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Infectious Causes of Cancers: A Novel Pathway to Integrate Oncogenic...
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Infectious Causes of Cancers: A Novel Pathway to Integrate Oncogenic Processes with Host–Pathogen Theory and Evolutionary Biology

A special issue of Pathogens (ISSN 2076-0817).

Deadline for manuscript submissions: closed (30 September 2022) | Viewed by 29315

Special Issue Editors

Dr. Rodrigo Hamede

E-Mail Website
Guest Editor
School of Natural Sciences, College of Sciences and Engineering, University of Tasmania, Hobart 7001, Australia
Interests: disease ecology; epidemiology; behavioral ecology; evolutionary biology
Prof. Dr. Frederic Thomas

E-Mail Website
Guest Editor
CREEC/CANECEV, MIVEGEC (CREES), University of Montpellier, CNRS, IRD, Montpellier, France
Interests: cancer; ecology; evolution; behavioral ecology; health ecology
Dr. Beata Ujvari

E-Mail Website
Guest Editor
School of Life and Environmental Sciences, Centre for Integrative Ecology, Deakin University, Waurn Ponds 3226, Australia
Interests: cancer; ecology; evolution; genetics; immunology; host–parasite interactions

Special Issue Information

Dear Colleagues,

Infections are a fundamental trait of cancer causation, with up to 20% of all human cancers being associated with pathogens, such as oncoviruses, bacteria, and parasites. The infectious agent leading to cancer development can also be the cancer cell-line itself, as in the case of directly transmissible cancers. Exploring the evolutionary and ecological dynamics of cancers with infectious origins is a fascinating topic, which provides novel insights for understanding the role of oncogenic processes in shaping cellular and organismal traits as well as improving our ability to find novel solutions for cancer prevention and therapies.

The reciprocal interactions of infectious cancers with their hosts are in many ways analogous to the interplay of immunological, ecological, and evolutionary processes in host–pathogen systems. The growing number of novel cancer cell lines and virus-associated oncogenes found in terrestrial and aquatic environments highlights the need to implement an adaptive and transdisciplinary framework for studying oncogenic phenomena. In that sense, cancers with an infectious causation or directly transmissible cancers present a unique opportunity for integrating host–pathogen theory and eco-evolutionary biology to cancer research.

Despite the ubiquitous nature of cancer in the animal kingdom, our historical knowledge of cancer has mostly been derived from human tumors and experimental research in laboratory mice. Studies in wildlife are now providing novel perspectives for understanding cancer with a holistic vision, bridging oncology and other biological sciences. Integrating host–pathogen theory and evolutionary biology with cancer research has the potential to reveal the cellular and environmental mechanisms of cancer emergence, help to understand disease progression, and evaluate evolutionary patterns. Developing comparative approaches in cancer research across humans, domestic species, and wildlife cancers will also provide valuable insights for understanding the genesis and lethality of tumors across taxa.

Recently, some efforts have been made to use transmissible cancers or those caused by pathogens as model systems for understanding how organisms respond and adapt to oncogenic threats. However, the integration of oncology with other biological sciences such as disease ecology and evolution is still in its early stages. In this Issue, we would like to focus on all aspects of infections and cancer research that increase our knowledge of cancer biology, ecology, evolution, and host–pathogen theory. Topics of interest include (but are not limited to) transmission pathways, host–tumor interactions, immunogenetics and mechanisms of immune evasion, disease ecology and epidemiology, vaccine research, clinical and pathological aspects, as well as the development and improvement of diagnostic techniques.

Dr. Rodrigo Hamede
Prof. Dr. Frederic Thomas
Dr. Beata Ujvari
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. Pathogens 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 2200 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

  • transmissible cancer
  • oncovirus
  • host–pathogen interactions
  • evolutionary biology
  • disease ecology
  • immunogenetics
  • immunoecology
  • oncogenesis
  • evolutionary medicine
  • life history trade-offs
  • epidemiology

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Published Papers (6 papers)

