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Veterinary Sciences
Special Issues
Genetic Diseases and Gene Mutation-Related Tumors in Small Animals
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Genetic Diseases and Gene Mutation-Related Tumors in Small Animals

A special issue of Veterinary Sciences (ISSN 2306-7381). This special issue belongs to the section "Veterinary Biomedical Sciences".

Deadline for manuscript submissions: 25 July 2024 | Viewed by 4901

Special Issue Editor

Dr. Yasunaga Yoshikawa

E-Mail Website1 Website2
Guest Editor
Laboratory of Veterinary Biochemistry, School of Veterinary Medicine, Kitasato University, Aomori 034–8628, Japan
Interests: DNA damage repair; BRCA2; Fanconi/BRCA pathway; comparative oncology; dog

Special Issue Information

Dear Colleagues,

Small animals, especially dogs and cats, have been consistently bred to obtain preferred phenotypes, resulting in the accumulation of genetic mutations and a high prevalence of genetic diseases. Some purebred breeds are particularly susceptible to specific diseases. These congenital genetic diseases are caused by mutations in specific genes, which can potentially be avoided by devising breeding strategies. However, this issue has not yet been completely solved.

In addition, tumors are the most common disease resulting from genetic mutations in small animals. While mutations in genes related to tumors lead to their development, the study of tumor-related genes in small animals has not been studied as extensively as in humans. In small animals, certain genes have been evidenced to be associated with tumors, but more detailed information is required.

This Special Issue will collect not only basic research, including pathological, pharmacological, and biochemical studies on congenital genetic diseases and tumors, but also comparative and clinical studies and case reports. Through these studies, we aim to further enhance our understanding of genetic diseases, including tumors in small animals, and further contribute to the concept of “one health” by facilitating comparisons between small animals and humans. Thank you for your contribution.

Dr. Yasunaga Yoshikawa
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. Veterinary Sciences 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.

Keywords

  • DNA damage repair
  • genomic stability and instability
  • DNA damage response
  • DNA replication
  • tumors and other diseases caused by DNA instability
  • radiotherapy and chemotherapy

Published Papers (2 papers)

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Research

19 pages, 3568 KiB  
Article
A Highly Conserved Region in BRCA2 Suppresses the RAD51-Interaction Activity of BRC Repeats
by Zida Zhu, Taisuke Kitano, Masami Morimatsu, Kazuhiko Ochiai, Toshina Ishiguro-Oonuma, Kosuke Oosumi, Xianghui Lin, Koichi Orino and Yasunaga Yoshikawa
Vet. Sci. 2023, 10(2), 145; https://doi.org/10.3390/vetsci10020145 - 10 Feb 2023
Cited by 1 | Viewed by 1958
Abstract
Mammary tumors are the most prevalent type of tumors in female dogs. Breast cancer 2, early onset (BRCA2) malignant mutations are associated with tumorigenesis in humans and dogs. BRCA2 plays a pivotal role in homologous recombination repair by recruiting RAD51 recombinase [...] Read more.
Mammary tumors are the most prevalent type of tumors in female dogs. Breast cancer 2, early onset (BRCA2) malignant mutations are associated with tumorigenesis in humans and dogs. BRCA2 plays a pivotal role in homologous recombination repair by recruiting RAD51 recombinase to DNA damage sites to maintain genome stability. To recruit RAD51, BRCA2 must interact with RAD51 via BRC repeats, but the regulation of this interaction has been unclear. In this study, we focused on a highly conserved region (HCR) near BRC repeats. Using co-immunoprecipitation and mammalian two-hybrid assay, we found that HCR suppressed the RAD51-interaction activity of BRC repeats and that substitutions of HCR phosphorylation sites affected it. In canine tumor samples, we found ten mutations, including a novel HCR mutation (I1110M) from canine tumor samples. The effect of four HCR mutations, including I1110M, on the RAD51-interaction activity of BRC repeats was tested. One of the HCR mutations found in canine mammary tumors increased the interaction, but the two mutations found in human breast cancers decreased it. This study suggested that the HCR regulated the RAD51-interacting activity of BRC repeats through HCR phosphorylation and that mutations in HCR may be related to tumorigenesis in both dogs and humans. Full article
(This article belongs to the Special Issue Genetic Diseases and Gene Mutation-Related Tumors in Small Animals)
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13 pages, 2818 KiB  
Article
Canine Mammary Tumor Cell Lines Derived from Metastatic Foci Show Increased RAD51 Expression but Diminished Radioresistance via p21 Inhibition
by Kei Shimakawa, Kazuhiko Ochiai, Sachi Hirose, Eri Tanabe, Masaki Michishita, Motoharu Sakaue, Yasunaga Yoshikawa, Masami Morimatsu, Tsuyoshi Tajima, Masami Watanabe and Yoshikazu Tanaka
Vet. Sci. 2022, 9(12), 703; https://doi.org/10.3390/vetsci9120703 - 17 Dec 2022
Viewed by 1799
Abstract
Due to the high incidence of mammary tumors in dogs, it is important to elucidate the pathogenesis of these tumors in veterinary medicine. Radiation therapy is often used to treat mammary tumors that target DNA lesions. RAD51 is a key molecule that repairs [...] Read more.
Due to the high incidence of mammary tumors in dogs, it is important to elucidate the pathogenesis of these tumors in veterinary medicine. Radiation therapy is often used to treat mammary tumors that target DNA lesions. RAD51 is a key molecule that repairs DNA damage via homologous recombination. We examined the relationship between RAD51 expression and radiosensitivity in mammary tumor cell lines. CHMp and CHMm from the same individual were selected based on the differences in RAD51 expression. The radiosensitivity of both cell lines was examined using MTT and scratch assays; CHMm, which has high RAD51 expression, showed higher sensitivity to radiation than CHMp. However, the nuclear focus of RAD51 during DNA repair was formed normally in CHMp, but not in most of CHMm. Since irradiation resulted in the suppression of cell cycle progression in CHMp, the expression of p21, a cell cycle regulatory factor, was detected in CHMp after 15 Gy irradiation but not in CHMm. These results indicate that functional expression is more important than the quantitative expression of RAD51 in canine mammary tumor cells in response to DNA damage. Full article
(This article belongs to the Special Issue Genetic Diseases and Gene Mutation-Related Tumors in Small Animals)
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