Abstract
Urogenital carcinoma is a highly metastatic cancer affecting California sea lions ( Zalophus californianus). The disease has high prevalence amongst stranded animals, and is one of the most commonly observed cancers in wildlife. The genital localisation of primary tumours suggests the possibility that coital transmission of an infectious agent could underlie this disease. Otarine herpesvirus type 1 has been associated with lesions, however a causative role for this virus has not been confirmed. We investigated the possibility that urogenital carcinoma might be clonally transmissible, spread by the direct transfer of cancer cells. Analysis of sequences at the mitochondrial DNA control region in seven matched tumour and host pairs confirmed that tumour genotypes were identical to those of their matched hosts and did not show similarity with tumours from other individuals. Thus our findings suggest that urogenital carcinoma in California sea lions is not clonally transmitted, but rather arises from transformed host cells.
Highlights
Urogenital carcinoma (UGC) is the most commonly observed neoplasm in California sea lions (Zalophus californianus
Otarine herpesvirus type 1 (OtHV-1), a gammaherpesvirus related to Kaposi’s sarcoma-linked human herpesvirus-85,6 has been associated with UGC5–7; this virus has not been confirmed as a causative agent
Our study does not support the hypothesis that UGC is clonally transmitted, but rather further confirms that UGC arises from host cells
Summary
Urogenital carcinoma (UGC) is the most commonly observed neoplasm in California sea lions (Zalophus californianus)1 This cancer was first reported in sea lions on the west coast of North America in 19792, and over a fifteen-year period, from 1998 to 2012, the disease was found in 26 per cent of adult animals examined post-mortem at The Marine Mammal Center, California. Genetic studies have indicated that individuals with high parental relatedness, homozygosity at the HSPE2 locus, or one or more copies of the Zaca-DRB.A MHC class II locus have increased risk of UGC. Environmental contaminants, such as organochlorines, have been proposed as causative agents in UGC carcinogenesis
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