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Research

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17 pages, 35966 KiB  
Article
Expression of the Nonclassical MHC Class I, Saha-UD in the Transmissible Cancer Devil Facial Tumour Disease (DFTD)
by Kathryn Hussey, Alison Caldwell, Alexandre Kreiss, Karsten Skjødt, Annalisa Gastaldello, Ruth Pye, Rodrigo Hamede, Gregory M. Woods and Hannah V. Siddle
Pathogens 2022, 11(3), 351; https://doi.org/10.3390/pathogens11030351 - 14 Mar 2022
Viewed by 4358
Abstract
Devil facial tumour disease (DFTD) is a transmissible cancer that has circulated in the Tasmanian devil population for >25 years. Like other contagious cancers in dogs and devils, the way DFTD escapes the immune response of its host is a central question to [...] Read more.
Devil facial tumour disease (DFTD) is a transmissible cancer that has circulated in the Tasmanian devil population for >25 years. Like other contagious cancers in dogs and devils, the way DFTD escapes the immune response of its host is a central question to understanding this disease. DFTD has a low major histocompatibility complex class I (MHC-I) expression due to epigenetic modifications, preventing host immune recognition of mismatched MHC-I molecules by T cells. However, the total MHC-I loss should result in natural killer (NK) cell activation due to the ‘missing self’. Here, we have investigated the expression of the nonclassical MHC-I, Saha-UD as a potential regulatory or suppressive mechanism for DFTD. A monoclonal antibody was generated against the devil Saha-UD that binds recombinant Saha-UD by Western blot, with limited crossreactivity to the classical MHC-I, Saha-UC and nonclassical Saha-UK. Using this antibody, we confirmed the expression of Saha-UD in 13 DFTD tumours by immunohistochemistry (n = 15) and demonstrated that Saha-UD expression is heterogeneous, with 12 tumours showing intratumour heterogeneity. Immunohistochemical staining for the Saha-UD showed distinct patterns of expression when compared with classical MHC-I molecules. The nonclassical Saha-UD expression by DFTD tumours in vivo may be a mechanism for immunosuppression, and further work is ongoing to characterise its ligand on immune cells. Full article
(This article belongs to the Special Issue Infectious Causes of Cancers: A Novel Pathway to Integrate Oncogenic Processes with Host–Pathogen Theory and Evolutionary Biology)
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14 pages, 1192 KiB  
Article
Survival and Detection of Bivalve Transmissible Neoplasia from the Soft-Shell Clam Mya arenaria (MarBTN) in Seawater
by Rachael M. Giersch, Samuel F. M. Hart, Satyatejas G. Reddy, Marisa A. Yonemitsu, María J. Orellana Rosales, Madelyn Korn, Brook M. Geleta, Peter D. Countway, José A. Fernández Robledo and Michael J. Metzger
Pathogens 2022, 11(3), 283; https://doi.org/10.3390/pathogens11030283 - 23 Feb 2022
Cited by 15 | Viewed by 4955
Abstract
Many pathogens can cause cancer, but cancer itself does not normally act as an infectious agent. However, transmissible cancers have been found in a few cases in nature: in Tasmanian devils, dogs, and several bivalve species. The transmissible cancers in dogs and devils [...] Read more.
Many pathogens can cause cancer, but cancer itself does not normally act as an infectious agent. However, transmissible cancers have been found in a few cases in nature: in Tasmanian devils, dogs, and several bivalve species. The transmissible cancers in dogs and devils are known to spread through direct physical contact, but the exact route of transmission of bivalve transmissible neoplasia (BTN) has not yet been confirmed. It has been hypothesized that cancer cells from bivalves could be released by diseased animals and spread through the water column to infect/engraft into other animals. To test the feasibility of this proposed mechanism of transmission, we tested the ability of BTN cells from the soft-shell clam (Mya arenaria BTN, or MarBTN) to survive in artificial seawater. We found that MarBTN cells are highly sensitive to salinity, with acute toxicity at salinity levels lower than those found in the native marine environment. BTN cells also survive longer at lower temperatures, with 50% of cells surviving greater than 12 days in seawater at 10 °C, and more than 19 days at 4 °C. With one clam donor, living cells were observed for more than eight weeks at 4 °C. We also used qPCR of environmental DNA (eDNA) to detect the presence of MarBTN-specific DNA in the environment. We observed release of MarBTN-specific DNA into the water of laboratory aquaria containing highly MarBTN-diseased clams, and we detected MarBTN-specific DNA in seawater samples collected from MarBTN-endemic areas in Maine, although the copy numbers detected in environmental samples were much lower than those found in aquaria. Overall, these data show that MarBTN cells can survive well in seawater, and they are released into the water by diseased animals. These findings support the hypothesis that BTN is spread from animal-to-animal by free cells through seawater. Full article
(This article belongs to the Special Issue Infectious Causes of Cancers: A Novel Pathway to Integrate Oncogenic Processes with Host–Pathogen Theory and Evolutionary Biology)
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16 pages, 9284 KiB  
Article
Disruption of Metapopulation Structure Reduces Tasmanian Devil Facial Tumour Disease Spread at the Expense of Abundance and Genetic Diversity
by Rowan Durrant, Rodrigo Hamede, Konstans Wells and Miguel Lurgi
Pathogens 2021, 10(12), 1592; https://doi.org/10.3390/pathogens10121592 - 8 Dec 2021
Cited by 2 | Viewed by 5988
Abstract
Metapopulation structure plays a fundamental role in the persistence of wildlife populations. It can also drive the spread of infectious diseases and transmissible cancers such as the Tasmanian devil facial tumour disease (DFTD). While disrupting this structure can reduce disease spread, it can [...] Read more.
Metapopulation structure plays a fundamental role in the persistence of wildlife populations. It can also drive the spread of infectious diseases and transmissible cancers such as the Tasmanian devil facial tumour disease (DFTD). While disrupting this structure can reduce disease spread, it can also impair host resilience by disrupting gene flow and colonisation dynamics. Using an individual-based metapopulation model we investigated the synergistic effects of host dispersal, disease transmission rate and inter-individual contact distance for transmission, on the spread and persistence of DFTD from local to regional scales. Disease spread, and the ensuing population declines, are synergistically determined by individuals’ dispersal, disease transmission rate and within-population mixing. Transmission rates can be magnified by high dispersal and inter-individual transmission distance. The isolation of local populations effectively reduced metapopulation-level disease prevalence but caused severe declines in metapopulation size and genetic diversity. The relative position of managed (i.e., isolated) local populations had a significant effect on disease prevalence, highlighting the importance of considering metapopulation structure when implementing metapopulation-scale disease control measures. Our findings suggest that population isolation is not an ideal management method for preventing disease spread in species inhabiting already fragmented landscapes, where genetic diversity and extinction risk are already a concern. Full article
(This article belongs to the Special Issue Infectious Causes of Cancers: A Novel Pathway to Integrate Oncogenic Processes with Host–Pathogen Theory and Evolutionary Biology)
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16 pages, 1636 KiB  
Article
Sea Turtles in the Cancer Risk Landscape: A Global Meta-Analysis of Fibropapillomatosis Prevalence and Associated Risk Factors
by Antoine M. Dujon, Gail Schofield, Roberto M. Venegas, Frédéric Thomas and Beata Ujvari
Pathogens 2021, 10(10), 1295; https://doi.org/10.3390/pathogens10101295 - 8 Oct 2021
Cited by 21 | Viewed by 4669
Abstract
Several cancer risk factors (exposure to ultraviolet-B, pollution, toxins and pathogens) have been identified for wildlife, to form a “cancer risk landscape.” However, information remains limited on how the spatiotemporal variability of these factors impacts the prevalence of cancer in wildlife. Here, we [...] Read more.
Several cancer risk factors (exposure to ultraviolet-B, pollution, toxins and pathogens) have been identified for wildlife, to form a “cancer risk landscape.” However, information remains limited on how the spatiotemporal variability of these factors impacts the prevalence of cancer in wildlife. Here, we evaluated the cancer risk landscape at 49 foraging sites of the globally distributed green turtle (Chelonia mydas), a species affected by fibropapillomatosis, by integrating data from a global meta-analysis of 31 publications (1994–2019). Evaluated risk factors included ultraviolet light exposure, eutrophication, toxic phytoplanktonic blooms, sea surface temperature, and the presence of mechanical vectors (parasites and symbiotic species). Prevalence was highest in areas where nutrient concentrations facilitated the emergence of toxic phytoplankton blooms. In contrast, ultraviolet light exposure and the presence of parasitic and/or symbiotic species did not appear to impact disease prevalence. Our results indicate that, to counter outbreaks of fibropapillomatosis, management actions that reduce eutrophication in foraging areas should be implemented. Full article
(This article belongs to the Special Issue Infectious Causes of Cancers: A Novel Pathway to Integrate Oncogenic Processes with Host–Pathogen Theory and Evolutionary Biology)
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Review

