Devil facial tumor disease, a contagious cancer spread through biting, has driven the Tasmanian devil to endangered status by killing the vast majority of infected animals and slashing wild populations since the mid-1990s. But the disease alone does not explain the species’ vulnerability. Tasmanian devils were already genetically impoverished before the tumors appeared, and a mix of roadkill, habitat fragmentation, and ecological disruption compounds the problem. The full story involves an unusual cancer, an unusual host, and a conservation effort racing to keep pace with both.
A Contagious Cancer Unlike Almost Anything Else in Nature
The central threat is devil facial tumor disease, or DFTD. Unlike most cancers, which begin and end in one individual, DFTD is transmissible. The tumor cells themselves are the infectious agent. When devils bite each other during mating or feeding disputes, living cancer cells from one animal lodge in the wounds of another and begin growing. The tumors are not caused by a virus or a bacterium; the cancer cells are passed directly as a kind of living tissue graft from devil to devil.
Research has traced these cells to Schwann cells, the type of cell that normally wraps around nerve fibers.1PubMed Central. The Tasmanian devil transcriptome reveals Schwann cell origins of a clonally transmissible cancer The tumors are clonal, meaning every DFTD tumor in every infected devil descends from a single original cancer that arose in one individual. That original devil is long dead, but its cancer cells live on, passed mouth-to-mouth across the population.2Nature. Transmission of devil facial-tumour disease The tumors typically grow on the face and mouth, eventually becoming so large that the animal can no longer eat. Death usually follows within months.
In 2014 and 2015, researchers discovered something alarming: a second, independent transmissible cancer had appeared in southern Tasmania. Named DFT2 to distinguish it from the original DFT1, this second lineage produces facial tumors that look similar to the naked eye but are genetically and histologically distinct. DFT2 carries a Y chromosome, indicating it originated in a male devil, whereas DFT1 came from a female. The two cancers share no detectable cytogenetic similarity.3PubMed Central. A second transmissible cancer in Tasmanian devils Genomic analysis places the emergence of DFT1 around 1986 and DFT2 around 2011.4PubMed Central. The evolution of two transmissible cancers in Tasmanian devils The fact that one species has independently spawned two transmissible cancers suggests something about devil biology makes them unusually susceptible, and that something is their immune system.
How the Tumors Dodge the Immune System
Normally, if foreign tissue is transplanted into an animal, the immune system recognizes it as “not self” and destroys it. This recognition depends heavily on molecules called MHC (major histocompatibility complex) on cell surfaces. MHC molecules display fragments of proteins from inside the cell, essentially broadcasting the cell’s identity. If those identity markers look foreign, immune cells attack.
DFT1 cells have found a way around this. They shut down expression of MHC molecules on their surface, making them effectively invisible to the immune cells that would normally reject a foreign graft.5PubMed Central. How the devil facial tumor disease escapes host immune responses The genes for making MHC molecules are still present in the tumor’s DNA and are not mutated. Instead, the shutdown is epigenetic: chemical modifications to the DNA packaging silence the relevant genes without altering their sequence. In laboratory experiments, treating DFT1 cells with drugs that reverse this epigenetic silencing can restore MHC expression.6PubMed Central. Reversible epigenetic down-regulation of MHC molecules by devil facial tumour disease illustrates immune escape by a contagious cancer This finding has been important for vaccine research, because it means the tumor’s cloak of invisibility is not permanent in principle.
DFT2 takes a different approach. Its cells do express MHC molecules, which initially puzzled researchers. But the MHC variants DFT2 displays happen to be extremely common among Tasmanian devils in the region where it circulates. Because most host devils share those same MHC types, the tumor does not look sufficiently foreign to trigger a strong immune response.7eLife. The newly-arisen Devil facial tumour disease 2 (DFT2) reveals a mechanism for the emergence of a contagious cancer Two cancers, two different immune-evasion strategies, both exploiting the same underlying problem: devils’ immune systems have trouble telling each other apart.
Why Devils Were Already Vulnerable
Low genetic diversity is the backdrop to almost everything that has gone wrong for Tasmanian devils. Their MHC genes are strikingly similar across individuals, which is why transplanted cancer cells can slip past immune defenses. But this lack of genetic variety is not a recent development. Studies of the species’ demographic history show that devil populations went through severe declines long before European colonizers arrived in Tasmania and long before DFTD emerged.8PubMed Central. Extensive population decline in the Tasmanian devil predates European settlement and devil facial tumour disease
Part of the explanation stretches back thousands of years. Tasmanian devils once lived across mainland Australia, alongside the thylacine and other now-vanished species. They disappeared from the mainland during the mid-Holocene, roughly 3,000 years ago. Two leading hypotheses compete to explain this loss. One points to the arrival of the dingo, which may have outcompeted devils as a predator. The other points to a surge in the Aboriginal human population around the same period, accompanied by new hunting technologies and more intensive resource use.9The Holocene. Causes of extinction of vertebrates during the Holocene of mainland Australia: arrival of the dingo, or human impact? Climate shifts linked to El Niño patterns may have played a role on both the mainland and in Tasmania, weakening devil populations at the same time that other pressures mounted.10Journal of Biogeography. Ancient DNA tracks the mainland extinction and island survival of the Tasmanian devil Recent modeling work has largely ruled out climate alone as the cause of mainland extinction, leaving dingoes and intensified human activity as the most likely drivers.11Ecography. Too hot for the devil? Did climate change cause the mid‐Holocene extinction of the Tasmanian devil Sarcophilus harrisii from mainland Australia?
