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Application of Animal Modeling in Cancer
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Application of Animal Modeling in Cancer

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

Deadline for manuscript submissions: closed (25 June 2024) | Viewed by 8732

Special Issue Editors

Dr. Dongyu Jia

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Guest Editor
Molecular and Cellular Biology, Department of Molecular and Cellular Biology, Kennesaw State University, Statesboro, GA, USA
Interests: cancer biology; human genetics; cell and molecular biology; drosophila
Special Issues, Collections and Topics in MDPI journals
Dr. Yinu Wang

E-Mail Website
Guest Editor
Department of Obstetrics and Gynecology, Northwestern University, Chicago, IL, USA
Interests: ovarian cancer; cancer stem cell; epigenetics; metabolism; ROS; chemo resistance
Special Issues, Collections and Topics in MDPI journals
Dr. Yoichiro Tamori

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Guest Editor
Graduate School of Medicine, Kyoto University, Kyoto, Japan
Interests: cancer cell evolution; polyploidy; tissue homeostasis; morphogenesis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Cancer is essentially a genetic disease. Accumulated genetic mutations accelerate genome instability, which eventually leads to the uncontrollable growth of the tumor. Many cancer types have poor prognosis due to their clinical heterogeneity and molecular diversity. There is a great need to understand cancer biology and to create animal models to advance scientific knowledge and facilitate cancer treatments.

This Special Issue of Genes aims to highlight the most recent advances in animal modeling and its application in the field of cancer research. We invite authors to submit reviews, original articles, new experimental and computational methods, and commentaries that focus on any of the following topics: different animal models of cancer, applications of animal modeling, and translational research using animals in cancer research and the clinical field. We look forward to your contributions.

Dr. Dongyu Jia
Dr. Yinu Wang
Dr. Yoichiro Tamori
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.

Keywords

  • animal model
  • cancer model
  • application
  • translational research
  • cancer biology

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Published Papers (4 papers)

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Research

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10 pages, 2160 KiB  
Article
Splice Variant of Spalax Heparanase Skipping Exon 12
by Nicola J. Nasser, Eviatar Nevo and Aaron Avivi
Genes 2024, 15(8), 1039; https://doi.org/10.3390/genes15081039 - 7 Aug 2024
Viewed by 1028
Abstract
The subterranean blind mole rat, Spalax, has evolved significantly over 47 million years to thrive in its underground habitat. A key enzyme in this adaptation is heparanase, which degrades heparan sulfate (HS) in the extracellular matrix (ECM), facilitating angiogenesis and releasing growth [...] Read more.
The subterranean blind mole rat, Spalax, has evolved significantly over 47 million years to thrive in its underground habitat. A key enzyme in this adaptation is heparanase, which degrades heparan sulfate (HS) in the extracellular matrix (ECM), facilitating angiogenesis and releasing growth factors for endothelial cells. Spalax heparanase has various splice variants influencing tumor growth and metastasis differently. We report a novel splice variant from a hypoxia-exposed kidney sample resulting from exon 12 skipping. This variant maintains the translation frame but lacks enzymatic activity, offering insights into Spalax’s unique adaptations. Full article
(This article belongs to the Special Issue Application of Animal Modeling in Cancer)
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21 pages, 13456 KiB  
Article
Tracking Ovine Pulmonary Adenocarcinoma Development Using an Experimental Jaagsiekte Sheep Retrovirus Infection Model
by Chris Cousens, James Meehan, David Collie, Steven Wright, Ziyuan Chang, Helen Todd, Jo Moore, Lynn Grant, Carola R. Daniel, Peter Tennant, Adrian Ritchie, James Nixon, Chris Proudfoot, Stefano Guido, Helen Brown, Calum D. Gray, Tom J. MacGillivray, R. Eddie Clutton, Stephen N. Greenhalgh, Rachael Gregson, David J. Griffiths, James Spivey, Nicole Storer, Chad E. Eckert and Mark Grayadd Show full author list remove Hide full author list
Genes 2024, 15(8), 1019; https://doi.org/10.3390/genes15081019 - 2 Aug 2024
Cited by 2 | Viewed by 1717
Abstract
Ovine pulmonary adenocarcinoma (OPA) is an infectious, neoplastic lung disease of sheep that causes significant animal welfare and economic issues throughout the world. Understanding OPA pathogenesis is key to developing tools to control its impact. Central to this need is the availability of [...] Read more.
Ovine pulmonary adenocarcinoma (OPA) is an infectious, neoplastic lung disease of sheep that causes significant animal welfare and economic issues throughout the world. Understanding OPA pathogenesis is key to developing tools to control its impact. Central to this need is the availability of model systems that can monitor and track events after Jaagsiekte sheep retrovirus (JSRV) infection. Here, we report the development of an experimentally induced OPA model intended for this purpose. Using three different viral dose groups (low, intermediate and high), localised OPA tumour development was induced by bronchoscopic JSRV instillation into the segmental bronchus of the right cardiac lung lobe. Pre-clinical OPA diagnosis and tumour progression were monitored by monthly computed tomography (CT) imaging and trans-thoracic ultrasound scanning. Post mortem examination and immunohistochemistry confirmed OPA development in 89% of the JSRV-instilled animals. All three viral doses produced a range of OPA lesion types, including microscopic disease and gross tumours; however, larger lesions were more frequently identified in the low and intermediate viral groups. Overall, 31% of JSRV-infected sheep developed localised advanced lesions. Of the sheep that developed localised advanced lesions, tumour volume doubling times (calculated using thoracic CT 3D reconstructions) were 14.8 ± 2.1 days. The ability of ultrasound to track tumour development was compared against CT; the results indicated a strong significant association between paired CT and ultrasound measurements at each time point (R2 = 0.799, p < 0.0001). We believe that the range of OPA lesion types induced by this model replicates aspects of naturally occurring disease and will improve OPA research by providing novel insights into JSRV infectivity and OPA disease progression. Full article
(This article belongs to the Special Issue Application of Animal Modeling in Cancer)
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21 pages, 1810 KiB  
Article
Translation of Data from Animal Models of Cancer to Immunotherapy of Breast Cancer and Chronic Lymphocytic Leukemia
by Reginald Gorczynski
Genes 2024, 15(3), 292; https://doi.org/10.3390/genes15030292 - 25 Feb 2024
Viewed by 1963
Abstract
The field of clinical oncology has been revolutionized over the past decade with the introduction of many new immunotherapies the existence of which have depended to a large extent on experimentation with both in vitro analysis and the use of various animal models, [...] Read more.
The field of clinical oncology has been revolutionized over the past decade with the introduction of many new immunotherapies the existence of which have depended to a large extent on experimentation with both in vitro analysis and the use of various animal models, including gene-modified mice. The discussion below will review my own laboratory’s studies, along with those of others in the field, on cancer immunotherapy. Our own studies have predominantly dwelt on two models of malignancy, namely a solid tumor model (breast cancer) and lymphoma. The data from our own laboratory, and that of other scientists, highlights the novel information so obtained, and the evidence that application of such information has already had an impact on immunotherapy of human oncologic diseases Full article
(This article belongs to the Special Issue Application of Animal Modeling in Cancer)
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Review

