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Research Article Open access CC BY 4.0

The Biology and Evolution of Canine Transmissible Venereal Tumour: A Review

Banoth Sai Nehru, Hariharan. R., Sathish Kumar M, Vigneshwaran B, Kushwanth Sai Kumar P, Pooja Kailas, Pamu Sushma

Asian Journal of Biology · pp. 11–17 · Published 18 Mar 2025

10.9734/ajob/2025/v21i4494

Abstract

The canine transmissible venereal tumour represents one fof only three known naturally occurring transmissible cancers, distinguished by its remarkable 11,000-year evolutionary history. This unique neoplasm, first documented in 1876, spreads through the transfer of viable cancer cells during physical contact, primarily affecting the external genitalia of dogs. It exhibits distinct genetic characteristics, including an aneuploid karyotype of 57-59 chromosomes and a characteristic LINE-1 insertion near the c-myc gene. The tumour demonstrates sophisticated host manipulation mechanisms, including the modulation of erythropoietin levels and immune responses. Its growth pattern follows three phases: progressive, static, and regression, with approximately 80% of cases eventually regressing due to host immune response. The tumour employs various immune evasion strategies, including the suppression of major histocompatibility complex molecule expression and the secretion of immunosuppressive factors. A notable adaptive feature is its ability to acquire mitochondrial deoxyribonucleic acid DNA from host cells, potentially contributing to its long-term survival. The disease shows particular prevalence in tropical and subtropical regions, with incidence rates of 23-43% among sexually active dogs. While primarily affecting dogs aged 2-5 years, it can be experimentally transmitted to other Canidae family members. The study of this tumour provides valuable insights into cancer evolution, host-pathogen relationships, and immune system interactions, offering potential applications for understanding cancer biology and developing novel therapeutic approaches.

Canine transmissible cancer immune evasion LINE-1

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