The dog as a patient rather than an experimental animal in cancer treatment: Implications for comparative oncology and translational medicine

Abstract

Comparative oncology leverages spontaneously occurring canine
malignancies as robust bidirectional models to bridge the translational
gap between preclinical laboratory discoveries and human clinical
applications. Unlike conventional genetically uniform rodent models,
which often fail to capture natural tumor dynamics, companion dogs
develop cancers within an intact, co-evolved immune system and
a shared anthropogenic environment. This comprehensive review
examines the deep histopathological, genomic, and molecular
homologies shared between canine and human neoplasms, with
particular emphasis on aggressive entities such as osteosarcoma,
malignant melanoma, mammary carcinoma, and non-Hodgkin
lymphoma. High-throughput sequencing confirms mutual somatic
driver mutations and identical signaling pathway aberrations (e.g.,
TP53, HER2, and PTEN), substantially increasing translational
predictability. Furthermore, companion dogs act as important
environmental sentinels for shared ecological carcinogens and provide
an accelerated clinical timeline due to their compressed lifespans.
Integrating veterinary clinical trials into drug development timelines
enables the realistic evaluation of therapeutic efficacy, systemic
toxicities, and immune-mediated resistances without compromising
animal welfare. Recent advancements in experimental therapeutics,
particularly Newcastle Disease Virus (NDV)-based oncolytic
virotherapy using the ZG1999HDS strain, underscore the immense
clinical and immunological potential of comparative frameworks.
Although challenges regarding international trial standardization
and cross-species regulatory frameworks persist, the companion
canine model represents an irreplaceable, ethically sound foundation
within the modern “One Health” paradigm, driving parallel medical
breakthroughs that directly benefit both human and veterinary
oncology.