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20 pages, 2111 KiB  
Review
Polyploid Cancer Cell Models in Drosophila
by Yuqing Wang and Yoichiro Tamori
Genes 2024, 15(1), 96; https://doi.org/10.3390/genes15010096 - 14 Jan 2024
Cited by 1 | Viewed by 3373
Abstract
Cells with an abnormal number of chromosomes have been found in more than 90% of solid tumors, and among these, polyploidy accounts for about 40%. Polyploidized cells most often have duplicate centrosomes as well as genomes, and thus their mitosis tends to promote [...] Read more.
Cells with an abnormal number of chromosomes have been found in more than 90% of solid tumors, and among these, polyploidy accounts for about 40%. Polyploidized cells most often have duplicate centrosomes as well as genomes, and thus their mitosis tends to promote merotelic spindle attachments and chromosomal instability, which produces a variety of aneuploid daughter cells. Polyploid cells have been found highly resistant to various stress and anticancer therapies, such as radiation and mitogenic inhibitors. In other words, common cancer therapies kill proliferative diploid cells, which make up the majority of cancer tissues, while polyploid cells, which lurk in smaller numbers, may survive. The surviving polyploid cells, prompted by acute environmental changes, begin to mitose with chromosomal instability, leading to an explosion of genetic heterogeneity and a concomitant cell competition and adaptive evolution. The result is a recurrence of the cancer during which the tenacious cells that survived treatment express malignant traits. Although the presence of polyploid cells in cancer tissues has been observed for more than 150 years, the function and exact role of these cells in cancer progression has remained elusive. For this reason, there is currently no effective therapeutic treatment directed against polyploid cells. This is due in part to the lack of suitable experimental models, but recently several models have become available to study polyploid cells in vivo. We propose that the experimental models in Drosophila, for which genetic techniques are highly developed, could be very useful in deciphering mechanisms of polyploidy and its role in cancer progression. Full article
(This article belongs to the Special Issue Application of Animal Modeling in Cancer)
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