ABSTRACT
Thyroid carcinomas are the most common endocrine neoplasms in humans, with a globally increasing incidence. Thyroid follicular cells and neuroendocrine (parafollicular) C cells are each susceptible to neoplastic transformation, resulting in thyroid cancers of differing phenotypes with unique associated genetic mutations and clinical outcomes. Over the past 15 years, several sophisticated genetically engineered mouse models of thyroid cancer have been created to further our understanding of the genetic events leading to thyroid carcinogenesis in vivo. The most significant mouse models of papillary, follicular, anaplastic, and medullary thyroid carcinoma are highlighted, with particular emphasis on the relationship between the relevant oncogenes in these models and genetic events in the naturally occurring human disease. Limitations of each model are presented, and the need for additional models to better recapitulate certain aspects of the human disease is discussed.
Subject(s)
Disease Models, Animal , Thyroid Neoplasms/genetics , Animals , Animals, Genetically Modified , Female , Humans , Male , Mice , Oncogenes , Thyroid Neoplasms/pathologyABSTRACT
A 10-year-old castrated male Standard Poodle presented with an acute onset of lethargy and abdominal pain. The animal had a history of traumatic splenic rupture requiring splenectomy 5 years previously. Surgical exploration revealed multiple cystic red nodules involving all liver lobes, several of which were submitted for histopathology. Microscopically, the cystic nodules were dilated bile ducts and lymphatics surrounded by ectopic splenic tissue. A diagnosis of intrahepatic splenosis was made.
