Deer Cancer: Rare Occurrences and Protective Factors

Cancer is relatively common in many mammals, but deer exhibit notably low rates of the disease. Researchers are investigating why these animals seem resistant to cancer despite rapid cell growth, particularly in antlers. Understanding the biological mechanisms behind this resistance could offer insights for human medicine.

Tumor Occurrence In Deer

Neoplastic growths in deer are rare compared to other mammals, a phenomenon that has intrigued wildlife biologists and veterinary pathologists. While tumors do occur, their prevalence remains low across species like white-tailed deer (Odocoileus virginianus), mule deer (Odocoileus hemionus), and elk (Cervus canadensis). Surveillance studies by wildlife health agencies and veterinary laboratories report sporadic cases, with most tumors being benign and rarely progressing to malignancy. This suggests underlying biological mechanisms that suppress tumorigenesis despite rapid cellular proliferation in certain tissues.

Epidemiological data indicate that when tumors appear in deer, they typically occur in the skin, lymphatic system, or internal organs. Cutaneous tumors, such as fibromas and papillomas, are the most frequently documented, though they rarely metastasize or impact survival. Internal malignancies, like lymphomas, are far less common but have been identified in necropsy reports. A study in the Journal of Wildlife Diseases found neoplastic lesions in less than 1% of examined deer, reinforcing the notion that cancer is uncommon in these animals.

The low incidence of tumors is particularly striking given deer’s exposure to environmental carcinogens, including pesticides, industrial pollutants, and naturally occurring toxins. Unlike domesticated livestock, which may develop neoplasms due to prolonged exposure to agricultural chemicals, wild deer encounter diverse environmental stressors yet exhibit notable resistance to tumor development. Researchers are exploring whether deer possess intrinsic protective factors that mitigate oncogenic processes, potentially offering insights into cancer resistance in other species.

Types Of Deer Cancers

Although cancer is rare in deer, certain tumor types have been documented in both wild and captive populations. These neoplasms primarily affect the skin and connective tissues, with malignant cases being far less frequent than benign growths. The most commonly observed tumors include papillomas, fibromas, and lymphomas, each with distinct characteristics.

Papillomas

Papillomas in deer result from species-specific papillomaviruses, which cause wart-like growths on the skin. These benign tumors appear as raised, keratinized lesions, often on the head, neck, and shoulders. White-tailed deer frequently develop cutaneous papillomas due to infection with Deer Papillomavirus (DPV). The lesions vary in size but rarely interfere with feeding or movement.

Transmission occurs through direct contact or exposure to contaminated surfaces like vegetation or feeding stations. Most papillomas regress as the deer’s skin cells turn over, though secondary bacterial infections can develop if lesions ulcerate. Unlike papillomavirus-induced cancers in humans, such as cervical cancer, malignant transformation in deer is exceedingly rare. Studies analyzing papilloma samples have found no significant evidence of progression to malignancy, suggesting that the virus-host interaction in deer differs from oncogenic papillomavirus infections in other species.

Fibromas

Fibromas, caused by Deer Fibroma Virus (DFV), a poxvirus, appear as firm, nodular masses that can range from a few millimeters to several centimeters. They are most often found on the face, neck, and limbs. Unlike papillomas, fibromas tend to be smoother in texture and may have darker pigmentation.

The virus is transmitted through biting insects like mosquitoes and ticks. While fibromas are generally benign and do not metastasize, large or strategically located tumors can interfere with vision, feeding, or mobility. In rare cases, secondary infections may develop. Research indicates that the immune system often clears the infection over time, leading to tumor regression. Unlike fibrosarcomas, which are malignant connective tissue tumors in other species, fibromas in deer do not exhibit invasive growth patterns or spread to distant organs.

Lymphomas

Lymphomas are among the few malignant cancers reported in deer but remain infrequent. These cancers originate in the lymphatic system and can affect organs such as the spleen, liver, and lymph nodes. Unlike papillomas and fibromas, which are externally visible, lymphomas are typically diagnosed post-mortem during necropsies of deer exhibiting signs of systemic illness, such as weight loss or respiratory distress.