The upshot is that by the time Europeans found devils in Tasmania, the species was already confined to a single island with a gene pool narrowed by millennia of bottlenecks. That reduced diversity set the stage for DFTD to spread with terrifying efficiency once it appeared.
Threats Beyond the Tumor
DFTD dominates any discussion of devil endangerment, and rightly so, but it is not the only pressure these animals face. Vehicle strikes kill a meaningful number of devils every year. A survey of Tasmanian highways estimated that roughly 3,400 devils were killed on roads annually, representing somewhere between about 4 and 6 percent of the total population at the time.12Wildlife Research. Distribution and abundance of roadkill on Tasmanian highways: human management options That figure is tolerable when a population is large and healthy, but for a species already collapsing from disease, losing thousands of animals each year to traffic adds up fast.
Habitat loss through land clearing, logging, and agricultural expansion also fragments devil populations, reducing the territory available for foraging and denning. In scattered, smaller populations, genetic diversity erodes even more quickly, and isolated groups are less likely to benefit from any natural resistance to DFTD that evolves in one area. Domestic dogs have also been identified as a disturbance agent for Tasmanian wildlife, though devil-specific predation data is limited. The cumulative effect of these secondary threats is that devils face a gauntlet of hazards beyond the disease itself.
What Happens When Devils Disappear
Tasmanian devils are the island’s largest surviving marsupial carnivore, and their decline has rippled through the ecosystem in measurable ways. As devil numbers have fallen, feral cats have increased in areas where the disease has been present the longest. The relationship is direct: cat occurrence is significantly and negatively associated with devil abundance. Meanwhile, the eastern quoll, a smaller native predator, has declined rapidly following DFTD’s arrival, likely because feral cats fill the niche left by devils while also preying on quolls.13PubMed. Trophic cascades following the disease-induced decline of an apex predator, the Tasmanian devil Some researchers have described this as a textbook mesopredator release: remove the top predator, and mid-level predators flourish at the expense of smaller species. The evidence for this particular cascade has been debated, however. A follow-up analysis cautioned that direct evidence for competitive suppression among devils, cats, and quolls remains limited.14PubMed Central. Devil declines and catastrophic cascades: is mesopredator release of feral cats inhibiting recovery of the eastern quoll?
Devils are also major scavengers. Using remote cameras and experimentally placed carcasses, researchers found that where devil populations have declined, carcasses persist roughly 2.6 times longer. Mesopredators do find and consume more carrion in those areas, but they cannot match the speed and thoroughness of devils. The invasive feral cat, in particular, seems to exploit a “relaxed landscape of fear” in areas where devils are rare, scavenging more boldly when the bigger animal is absent.15PubMed Central. Top carnivore decline has cascading effects on scavengers and carrion persistence Slower carcass removal can increase disease risk for livestock and other wildlife, making devil decline a concern well beyond devil conservation alone.
Signs That Devils Are Fighting Back
One of the more encouraging developments in devil biology is evidence that the species is evolving in response to DFTD, and doing so quickly. Researchers comparing devil genomes from populations that had been exposed to the disease for varying lengths of time found signs of rapid, parallel selection at two genomic regions containing genes related to immune function and cancer risk. These signatures appeared independently in three separate populations, suggesting the evolutionary pressure from DFTD is strong enough to shift gene frequencies within just a few generations.16PubMed Central. Rapid evolutionary response to a transmissible cancer in Tasmanian devils
Devils have also changed their life-history patterns. In areas ravaged by DFTD, where adult survival has plummeted, a far greater proportion of young females now breed in their first year of life, rather than waiting until their second or third year as was previously typical. One study documented a 16-fold increase in the proportion of individuals showing precocious sexual maturity.17PubMed Central. Life-history change in disease-ravaged Tasmanian devil populations By breeding earlier, these devils can produce offspring before the disease kills them. It is a grim kind of adaptation, trading longevity for reproduction, but it helps populations persist even as adult mortality remains extremely high.
Whether these natural responses are enough to save the species on their own is far from certain. The evolutionary changes are real but may not proceed fast enough to outpace the disease, especially with DFT2 adding a second, independently evolving cancer to the picture.