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12 pages, 1727 KiB  
Review
Challenges of an Emerging Disease: The Evolving Approach to Diagnosing Devil Facial Tumour Disease
by Camila Espejo, Amanda L. Patchett, Richard Wilson, A. Bruce Lyons and Gregory M. Woods
Pathogens 2022, 11(1), 27; https://doi.org/10.3390/pathogens11010027 - 28 Dec 2021
Cited by 2 | Viewed by 4185
Abstract
Devil Facial Tumour Disease (DFTD) is an emerging infectious disease that provides an excellent example of how diagnostic techniques improve as disease-specific knowledge is generated. DFTD manifests as tumour masses on the faces of Tasmanian devils, first noticed in 1996. As DFTD became [...] Read more.
Devil Facial Tumour Disease (DFTD) is an emerging infectious disease that provides an excellent example of how diagnostic techniques improve as disease-specific knowledge is generated. DFTD manifests as tumour masses on the faces of Tasmanian devils, first noticed in 1996. As DFTD became more prevalent among devils, karyotyping of the lesions and their devil hosts demonstrated that DFTD was a transmissible cancer. The subsequent routine diagnosis relied on microscopy and histology to characterise the facial lesions as cancer cells. Combined with immunohistochemistry, these techniques characterised the devil facial tumours as sarcomas of neuroectodermal origin. More sophisticated molecular methods identified the origin of DFTD as a Schwann cell, leading to the Schwann cell-specific protein periaxin to discriminate DFTD from other facial lesions. After the discovery of a second facial cancer (DFT2), cytogenetics and the absence of periaxin expression confirmed the independence of the new cancer from DFT1 (the original DFTD). Molecular studies of the two DFTDs led to the development of a PCR assay to differentially diagnose the cancers. Proteomics and transcriptomic studies identified different cell phenotypes among the two DFTD cell lines. Phenotypic differences were also reflected in proteomics studies of extracellular vesicles (EVs), which yielded an early diagnostic marker that could detect DFTD in its latent stage from serum samples. A mesenchymal marker was also identified that could serve as a serum-based differential diagnostic. The emergence of two transmissible cancers in one species has provided an ideal opportunity to better understand transmissible cancers, demonstrating how fundamental research can be translated into applicable and routine diagnostic techniques. Full article
(This article belongs to the Special Issue Infectious Causes of Cancers: A Novel Pathway to Integrate Oncogenic Processes with Host–Pathogen Theory and Evolutionary Biology)
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Other

