Feline hereditary tumors possess carcinogenic mechanisms common with humans

A joint research team including Special Postdoctoral Researcher Namiko Ikeda and Team Director Yukihide Momozawa at the Laboratory for Genotyping Development, RIKEN Center for Integrative Medical Sciences, together with Professor Ryohei Nishimura (Professor at the time of research, currently Professor Emeritus at the University of Tokyo) and Associate Professor Hirotaka Tomiyasu at the Graduate School of Agricultural and Life Sciences, the University of Tokyo, identified genetic variants (differences between individuals in DNA sequences) potentially becoming causes of cancers in cats, clarifying these clinical characteristics. It was found by analyzing genetic variants of 784 cats. This finding could also lead to new comparative oncology models in human cancer research. The achievements were published in Scientific Reports on August 8.

Cancers are one of the primary death causes in cats as well, with 30 to 40% of overall cats developing tumors, and 50 to 85% among them developing malignant tumors (cancers). Cats serve as companion animals sharing living environments with humans. Since they develop cancers while receiving influences of aging or environmental factors similarly to humans, they are considered to serve as important research targets as model animals of cancer research.

Hereditary tumors show onset risks becoming high by several times to several tens of times via the existence of specific variants, occupying 5 to 10 percent of cancers. On the other hand, regarding cats, how genetic factors act was unclarified.

Therefore, targeting 813 cats where consent was obtained from owners among cats visiting the Veterinary Medical Center, the University of Tokyo, which is a facility that sees a high volume of cancer cases, the research team extracted DNA from surplus samples of blood.

They modified multiplex target sequencing methods which RIKEN developed independently and utilized for human genome analyses for cat genomes. They newly developed experimental systems capable of analyzing hereditary tumor-related genes efficiently.

When investigating 27 types of hereditary tumor-related candidate genes using this method, sequence data sufficient for analyses were obtained from 792 out of 813 cats. As a result, they succeeded in identifying 13 types of pathogenic variants.

In 7 out of 18 cats holding pathogenic variants, diverse cancer types such as lymphomas, breast cancers, mast cell tumors, and bone cancers were confirmed. It was found that even when holding pathogenic variants of hereditary tumor-related genes common with humans, individuals do not necessarily develop cancers known in humans.

In research into dogs, pathogenic variants of APC genes serving also as target genes of this analysis are recognized with high frequencies in Jack Russell Terriers, with reports existing where polyps arise frequently in large intestines. In cats, however, tendencies recognized with biases toward specific breeds did not exist.

Several mutations exist that are common with human cancers. Genes such as BRCA2, TP53, ATM, MSH2, and MSH6 playing important roles in human hereditary tumors were involved. Contributions are expected toward the understanding of carcinogenic mechanisms and pathological states preserved across species.

Ikeda stated: "In humans, efforts are advancing into investigating genetic factors behind cancers, leading to diagnoses and treatments suited for individuals. On the other hand, in cats, hereditary tumors were mostly unclarified thus far. Through this research, I feel that we were able to take that first step. In the future, I expect that this achievement will lead to better cancer medical treatment for cats, while contributing to the understanding of mechanisms of carcinogenesis and developments of new therapeutic methods by comparing humans and cats."

Journal Information
Publication: Scientific Reports
Title: Characterization of putative germline pathogenic variants in 27 candidate cancer-predisposing genes in 813 cats using a feline-specific multiplex targeted sequencing
DOI: 10.1038/s41598-026-61718-w