Hello, My co-authors and I are excited to share our new research article exploring the genomic signatures of Urogenital Carcinoma in the California sea lion.
This research uses cancer in California sea lions as a powerful comparative model to understand how tumors arise and evade the immune system across mammals. By identifying genomic changes shared between sea lion cancers and human cancers, the study provides insight into immune-related pathways that may inform future cancer immunotherapies and earlier diagnostic approaches. At the same time, the work underscores the role of wildlife as sentinels of environmental health, showing how studying naturally occurring cancers in wild species can benefit both conservation efforts and human medicine. Livingston, I.G.; Wise, C.F.; Dickey, A.N.; Thomas, R.; Demming, A.C.; Halaska, B.; Gulland, F.M.D.; Colegrove, K.M.; Duignan, P.; Breen, M. Cross-Species Exome Sequencing Reveals Recurrent Genomic Alterations in California Sea Lion (*Zalophus californianus*) Urogenital Carcinoma and Highlights a Recurrent PD-L1 Variant. *Genes* 2026, *17*, 222. https://doi.org/10.3390/genes17020222 Abstract: Background/Objectives: Human-driven environmental change can promote cancer development in wild species, yet the pathophysiology of wildlife cancers remain largely unexplored. Urogenital carcinoma (UGC) in the California sea lion (CSL) (Zalophus californianus) is one of the most common cancer types documented in any wild mammal. The pathogenesis of UGC in CSLs is known to be multifactorial, with links to environmental contaminant exposure and infection by Otarine Herpesvirus-1 (OtHV-1); however, the genomic features of these cancers have not been thoroughly explored. Understanding UGC pathogenesis in the CSL has important implications for the health of humans and other species that share environment and diet. Methods: We leveraged the evolutionary conservation between the domestic dog and CSL genomes to perform cross-species whole-exome sequencing (WES) of CSL UGC tumors and matched normal tissue pairs. We also used PCR and Sanger sequencing to investigate the prevalence of DNA from OtHV-1. Results: Bioinformatic analyses identified shared somatic variants and DNA copy number aberrations in UGC tumor samples, including recurrent exonic single-nucleotide variants in CD274/PD-L1, and recurrent copy number gains in CD274/PD-L1, TNFRSF14, CD200, CDK4, and PLCG2. In an extended cohort of 70 CSLs (tumor, matched normals, and controls), a recurrent C > T single-nucleotide variant in exon 4 of CD274/PD-L1 was identified in 54 of 68 (79.4%) CSLs with diagnosed UGC. OtHV-1 DNA was detected in 67 of 70 individuals (95.8%). Conclusions: These results demonstrate that cross-species exome capture provides a means to identify genomic alterations that may play a role in the molecular pathogenesis of UGC in the CSL and adds to the body of evidence for an association between OtHV-1 and UGC in this species. Link to paper: https://www.mdpi.com/2073-4425/17/2/222 Cheers, Isabella Livingston | she/her/hers Genetics and Genomics Ph.D.Candidate Genetics and Genomics Scholar GAANN Biotechnology Fellow Dept. of Molecular Biomedical Sciences, College of Veterinary Medicine North Carolina State University Raleigh, NC 27695 breenlab.org
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