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Expression of β-catenin and cyclin-D1 in sporadic parathyroid adenomas / 中华内分泌外科杂志
Chinese Journal of Endocrine Surgery ; (6): 221-224, 2012.
Artigo em Chinês | WPRIM | ID: wpr-622205
ABSTRACT
Objective To study the expression of β-catenin and cyclin-D1 in sporadic parathyroid adenomas and the clinical significance.Methods Immunohistochemistry and RT-PCR were used to examine the expression of β-catenin and cyclin-Dl in 20 cases of sporadic parathyroid adenomas,10 cases of parathyroid hyperplasia tissues and 8 cases of normal parathyroid tissues respectively.Results The results of immunohistochemistry showed that the expression of β-catenin was decreased on cell membrane of normal parathyroid tissues,parathyroid hyperplasia tissues and sporadic parathyroid adenomas,and was increased in the cytoplasm and the nucleus.The expression of cyclin-Dl was significantly higher in the adenoma group and hyperplasia group than in the normal group( P < 0.05 ).The difference had no statistical significance in terms of cyclin-Dl expression between the adenoma group and the hyperplasia group( P >0.05 ).The abnormal expression of β-catenin was significantly correlated with the overexpression of cyclin-D1 in sporadic parathyroid adenomas( P < 0.05 ).RT-PCR analysis showed that the expression of cyclin-D1 mRNA was 2.36 ± 1.12 vs 1.50 ± 1.03 ( P < 0.05 ),and the expression of β-catenin mRNA was 1.02 ± 0.45 vs 0.88 ± 0.56( P > 0.05 ) in adenomas and normal parathyroid tissues respectively.Conclusion The abnormal expression of β-catenin activates cyclin-Dl and thus leads to the uncontrolled cell proliferation and differentiation,which may be one of the mechanisms of the occurrence of sporadic parathyroid tumors.

Texto completo: DisponíveL Índice: WPRIM (Pacífico Ocidental) Idioma: Chinês Revista: Chinese Journal of Endocrine Surgery Ano de publicação: 2012 Tipo de documento: Artigo

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Texto completo: DisponíveL Índice: WPRIM (Pacífico Ocidental) Idioma: Chinês Revista: Chinese Journal of Endocrine Surgery Ano de publicação: 2012 Tipo de documento: Artigo