|Título||Expressão da iodotironina desiodase tipo 3 no carcinoma diferenciado de tireóide
Maia, Ana Luiza Silva
|Instituição||Universidade Federal do Rio Grande do Sul. Faculdade de Medicina. Programa de Pós-Graduação em Ciências Médicas: Endocrinologia.|
Carcinoma papilar, variante folicular
Neoplasias da glândula tireóide
|Abstract||Thyroid carcinoma is the most common endocrine malignant neoplasia. Differentiated thyroid carcinomas (DTC), represent more than 90% of all thyroid carcinomas and comprise the papillary (PTC) and follicular thyroid carcinomas (FTC) subtypes. Anaplastic thyroid carcinoma (ATC) corresponds to less than 5% of all thyroid tumors. The etiology of DTC is not fully understood. Several genetic events have been implicated on differentiated thyroid tumorigenesis. Point mutations in BRAF and RAS genes and RET/PTC rearrangements are observed in about 70% of PTC cases. Follicular carcinomas commonly harbor RAS mutations and PAX8-PPARJ rearrangements. Anaplastic carcinomas may harbor a wide set of genetic alterations, as in genes encoding effectors in the mitogen-activated protein kinase (MAPK), phosphatidylinositol 3-kinases (PI3K) and G-Catenin signaling pathways. These distinct genetic alterations are able to activate constitutively several signaling pathways as MAPK, PI3K and G-Catenin, which have been implicated on thyroid cancer development and progression. In this context, the evaluation of the specific oncogenes, as well as the knowledge of their effects on thyroid carcinomas can provide important information about the disease presentation, prognosis and therapy, through the development of specific tyrosine kinase targets. Particularly in this review, we explore the main genetic alterations observed in follicular cell-derived thyroid carcinomas as well as the molecular mechanisms involved in thyroid tumors development and progression.
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