Data/hora: 10/06/2024 05:36:46

Provedor de dados: | 56
País: | Brazil
Título: | Role of ACTH receptor in adrenocortical tumor formation
Autores: | Latronico,A.C.
Data: | 2000-10-01
Ano: | 2000
Palavras-chave: | Adrenocorticotrophin receptor; Adrenocortical tumors; Tumorigenesis.
Resumo: | Adrenocorticotrophin (ACTH) is the major regulatory hormone of steroid synthesis and secretion by adrenocortical cells. The actions of ACTH are mediated by its specific membrane receptor (ACTH-R). The human ACTH-R gene was recently cloned, allowing systematic determination of its sequence, expression and function in adrenal tumorigenesis. The presence of oncogenic mutations of the ACTH-R gene in adrenocortical tumors has been reported. Direct sequencing of the entire coding region of the ACTH-R gene of sporadic adrenocortical adenomas and carcinomas did not reveal constitutive activating mutations, indicating that this mechanism is not frequent in human adrenocortical tumorigenesis. Recent studies demonstrated allelic loss of the ACTH-R gene in a subset of sporadic adrenocortical tumors using a PstI polymorphism located in the promoter region of the ACTH-R gene. Loss of heterozygosity of the ACTH-R was analyzed in 20 informative patients with a variety of benign and malignant adrenocortical tumors. Three of them showed loss of heterozygosity of the ACTH-R gene. In addition, Northern blot experiments demonstrated reduced expression of ACTH-R mRNA in these three tumors with loss of heterozygosity, suggesting the functional significance of this finding at the transcriptional level. Deletion of the ACTH-R gene seems to be involved in a subset of human adrenocortical tumors, contributing to cellular dedifferentiation.
Tipo: | Info:eu-repo/semantics/article
Idioma: | Inglês
Identificador: | http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2000001000016
Editor: | Associação Brasileira de Divulgação Científica
Relação: | 10.1590/S0100-879X2000001000016
Formato: | text/html
Fonte: | Brazilian Journal of Medical and Biological Research  v.33 n.10 2000
Fonte: | info:eu-repo/semantics/openAccess