Peer-reviewed veterinary case report
No USP8 gene mutations found in dog pituitary tumors causing
By Sbiera, Silviu et al.·Published in PloS one·2016·Department of Internal Medicine I, Germany·View original on PubMed →
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Original publication title: Lack of Ubiquitin Specific Protease 8 (USP8) Mutations in Canine Corticotroph Pituitary Adenomas.
- Species:
- dog
Plain-English summary
A group of dogs with Cushing's disease, which causes symptoms like excessive thirst, increased urination, and a pot-bellied appearance, were studied to see if a specific gene mutation (USP8) linked to similar tumors in humans was present. Researchers found that none of the dogs had mutations in this gene, suggesting that the genetic causes of pituitary tumors in dogs are different from those in humans. However, some tumors showed increased levels of the USP8 protein, which was associated with smaller tumor sizes but higher hormone production. This indicates that while the genetic backgrounds differ, there may be some similarities in how the disease manifests.
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Abstract
PURPOSE: Cushing's disease (CD), also known as pituitary-dependent hyperadrenocorticism, is caused by adrenocorticotropic hormone (ACTH)-secreting pituitary tumours. Affected humans and dogs have similar clinical manifestations, however, the incidence of the canine disease is thousand-fold higher. This makes the dog an obvious model for studying the pathogenesis of pituitary-dependent hyperadrenocorticism. Despite certain similarities identified at the molecular level, the question still remains whether the two species have a shared oncogenetic background. Recently, hotspot recurrent mutations in the gene encoding for ubiquitin specific protease 8 (USP8) have been identified as the main driver behind the formation of ACTH-secreting pituitary adenomas in humans. In this study, we aimed to verify whether USP8 mutations also play a role in the development of such tumours in dogs. METHODS: Presence of USP8 mutations was analysed by Sanger and PCR-cloning sequencing in 38 canine ACTH-secreting adenomas. Furthermore, the role of USP8 and EGFR protein expression was assessed by immunohistochemistry in a subset of 25 adenomas. RESULTS: None of the analysed canine ACTH-secreting adenomas presented mutations in the USP8 gene. In a subset of these adenomas, however, we observed an increased nuclear expression of USP8, a phenotype characteristic for the USP8 mutated human tumours, that correlated with smaller tumour size but elevated ACTH production in those tumours. CONCLUSIONS: Canine ACTH-secreting pituitary adenomas lack mutations in the USP8 gene suggesting a different genetic background of pituitary tumourigenesis in dogs. However, elevated nuclear USP8 protein expression in a subset of tumours was associated with a similar phenotype as in their human counterparts, indicating a possible end-point convergence of the different genetic backgrounds in the two species. In order to establish the dog as a useful animal model for the study of CD, further comprehensive studies are needed.
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Search related cases →Original publication on PubMed: https://pubmed.ncbi.nlm.nih.gov/28005997/