Special Issue "DNA and Chromosomal Lesions in Tumorigenesis"

A special issue of Genes (ISSN 2073-4425). This special issue belongs to the section "Molecular Genetics and Genomics".

Deadline for manuscript submissions: closed (30 April 2021) | Viewed by 3125

Special Issue Editors

Department of Environmental & Radiological Health Sciences, Colorado State University, Fort Collins, CO 80523, USA
Interests: DNA damage; flavonoids; DNA repair; cytogenetics; radiobiology
Special Issues, Collections and Topics in MDPI journals
Faculty of Applied Sciences, Gifu University, Gifu, Japan
Interests: clinical oncology; pathology; tumorigenesis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

DNA and chromosomal lesions are one of the most important processes to initiate tumorigenesis. DNA damages including base damage, single strand breaks, double strand breaks, inter- and intra-strand crosslinks, and DNA–protein crosslinks can act as initiators. Chromosomal lesions including amplifications, deletions, inversions, translocations, and aneuploidy are often microscopically observable loss, gain or rearrangement of a particular or whole segment of a chromosome. These small or large lesions can cause alterations in oncogenes and tumor suppressor genes of somatic cells. These mutations occur spontaneously and via endogenous stress including ionizing radiation, ultraviolet light, oxidative stress, anticancer agents, and toxic mutagens.

This Special Issue will provide readers with information on "DNA and Chromosomal Lesions in Tumorigenesis". In particular, it will collect papers on the spontaneous and exogeneous stress altering genomic information and contributing transformation and tumorigenesis in in vitro cell cultures, in vivo animal experiments, and in human cancer patients. The mechanisms of generation of DNA and chromosomal lesions and the repair process are also topics of interest.

In this Special Issue, we expect to publish research manuscripts reporting computer software simulations, in vitro chemical reactions, and cellular and in vivo analyses. In addition, studies on novel methods to detect genomic alterations and translational research regarding experimental chemoprevention of tumorigenesis in cells and model animals are welcome. Therefore, this collection of interdisciplinary papers on DNA and chromosomal lesions in tumorigenesis will be a good reference for a broad range of readers, including modelers, chemists, biologists, and clinical researchers.

Prof. Takamitsu Kato
Prof. Mami Murakami
Guest Editors

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. Genes is an international peer-reviewed open access monthly 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 2600 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.


  • DNA damage
  • chromosomal aberrations
  • initiators
  • DNA repair
  • mutations
  • transformation
  • tumorigenesis
  • carcinogenesis
  • chemoprevention

Published Papers (1 paper)

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16 pages, 2608 KiB  
Cytotoxicity and Mutagenicity of Narrowband UVB to Mammalian Cells
Genes 2020, 11(6), 646; https://doi.org/10.3390/genes11060646 - 11 Jun 2020
Cited by 8 | Viewed by 2720
Phototherapy using narrowband ultraviolet-B (NB-UVB) has been shown to be more effective than conventional broadband UVB (BB-UVB) in treating a variety of skin diseases. To assess the difference in carcinogenic potential between NB-UVB and BB-UVB, we investigated the cytotoxicity via colony formation assay, [...] Read more.
Phototherapy using narrowband ultraviolet-B (NB-UVB) has been shown to be more effective than conventional broadband UVB (BB-UVB) in treating a variety of skin diseases. To assess the difference in carcinogenic potential between NB-UVB and BB-UVB, we investigated the cytotoxicity via colony formation assay, genotoxicity via sister chromatid exchange (SCE) assay, mutagenicity via hypoxanthine phosphoribosyltransferase (HPRT) mutation assay, as well as cyclobutane pyrimidine dimer (CPD) formation and reactive oxygen species (ROS) generation in Chinese hamster ovary (CHO) and their NER mutant cells. The radiation dose required to reduce survival to 10% (D10 value) demonstrated BB-UVB was 10 times more cytotoxic than NB-UVB, and revealed that NB-UVB also induces DNA damage repaired by nucleotide excision repair. We also found that BB-UVB more efficiently induced SCEs and HPRT mutations per absorbed energy dosage (J/m2) than NB-UVB. However, SCE and HPRT mutation frequencies were observed to rise in noncytotoxic dosages of NB-UVB exposure. BB-UVB and NB-UVB both produced a significant increase in CPD formation and ROS formation (p < 0.05); however, higher dosages were required for NB-UVB. These results suggest that NB-UVB is less cytotoxic and genotoxic than BB-UVB, but can still produce genotoxic effects even at noncytotoxic doses. Full article
(This article belongs to the Special Issue DNA and Chromosomal Lesions in Tumorigenesis)
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