Conservation Efforts on Multiple Fronts
The most established conservation strategy has been the creation of insurance populations: groups of disease-free devils held in captivity or on isolated islands, kept as a genetic reserve in case wild populations collapse entirely. An insurance metapopulation was established in 2006, drawing founders from across Tasmania to capture as much of the remaining genetic diversity as possible.18PubMed Central. No evidence of inbreeding depression in a Tasmanian devil insurance population despite significant variation in inbreeding Genetic monitoring using purpose-built DNA assays helps managers make breeding recommendations that minimize inbreeding and maintain diversity.19PubMed Central. Development of a SNP-based assay for measuring genetic diversity in the Tasmanian devil insurance population So far, genetic analysis suggests the insurance metapopulation has remained reasonably representative of wild genetic diversity, including at loci thought to be important for DFTD resistance.20PubMed Central. Restoring faith in conservation action: Maintaining wild genetic diversity through the Tasmanian devil insurance program
In 2012, devils were introduced to Maria Island, off Tasmania’s east coast, as a free-ranging insurance population separate from the captive colonies. The Maria Island population grew successfully and provided a disease-free reservoir. But the introduction also illustrated the trade-offs inherent in moving predators to new ecosystems. Devil presence on the island suppressed invasive mesopredators, a benefit, but also eliminated a breeding colony of little penguins, a significant cost.21Biological Conservation. Conservation trade-offs: Island introduction of a threatened predator suppresses invasive mesopredators but eliminates a seabird colony This outcome is a useful reminder that conservation interventions can have cascading and sometimes unwelcome consequences.
Vaccine development has been another avenue of research. Early trials immunized healthy devils with killed DFTD tumor cells combined with immune-boosting agents. Five of six vaccinated devils mounted detectable immune responses, including antibody production and cytotoxic activity against tumor cells. One devil was temporarily protected against a challenge with live DFTD cells, though the protection did not last when the animal was re-challenged a year later.22PubMed. Evidence for induction of humoral and cytotoxic immune responses against devil facial tumor disease cells in Tasmanian devils (Sarcophilus harrisii) immunized with killed cell preparations The results were promising enough to confirm that the devil immune system is not fundamentally incapable of recognizing DFTD. The challenge is developing a formulation that generates durable, long-lasting protection that could be deployed across wild populations, a logistical as well as a scientific hurdle.
The Mainland Reintroduction Question
One of the more ambitious ideas floated in recent years is reintroducing Tasmanian devils to mainland Australia, where they have been absent for about 3,000 years. The rationale is partly about giving the species additional range beyond Tasmania and partly about restoring ecological function. Species distribution modeling suggests that suitable climatic conditions for devils exist in southeastern Australia. Ecosystem modeling predicted that reintroduced devils would have cascading effects on mainland food webs, reducing invasive mesopredators and herbivores while modestly boosting small and medium-sized native mammals. The predicted effects were similar to those of dingoes, but weaker.23Biological Conservation. Reintroduction of Tasmanian devils to mainland Australia can restore top-down control in ecosystems where dingoes have been extirpated
A small rewilding project released a group of devils into a fenced sanctuary in New South Wales in 2020, marking the first time devils had lived on the mainland in millennia. Whether devils can be sustained in mainland conditions long-term, and whether they would encounter the same disease pressures they face in Tasmania, remains an open question. The mainland is not dingo-free, and the interaction between devils and dingoes is the very dynamic that may have driven devils to extinction there in the first place. Still, as insurance against catastrophic loss in Tasmania, having at least some devils on the mainland provides a geographic hedge that did not exist a decade ago.
A Rare Window Into Transmissible Cancer
Tasmanian devils share a strange distinction with only a handful of other species. Contagious cancers, where the tumor cells themselves hop between hosts, are vanishingly rare in nature. The best-known comparison is canine transmissible venereal tumor, or CTVT, a sexually transmitted cancer in dogs that has been circulating globally for thousands of years. Both DFTD and CTVT demonstrate the ability to evade host immune systems, though they do so through different molecular strategies.24PubMed Central. Transmissible Cancers and Immune Downregulation in Tasmanian Devil (Sacrophilus harrisii) and Canine Populations CTVT typically regresses on its own after a few months. DFTD almost never does, which is why it has been so devastating.
The emergence of two independent transmissible cancers in devils within roughly 25 years of each other raises an unsettling possibility: that transmissible cancers may arise more frequently in nature than scientists once assumed, particularly in populations with low genetic diversity and frequent physical contact involving tissue transfer.3PubMed Central. A second transmissible cancer in Tasmanian devils For researchers studying cancer biology broadly, devils have become a living laboratory. Understanding how DFTD cells silence their identity markers, how devil immune systems sometimes begin to fight back, and why certain populations show signs of evolving resistance all have implications well beyond a single species on a single island. The tragedy of the Tasmanian devil’s endangerment has, in a grim irony, produced some of the richest data available on how cancers evade immunity and how wild populations respond to novel diseases in real time.