Wild animals are subject to the same fundamental biological processes as humans, and this includes the development of cancer. The phenomenon of uncontrolled cell division is found across the animal kingdom, from fish and reptiles to birds and mammals. While the core mechanics of the disease are consistent, its occurrence and visibility in wild populations are shaped by a different set of environmental pressures and observational challenges.
Documented Cancer Cases in Wild Animals
A well-studied example of wildlife cancer is Devil Facial Tumour Disease (DFTD) in Tasmanian devils. This is a rare, transmissible cancer where cells spread between animals through biting during fights over food or mates. First identified in 1996, DFTD causes large tumors around the mouth and head that prevent the animal from eating, causing population declines of over 80% and pushing the species toward extinction.
The marine environment also provides evidence of cancer in wildlife. Beluga whales in the St. Lawrence River estuary exhibit high rates of intestinal cancer, which is their second leading cause of death. Studies have linked this to high concentrations of industrial pollutants, specifically polycyclic aromatic hydrocarbons (PAHs), released from local industry. These chemicals accumulate in the river sediment where the whales feed, concentrating in their bodies over their long lifespans.
Another case in marine life is fibropapillomatosis, a disease that causes large tumors on the skin, eyes, and internal organs of sea turtles, particularly green turtles. This condition is associated with a herpesvirus, but its development into tumors is likely triggered by environmental stressors, including pollution. These growths can impair a turtle’s vision, movement, and ability to feed, often leading to death.
Beyond these specific cases, tumors have been documented in a wide array of other vertebrates. Researchers have identified melanomas in wild fish populations and various tumors in snakes and birds. These instances demonstrate that cancer is a widespread natural phenomenon, and the challenges of observing these animals mean the true incidence is likely much higher than documented cases suggest.
Why Cancer Appears Less Common in the Wild
A primary reason cancer seems rare in nature is observational bias. An animal weakened by a developing tumor is an immediate target for predators. A wild animal showing signs of illness is quickly removed from the ecosystem, either by predation or by hiding to avoid it, meaning researchers rarely encounter animals in the advanced stages of the disease.
Many cancers are diseases of old age. In the wild, life is often short due to the constant pressures of finding food, avoiding predators, and surviving harsh weather. Most wild animals do not live long enough to reach the advanced ages where age-related cancers would develop, succumbing to other causes of mortality long before a tumor could grow to a detectable stage.
The logistics of studying wildlife present another hurdle. Tracking individual animals over their entire lifespans to monitor for disease is a major challenge. Diagnosing cancer requires procedures like biopsies and necropsies, which are difficult to perform on free-ranging populations. Without systematic health screening, the data on wildlife cancer remains sparse and likely underestimates its true prevalence.
Known Causes of Wildlife Cancer
Viruses are a significant natural cause of cancer in some animal populations. For example, certain viruses can induce genital tumors in marine mammals like California sea lions. These oncogenic viruses work by altering the host’s cellular machinery, leading to uncontrolled cell growth.
Genetic predisposition also plays a role. Some animal lineages may be more susceptible to developing certain types of cancers. This can be exacerbated in small, isolated populations where low genetic diversity is common. When the gene pool is limited, mutations that increase cancer risk can become more frequent, making the population more vulnerable.
Human activities have introduced a host of cancer-causing elements into the environment. Pollutants, including pesticides, chemical runoff, and radioactive materials from accidents, act as environmental carcinogens that wildlife are increasingly exposed to. These carcinogenic chemicals accumulate in the food web, reaching dangerous concentrations in top predators.
Evolution’s Role in Animal Cancer Resistance
The question of how large, long-lived animals manage their cancer risk leads to an observation known as “Peto’s Paradox.” An animal with trillions more cells and a longer lifespan, like a whale or an elephant, should have a much higher probability of developing cancer than a small animal like a mouse. However, cancer rates do not correlate with body size or lifespan across species, suggesting that larger animals have evolved robust cancer-suppression mechanisms.
Elephants provide a clear example of this evolutionary adaptation. While humans have a single copy of a tumor-suppressor gene called TP53, elephants have twenty copies. This gene’s protein product, p53, identifies and responds to DNA damage. If a cell’s DNA becomes damaged, the p53 protein can halt cell division for repairs or trigger programmed cell death, known as apoptosis, to eliminate the potentially cancerous cell.
With multiple copies of TP53, elephants have a highly sensitive and redundant system for detecting and destroying damaged cells before they can form tumors. Studies have shown that elephant cells are much quicker to undergo apoptosis in response to DNA damage compared to human cells. This enhanced cellular defense mechanism is an evolutionary solution that likely enabled the evolution of their large body size by counteracting the increased cancer risk.