Thyroid hormone receptor beta mutations in the 'hot-spot region' are rare events in thyroid carcinomas

• Tipo: Artigo em Revista Científica Internacional
• Data: 2007

Autores

Ana Sofia Rocha (Autor) Outra; Ricardo Marques (Autor) Outra; Ines Bento (Autor) Outra; Ricardo Soares (Autor) Outra; Joao Magalhaes (Autor) Outra; Ines Vieira de Castro (Autor) Outra; Paula Soares (Autor) FMUP

Revista

Título: Journal of Endocrinology

Vol. 192 Nº 3

Páginas: 83-86

ISSN: 0022-0795

Editora: BioScientifica Ltd.

Indexação

ISI Web of Knowledge - 17 Citações

ISI Web of Science

Scopus - 17 Citações

Pubmed / Medline

Classificação Científica

FOS: Ciências médicas e da saúde > Medicina clínica

Outras Informações

ID Authenticus: P-004-DNF

DOI: 10.1677/joe-06-0009

Abstract (EN): Thyroid cancer constitutes the most frequent endocrine neoplasia. Targeted expression of rearranged during transfection (RET)/papillary thyroid carcinoma (PTC) and V600E V-raf murine sarcoma viral oncogene homolog B1 (BRAF) to the thyroid glands of transgenic mice results in tumours similar to those of human PTC, providing evidence for the involvement of these oncogenes in PTC. Kato et al. developed a mouse model that mimics the full spectrum of the human follicular form of thyroid cancer (FTC). FTC rapidly develops in these mice through introduction of the thyroid hormone receptor beta (THRB)(PV) mutant on the background of the inactivatedTHRB wt locus. Our aim was to verify if, in the context of human follicular thyroid carcinogenesis, THRB acted as a tumour suppressor gene. We screened for mutations of the THRB gene in the hot-spot region, spanning exons 7-10, in 51 thyroid tumours and six thyroid cancer cell lines by PCR and direct sequencing. We did not find mutations in any of the tumours or cell lines analysed. Our findings suggest that, in contrast to the findings on the THRB-mutant transgenic mice, THRB gene mutations are not a relevant mechanism for human thyroid carcinogenesis.

Idioma: Inglês

Tipo (Avaliação Docente): Científica

Nº de páginas: 4