Patogênese dos tumores diferenciados da tiróide (papilífero e folicular)
Differentiated thyroid cancers (papillary - PTC and follicular - FTC) are the most common endocrine malignancies. The recent progresses in the understanding of PTC and FTC pathogenesis are summarized in this review. In PTC, a single mutation of BRAF (the gene for the B-type Raf kinase) (V600E) is re...
| Autores: | , , |
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| Tipo de recurso: | artículo |
| Estado: | Versión publicada |
| Fecha de publicación: | 2005 |
| País: | Brasil |
| Institución: | Universidade Federal de São Paulo (UNIFESP) |
| Repositorio: | Repositório Institucional da UNIFESP |
| Idioma: | portugués |
| OAI Identifier: | oai:repositorio.unifesp.br:11600/2718 |
| Acceso en línea: | http://dx.doi.org/10.1590/S0004-27302005000500009 http://repositorio.unifesp.br/handle/11600/2718 |
| Access Level: | acceso abierto |
| Palabra clave: | Papillary thyroid carcinoma Follicular thyroid carcinoma RET; BRAF; RET/PTC; RAS; PAX8/PPARgamma Carcinoma papilífero da tiróide Carcinoma folicular da tiróide RET; BRAF; RET/PTC; RAS; PAX8/PPARgama |
| Sumario: | Differentiated thyroid cancers (papillary - PTC and follicular - FTC) are the most common endocrine malignancies. The recent progresses in the understanding of PTC and FTC pathogenesis are summarized in this review. In PTC, a single mutation of BRAF (the gene for the B-type Raf kinase) (V600E) is responsible for the disease in 40-50% of patients, especially in older people and is associated with a poorer clinicopathological outcome. Due to these characteristics, its use as a specific diagnostic and prognostic marker for PTC in cytological specimens is being implemented. Another important cause of PTC is rearrangements of the RET tyrosine kinase receptor (RET/PTC), which represent a recombination of the promoter and N-terminal domain of a partner gene with the C-terminal region of the RET gene, resulting in a chimeric gene with a protein product containing a constitutively activated RET tyrosine kinase, responsible for 20-30% patients, specially the younger or after radiation. The pathogenesis of FTC is less understood. A chromosomal translocation between the transcription factor PAX8 and the peroxisome proliferator-activated receptorgamma (PPARgamma) occurs in 30-50% of patients; however, the presence of PAX8-PPARgamma is also demonstrated in follicular adenomas. Therefore, there is no complete evidence that PAX8-PPARgamma is the cause of FTC. Another finding in FTC is mutations on the RAS gene, which excludes PAX8-PPARgamma rearrangements. Several genes, as TRgamma, PTEN, PKAR1A, DDIT3, ARG2, ITM1 and C1orf24 - some discovered by techniques of differential gene expression -, have been recently implicated in the pathogenesis of FTC. |
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