Darwin, the devil, and the management of transmissible cancers

Hamede, Rodrigo; Madsen, Thomas; McCallum, Hamish; Storfer, Andrew; Hohenlohe, Paul A.; Siddle, Hannah V.; Kaufman, Jim; Giraudeau, Mathieu; Jones, Menna Lloyd; Thomas, Fréderic; Újvári, Beáta

doi:10.1111/cobi.13644

Cited by 14 publications

(22 citation statements)

References 28 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…2019; Hamede et al . 2020). It is, however, important to recognise the potential for DFTD to evolve in response to changes in the host population, and that selecting for resistant devils might inadvertently select for more virulent tumours.…”

Section: Discussionmentioning

confidence: 99%

“…A third exciting priority is that we can attempt to accelerate the pace of evolution by identifying and then moving advantageous genotypes to areas lacking them (McCallum 2012). Crucially, these genotypes need to come from populations that are under selective pressure by DFTD (Hohenlohe et al 2019;Hamede et al 2020). It is, however, important to recognise the potential for DFTD to evolve in response to changes in the host population, and that selecting for resistant devils might inadvertently select for more virulent tumours.…”

Section: Population Trends and Conservationmentioning

confidence: 99%

See 1 more Smart Citation

Quantifying 25 years of disease‐caused declines in Tasmanian devil populations: host density drives spatial pathogen spread

et al. 2021

Self Cite

View full text Add to dashboard Cite

Infectious diseases are strong drivers of wildlife population dynamics, however, empirical analyses from the early stages of pathogen emergence are rare. Tasmanian devil facial tumour disease (DFTD), discovered in 1996, provides the opportunity to study an epizootic from its inception. We use a pattern‐oriented diffusion simulation to model the spatial spread of DFTD across the species' range and quantify population effects by jointly modelling multiple streams of data spanning 35 years. We estimate the wild devil population peaked at 53 000 in 1996, less than half of previous estimates. DFTD spread rapidly through high‐density areas, with spread velocity slowing in areas of low host densities. By 2020, DFTD occupied >90% of the species' range, causing 82% declines in local densities and reducing the total population to 16 900. Encouragingly, our model forecasts the population decline should level‐off within the next decade, supporting conservation management focused on facilitating evolution of resistance and tolerance.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Population Trends and Conservationmentioning

confidence: 99%

Quantifying 25 years of disease‐caused declines in Tasmanian devil populations: host density drives spatial pathogen spread

et al. 2021

Self Cite

View full text Add to dashboard Cite

show abstract

“…Further experiments are needed to explore this potential method for the future of cancer prevention and treatment (e.g., Thomas et al, 2018a). This area is still in its infancy concerning wildlife species, remaining the source of an important debate concerning its application and real efficiency (see Hamede et al, 2021).…”

Section: Could We Boost Cost-free Cancer Defenses In Organisms?mentioning

confidence: 99%

Ecological and Evolutionary Consequences of Anticancer Adaptations

et al. 2020

Self Cite

View full text Add to dashboard Cite

Summary Cellular cheating leading to cancers exists in all branches of multicellular life, favoring the evolution of adaptations to avoid or suppress malignant progression, and/or to alleviate its fitness consequences. Ecologists have until recently largely neglected the importance of cancer cells for animal ecology, presumably because they did not consider either the potential ecological or evolutionary consequences of anticancer adaptations. Here, we review the diverse ways in which the evolution of anticancer adaptations has significantly constrained several aspects of the evolutionary ecology of multicellular organisms at the cell, individual, population, species, and ecosystem levels and suggest some avenues for future research.

show abstract

“…Furthermore, empirical and theoretical evidence suggest that vaccinations that do not prevent transmission and spread of disease (often referred to as leaky or imperfect vaccines) can create ecological and epidemiological conditions that would allow more virulent pathogen strains to emerge and persist [61,62]. In the case of the Tasmanian devils and DFTD, an increasing number of studies have demonstrated natural adaptations to the epidemic [63,64], with devils developing defence mechanisms against infection, such as immune responses against DFTD, the upregulation of a tumour suppressor gene [65,66] and genetic changes in the tumour, leading to reduced transmission and epidemic outcomes [40,67]. Future research should integrate these deviltumour evolutionary processes to evaluate their long-term effects on disease spread and metapopulation dynamics.…”

Section: Discussionmentioning

confidence: 99%

Disruption of Metapopulation Structure Reduces Tasmanian Devil Facial Tumour Disease Spread at the Expense of Abundance and Genetic Diversity

et al. 2021

Self Cite

View full text Add to dashboard Cite

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.

show abstract

Darwin, the devil, and the management of transmissible cancers

Cited by 14 publications

References 28 publications

Quantifying 25 years of disease‐caused declines in Tasmanian devil populations: host density drives spatial pathogen spread

Quantifying 25 years of disease‐caused declines in Tasmanian devil populations: host density drives spatial pathogen spread

Ecological and Evolutionary Consequences of Anticancer Adaptations

Disruption of Metapopulation Structure Reduces Tasmanian Devil Facial Tumour Disease Spread at the Expense of Abundance and Genetic Diversity

Contact Info

Product

Resources

About