage
DNA repair
Mutagenesis
Carcinogenesis
Cell signaling
Oxidative stress
Integrated pathway analysis
Tumor microenvironment
DNA damage response
Cellular proliferation

Published Papers (2 papers)

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Research

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25 pages, 3489 KiB

Open AccessArticle

Human Recombinant DNase I (Pulmozyme^®) Inhibits Lung Metastases in Murine Metastatic B16 Melanoma Model That Correlates with Restoration of the DNase Activity and the Decrease SINE/LINE and c-Myc Fragments in Blood Cell-Free DNA

by Ludmila Alekseeva, Aleksandra Sen’kova, Innokenty Savin, Marina Zenkova and Nadezhda Mironova

Int. J. Mol. Sci. 2021, 22(21), 12074; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms222112074 - 08 Nov 2021

Cited by 5 | Viewed by 3548

Abstract

Tumor-associated cell-free DNAs (cfDNA) play an important role in the promotion of metastases. Previous studies proved the high antimetastatic potential of bovine pancreatic DNase I and identified short interspersed nuclear elements (SINEs) and long interspersed nuclear elements (LINEs)and fragments of oncogenes in cfDNA as the main molecular targets of enzyme in the bloodstream. Here, recombinant human DNase I (commercial name Pulmozyme^®), which is used for the treatment of cystic fibrosis in humans, was repurposed for the inhibition of lung metastases in the B16 melanoma model in mice. We found that Pulmozyme^® strongly reduced migration and induced apoptosis of B16 cells in vitro and effectively inhibited metastases in lungs and liver in vivo. Pulmozyme^® was shown to be two times more effective when administered intranasally (i.n.) than bovine DNase I, but intramuscular (i.m.) administration forced it to exhibit as high an antimetastatic activity as bovine DNase I. Both DNases administered to mice either i.m. or i.n. enhanced the DNase activity of blood serum to the level of healthy animals, significantly decreased cfDNA concentrations, efficiently degraded SINE and LINE repeats and c-Myc fragments in the bloodstream and induced apoptosis and disintegration of neutrophil extracellular traps in metastatic foci; as a result, this manifested as the inhibition of metastases spread. Thus, Pulmozyme^®, which is already an approved drug, can be recommended for use in the treatment of lung metastases. Full article

(This article belongs to the Special Issue New Findings and Insights in Inflammation-Induced DNA Damage, Mutations and Cancer)

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Review

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21 pages, 18439 KiB

Open AccessReview

Role of Cell-Free DNA and Deoxyribonucleases in Tumor Progression

by Ludmila Alekseeva and Nadezhda Mironova

Int. J. Mol. Sci. 2021, 22(22), 12246; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms222212246 - 12 Nov 2021

Cited by 11 | Viewed by 2696

Abstract

Many studies have reported an increase in the level of circulating cell-free DNA (cfDNA) in the blood of patients with cancer. cfDNA mainly comes from tumor cells and, therefore, carries features of its genomic profile. Moreover, tumor-derived cfDNA can act like oncoviruses, entering the cells of vulnerable organs, transforming them and forming metastatic nodes. Another source of cfDNA is immune cells, including neutrophils that generate neutrophil extracellular traps (NETs). Despite the potential eliminative effect of NETs on tumors, in some cases, their excessive generation provokes tumor growth as well as invasion. Considering both possible pathological contributions of cfDNA, as an agent of oncotransformation and the main component of NETs, the study of deoxyribonucleases (DNases) as anticancer and antimetastatic agents is important and promising. This review considers the pathological role of cfDNA in cancer development and the role of DNases as agents to prevent and/or prohibit tumor progression and the development of metastases. Full article

(This article belongs to the Special Issue New Findings and Insights in Inflammation-Induced DNA Damage, Mutations and Cancer)

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