Imunolocalização de B-Catenina, GSK3, APC, LEF-1, e-Caderina e p63 em adenomas de células basais de glândula salivar

• Ano de defesa: 2014
• Autor(a) principal: Crispim, Leana Ferreira
• Tipo de documento: Dissertação
• Tipo de acesso: Acesso aberto
• Idioma: por
• Instituição de defesa: Universidade Federal de Uberlândia; BR; Programa de Pós-graduação em Biologia Celular e Estrutural Aplicadas; Ciências Biomédicas; UFU
• Palavras-chave em Português: Adenoma de células basais; Via de sinalização Wnt; B-Catenina; Tumores; Citologia; Câncer; Basal cell adenoma; Wnt signaling pathway; B-catenin; CNPQ::CIENCIAS BIOLOGICAS::MORFOLOGIA::CITOLOGIA E BIOLOGIA CELULAR
• Link de acesso: https://repositorio.ufu.br/handle/123456789/12423; https://doi.org/10.14393/ufu.di.2014.521

Basal cell adenoma (BCA) is a rare benign salivary gland neoplasm that mainly affects the parotid salivary gland. The knowledge of the causes and mechanisms enrolled in BCA pathogenesis is poorly understood. Some research shows that a peculiar feature of the BCA that distinguishes it from other salivary gland tumors is the nuclear accumulation of β-catenin, through activation of the canonical Wnt signaling pathway. Therefore, the aim of this study was to investigate if nuclear β-catenin accumulation in BCA was been related to Wnt/ β- catenin signaling activation, and then, improve the understanding of the pathogenesis of the lesion. For this, we selected 25 cases diagnosed as BCA. So, it was investigated by immunohistochemistry the expression of some key molecules of canonical Wnt / β-catenin signaling pathway, such as APC, GSK3β, β-Catenin, LEF-1, and e-cadherin as p63. Each reaction was analyzed qualitative and quantitatively by QuickScore index (Detre et al., 1995). The nuclear reactivity for β-catenin was found in 22 cases (88% of sample), with significantly higher reactivity in abluminal cell than in the luminal cell. We found a statistically significant correlation between QuickScore to β-catenin and GSK3β and p63 (Pearson correlation test). These results open new possibilities for research on the pathogenesis of the BCA, when suggest that GSK3β may be related to an alteration in the expression of β-catenin, and this change may result in a change in the expression of p63.