Mitochondrial Capture by a Transmissible Cancer

Science ◽  
2011 ◽  
Vol 331 (6015) ◽  
pp. 303-303 ◽  
Author(s):  
C. A. Rebbeck ◽  
A. M. Leroi ◽  
A. Burt
Keyword(s):  
Transmissible Cancer

scholarly journals Prevalence and polymorphism of a mussel transmissible cancer in Europe

2021 ◽  
Author(s):  
Maurine Hammel ◽  
Alexis Simon ◽  
Christine Arbiol ◽  
Antonio Villalba ◽  
Erika AV Burioli ◽  
...  
Keyword(s):  
Transmissible Cancer

scholarly journals Evolution and lineage dynamics of a transmissible cancer in Tasmanian devils

PLoS Biology ◽  
2020 ◽  
Vol 18 (11) ◽  
pp. e3000926 ◽  
Author(s):  
Young Mi Kwon ◽  
Kevin Gori ◽  
Naomi Park ◽  
Nicole Potts ◽  
Kate Swift ◽  
...  
Keyword(s):  
Positive Selection ◽  
Cancer Cells ◽  
Cell Lines ◽  
Copy Number ◽  
Convergent Evolution ◽  
Evolutionary History ◽  
Genome Instability ◽  
Copy Number Variants ◽  
Tasmanian Devil ◽  
Transmissible Cancer

Devil facial tumour 1 (DFT1) is a transmissible cancer clone endangering the Tasmanian devil. The expansion of DFT1 across Tasmania has been documented, but little is known of its evolutionary history. We analysed genomes of 648 DFT1 tumours collected throughout the disease range between 2003 and 2018. DFT1 diverged early into five clades, three spreading widely and two failing to persist. One clade has replaced others at several sites, and rates of DFT1 coinfection are high. DFT1 gradually accumulates copy number variants (CNVs), and its telomere lengths are short but constant. Recurrent CNVs reveal genes under positive selection, sites of genome instability, and repeated loss of a small derived chromosome. Cultured DFT1 cell lines have increased CNV frequency and undergo highly reproducible convergent evolution. Overall, DFT1 is a remarkably stable lineage whose genome illustrates how cancer cells adapt to diverse environments and persist in a parasitic niche.

scholarly journals A Devil of a Transmissible Cancer

2020 ◽  
Vol 5 (2) ◽  
pp. 50 ◽  
Author(s):  
Gregory M. Woods ◽  
A. Bruce Lyons ◽  
Silvana S. Bettiol
Keyword(s):  
Cancer Cells ◽  
Direct Contact ◽  
Life Cycles ◽  
Host Organism ◽  
Independent Vector ◽  
Transmissible Cancer ◽  
Control And Prevention ◽  
Devil Facial Tumor Disease ◽  
Vector Borne ◽  
The Devil

Devil facial tumor disease (DFTD) encompasses two independent transmissible cancers that have killed the majority of Tasmanian devils. The cancer cells are derived from Schwann cells and are spread between devils during biting, a common behavior during the mating season. The Centers for Disease Control and Prevention (CDC) defines a parasite as “An organism that lives on or in a host organism and gets its food from, or at, the expense of its host.” Most cancers, including DFTD, live within a host organism and derive resources from its host, and consequently have parasitic-like features. Devil facial tumor disease is a transmissible cancer and, therefore, DFTD shares one additional feature common to most parasites. Through direct contact between devils, DFTD has spread throughout the devil population. However, unlike many parasites, the DFTD cancer cells have a simple lifecycle and do not have either independent, vector-borne, or quiescent phases. To facilitate a description of devil facial tumor disease, this review uses life cycles of parasites as an analogy.

scholarly journals Infectious disease and sickness behaviour: tumour progression affects interaction patterns and social network structure in wild Tasmanian devils

2020 ◽  
Vol 287 (1940) ◽  
pp. 20202454
Author(s):  
David G. Hamilton ◽  
Menna E. Jones ◽  
Elissa Z. Cameron ◽  
Douglas H. Kerlin ◽  
Hamish McCallum ◽  
...  
Keyword(s):  
Social Network ◽  
Cancer Progression ◽  
Population Change ◽  
Tumour Progression ◽  
Interaction Patterns ◽  
Social Network Structure ◽  
Devil Facial Tumour Disease ◽  
The Social ◽  
Transmissible Cancer ◽  
Host Behaviour

Infectious diseases, including transmissible cancers, can have a broad range of impacts on host behaviour, particularly in the latter stages of disease progression. However, the difficulty of early diagnoses makes the study of behavioural influences of disease in wild animals a challenging task. Tasmanian devils ( Sarcophilus harrisii ) are affected by a transmissible cancer, devil facial tumour disease (DFTD), in which tumours are externally visible as they progress. Using telemetry and mark–recapture datasets, we quantify the impacts of cancer progression on the behaviour of wild devils by assessing how interaction patterns within the social network of a population change with increasing tumour load. The progression of DFTD negatively influences devils' likelihood of interaction within their network. Infected devils were more active within their network late in the mating season, a pattern with repercussions for DFTD transmission. Our study provides a rare opportunity to quantify and understand the behavioural feedbacks of disease in wildlife and how they may affect transmission and population dynamics in general.

scholarly journals Somatic evolution and global expansion of an ancient transmissible cancer lineage

Science ◽  
2019 ◽  
Vol 365 (6452) ◽  
pp. eaau9923 ◽  
Author(s):  
Adrian Baez-Ortega ◽  
Kevin Gori ◽  
Andrea Strakova ◽  
Janice L. Allen ◽  
Karen M. Allum ◽  
...  
Keyword(s):  
Cancer Evolution ◽  
Time Resolved ◽  
Somatic Evolution ◽  
Dominant Feature ◽  
Transmissible Cancer ◽  
Clonal Organisms ◽  
Context Specific ◽  
Neutral Genetic Drift ◽  
Mutational Process

