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Origin and evolution of adrenocortical neoplasias
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Adrenocortical neoplasias leading to the clinical signs of hypercortisolemia are not too rare in dogs especially in those of larger breeds. Although there are unanswered questions about the origin and evolution of adrenocortical neoplasms, analysis of human tumor specimens and animal models indicates that adrenocortical tumorigenesis involves both genetic and epigenetic alterations. A fascinating review from Finland!
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Chromosomal changes accumulate during tumor progression, and aberrant telomere function is one of the key mechanisms underlying chromosome instability during this process.
Epigenetic changes serve to expand the size of the uncommitted adrenal progenitor population, modulate their phenotypic plasticity (i.e., responsiveness to extracellular signals), and increase the likelihood of subsequent genetic alterations.
Analyses of heritable and spontaneous types of human adrenocortical tumors documented alterations in either cell surface receptors or their downstream effectors that impact neoplastic transformation.
Many of the mutations associated with benign human adrenocortical tumors result in dysregulated cyclic adenosine monophosphate signaling, whereas key factors and/or signaling pathways associated with adrenocortical carcinomas include dysregulated expression of the IGF2 gene cluster, activation of the Wnt/â-catenin pathway, and inactivation of the p53 tumor suppressor.
A better understanding of the factors and signaling pathways involved in adrenal tumorigenesis is necessary to develop targeted pharmacologic and genetic therapies.
Source: M. Bielinska, H. Parviainen, S. Kiiveri, M. Heikinheimo and D. B. Wilson (2009): Origin and Molecular Pathology of Adrenocortical Neoplasms. In: Vet Pathol 46:194-210 (2009)
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