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6 pages, 720 KiB  
Perspective
Transmissible Cancer Evolution: The Under-Estimated Role of Environmental Factors in the “Perfect Storm” Theory
by Sophie Tissot, Anne-Lise Gérard, Justine Boutry, Antoine M. Dujon, Tracey Russel, Hannah Siddle, Aurélie Tasiemski, Jordan Meliani, Rodrigo Hamede, Benjamin Roche, Beata Ujvari and Frédéric Thomas
Pathogens 2022, 11(2), 241; https://doi.org/10.3390/pathogens11020241 - 12 Feb 2022
Cited by 8 | Viewed by 3784
Abstract
Although the true prevalence of transmissible cancers is not known, these atypical malignancies are likely rare in the wild. The reasons behind this rarity are only partially understood, but the “Perfect Storm hypothesis” suggests that transmissible cancers are infrequent because a precise confluence [...] Read more.
Although the true prevalence of transmissible cancers is not known, these atypical malignancies are likely rare in the wild. The reasons behind this rarity are only partially understood, but the “Perfect Storm hypothesis” suggests that transmissible cancers are infrequent because a precise confluence of tumor and host traits is required for their emergence. This explanation is plausible as transmissible cancers, like all emerging pathogens, will need specific biotic and abiotic conditions to be able to not only emerge, but to spread to detectable levels. Because those conditions would be rarely met, transmissible cancers would rarely spread, and thus most of the time disappear, even though they would regularly appear. Thus, further research is needed to identify the most important factors that can facilitate or block the emergence of transmissible cancers and influence their evolution. Such investigations are particularly relevant given that human activities are increasingly encroaching into wild areas, altering ecosystems and their processes, which can influence the conditions needed for the emergence and spread of transmissible cell lines. Full article
(This article belongs to the Special Issue Infectious Causes of Cancers: A Novel Pathway to Integrate Oncogenic Processes with Host–Pathogen Theory and Evolutionary Biology)
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