The canine transmissible venereal tumor (CTVT) is a cancer lineage that arose several millennia ago and survives by “metastasizing” between hosts through cell transfer. The somatic mutations in this cancer record its phylogeography and evolutionary history. We constructed a time-resolved phylogeny from 546 CTVT exomes and describe the lineage’s worldwide expansion. Examining variation in mutational exposure, we identify a highly context-specific mutational process that operated early in the cancer’s evolution but subsequently vanished, correlate ultraviolet-light mutagenesis with tumor latitude, and describe tumors with heritable hyperactivity of an endogenous mutational process. CTVT displays little evidence of ongoing positive selection, and negative selection is detectable only in essential genes. We illustrate how long-lived clonal organisms capture changing mutagenic environments, and reveal that neutral genetic drift is the dominant feature of long-term cancer evolution.

scholarly journals Changes in spatial organization following an acute epizootic: Tasmanian devils and their transmissible cancer

2020 ◽  
Vol 22 ◽  
pp. e00993 ◽  
Author(s):  
Sebastien Comte ◽  
Scott Carver ◽  
Rodrigo Hamede ◽  
Menna Jones
Keyword(s):  
Spatial Organization ◽  
Transmissible Cancer

scholarly journals Tasman-PCR: a genetic diagnostic assay for Tasmanian devil facial tumour diseases

2018 ◽  
Vol 5 (10) ◽  
pp. 180870 ◽  
Author(s):  
Young Mi Kwon ◽  
Maximilian R. Stammnitz ◽  
Jinhong Wang ◽  
Kate Swift ◽  
Graeme W. Knowles ◽  
...  
Keyword(s):  
High Sensitivity ◽  
Diagnostic Methods ◽  
Tasmanian Devil ◽  
Polymorphic Markers ◽  
Diagnostic Assay ◽  
Chain Reaction ◽  
Geographic Ranges ◽  
Processing Times ◽  
Transmissible Cancer ◽  
Polymerase Chain

Tasmanian devils have spawned two transmissible cancer clones, known as devil facial tumour 1 (DFT1) and devil facial tumour 2 (DFT2). DFT1 and DFT2 are transmitted between animals by the transfer of allogeneic contagious cancer cells by biting, and both cause facial tumours. DFT1 and DFT2 tumours are grossly indistinguishable, but can be differentiated using histopathology, cytogenetics or genotyping of polymorphic markers. However, standard diagnostic methods require specialist skills and equipment and entail long processing times. Here, we describe Tasman-PCR: a simple polymerase chain reaction (PCR)-based diagnostic assay that identifies and distinguishes DFT1 and DFT2 by amplification of DNA spanning tumour-specific interchromosomal translocations. We demonstrate the high sensitivity and specificity of this assay by testing DNA from 546 tumours and 804 normal devils. A temporal–spatial screen confirmed the reported geographic ranges of DFT1 and DFT2 and did not provide evidence of additional DFT clones. DFT2 affects disproportionately more males than females, and devils can be co-infected with DFT1 and DFT2. Overall, we present a PCR-based assay that delivers rapid, accurate and high-throughput diagnosis of DFT1 and DFT2. This tool provides an additional resource for devil disease management and may assist with ongoing conservation efforts.

scholarly journals Author response: Mitochondrial genetic diversity, selection and recombination in a canine transmissible cancer

2016 ◽  
Author(s):  
Andrea Strakova ◽  
Máire Ní Leathlobhair ◽  
Guo-Dong Wang ◽  
Ting-Ting Yin ◽  
Ilona Airikkala-Otter ◽  
...  
Keyword(s):  
Genetic Diversity ◽  
Author Response ◽  
Transmissible Cancer

scholarly journals Traits of a mussel transmissible cancer are reminiscent of a parasitic life style

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
E. A. V. Burioli ◽  
M. Hammel ◽  
N. Bierne ◽  
F. Thomas ◽  
M. Houssin ◽  
...  
Keyword(s):  
Carrying Capacity ◽  
Host Population ◽  
Phenotypic Traits ◽  
Related Genome ◽  
Animal Kingdom ◽  
Transmissible Cancer ◽  
Marine Mussels ◽  
Parasitic Lifestyle ◽  
Biological Entities ◽  
Cancerous Cells

AbstractSome cancers have evolved the ability to spread from host to host by transmission of cancerous cells. These rare biological entities can be considered parasites with a host-related genome. Still, we know little about their specific adaptation to a parasitic lifestyle. MtrBTN2 is one of the few lineages of transmissible cancers known in the animal kingdom. Reported worldwide, MtrBTN2 infects marine mussels. We isolated MtrBTN2 cells circulating in the hemolymph of cancerous mussels and investigated their phenotypic traits. We found that MtrBTN2 cells had remarkable survival capacities in seawater, much higher than normal hemocytes. With almost 100% cell survival over three days, they increase significantly their chances to infect neighboring hosts. MtrBTN2 also triggered an aggressive cancerous process: proliferation in mussels was ~ 17 times higher than normal hemocytes (mean doubling time of ~ 3 days), thereby favoring a rapid increase of intra-host population size. MtrBTN2 appears to induce host castration, thereby favoring resources re-allocation to the parasites and increasing the host carrying capacity. Altogether, our results highlight a series of traits of MtrBTN2 consistent with a marine parasitic lifestyle that may have contributed to the success of its persistence and dissemination in different mussel populations across the globe.

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