The exact causes of lymphoma in deer are not well understood, though some cases have been linked to retroviral infections. Histopathological examinations reveal abnormal lymphocyte proliferation, often accompanied by organ enlargement and hemorrhagic lesions. While lymphoma is rare in wild deer, sporadic cases have been documented in captive populations, where environmental and genetic factors may contribute. Unlike domestic cattle, which can develop bovine leukemia virus-associated lymphomas, no direct viral cause has been confirmed in deer. The low incidence of lymphoma suggests these animals may possess biological mechanisms that limit uncontrolled lymphoid cell proliferation, though further research is needed.

Antler Regeneration And Cell Growth

Deer possess a unique biological trait—the ability to regenerate antlers annually. This process involves one of the fastest rates of organ regrowth among mammals, with antler tissue expanding up to an inch per day during peak growth periods. Unlike other instances of regeneration, such as limb regrowth in amphibians, deer antlers develop from a specialized structure known as the pedicle, a bony protuberance on the skull that serves as the foundation for new antler formation each year.

At the core of antler regrowth is the rapid expansion of mesenchymal stem cells, which originate in the periosteum of the pedicle and differentiate into chondrocytes and osteoblasts. These cells orchestrate the transformation of soft, cartilaginous tissue into fully mineralized bone over months. Unlike typical bone growth, which occurs through gradual ossification, antlers develop through a process resembling endochondral ossification, where cartilage serves as a scaffold for new bone deposition.

The molecular pathways governing antler growth share similarities with those involved in tumor development, particularly in their reliance on growth factors such as insulin-like growth factor 1 (IGF-1), fibroblast growth factors (FGFs), and vascular endothelial growth factor (VEGF). These signaling molecules promote cell division and angiogenesis, ensuring expanding antler tissue receives adequate blood supply and nutrients. Despite intense cell proliferation, deer do not exhibit uncontrolled tumor-like growth in their antlers, suggesting regulatory mechanisms prevent aberrant cell behavior. Investigations into gene expression during antler regeneration have identified tumor suppressor genes that remain active, maintaining cellular order and preventing unchecked proliferation.

Genetic Mechanisms Supporting Low Cancer Rates

The rarity of cancer in deer suggests their genetic makeup plays a role in suppressing tumor formation despite rapid cellular turnover. Comparative genomic analyses reveal that deer possess adaptations in genes related to cell cycle regulation and DNA repair, which may contribute to their resistance to malignancies.

One key factor is enhanced tumor suppressor gene activity, particularly within the TP53 gene, which encodes the p53 protein. This protein, often called the “guardian of the genome,” detects DNA damage, halts cell division, and initiates repair or apoptosis. Studies on long-lived and cancer-resistant mammals, such as elephants and naked mole rats, show that increased TP53 activity reduces cancer susceptibility. While deer do not have additional copies of this gene, they exhibit heightened regulatory control, ensuring damaged cells are eliminated before becoming malignant.

Another genetic factor influencing cancer resistance in deer is the regulation of proto-oncogenes, which, when mutated or overexpressed, can drive uncontrolled cell growth. In cancer-prone species, dysregulation of proto-oncogenes such as MYC and RAS contributes to tumorigenesis. In deer, these genes appear tightly controlled by regulatory elements that prevent aberrant activation. Genome sequencing efforts have identified variations in promoter regions and microRNA networks that fine-tune proto-oncogene expression, preventing unchecked proliferation. Additionally, deer exhibit efficient DNA damage response pathways, minimizing the accumulation of mutations that could lead to oncogenesis.

Environmental Influences

While genetic factors contribute to deer’s low cancer rates, environmental conditions also play a role. Wild populations encounter potential carcinogens, including naturally occurring toxins, industrial pollutants, and radiation. Despite this exposure, malignant tumors remain rare, suggesting that either these exposures do not reach harmful thresholds or deer possess biological adaptations to mitigate their effects.

One possible explanation is their diet, which consists primarily of vegetation containing antioxidants and phytochemicals that may neutralize free radicals and reduce oxidative stress, a known contributor to DNA mutations and cancer development. Additionally, deer’s roaming behavior prevents prolonged contact with localized pollutants, unlike domesticated animals that remain in fixed grazing areas where contaminants can concentrate. Studies on deer near industrial sites have found low levels of heavy metals and persistent organic pollutants, suggesting that their metabolism and foraging habits may reduce bioaccumulation.