Please use this identifier to cite or link to this item: http://repositorio.ufc.br/handle/riufc/21487
Type: Artigo de Periódico
Title: Evaluation of the p-AKT, p-JNK and FoxO3a function in the oral epithelial dysplasia malignance
Authors: Chaves, Filipe Nobre
Marinho, Thâmara Manoela Bezerra
Silva, Paulo Goberlânio de Barros
Oliveira, Francisco Artur Forte
Sousa, Fabrício Bitu
Costa, Fábio Wildson Gurgel
Alves, Ana Paula Negreiros Nunes
Pereira, Karuza Maria Alves
Keywords: Carcinoma;Citoplasma;Cytoplasm
Issue Date: 2016
Publisher: Oral Diseases
Citation: CHAVES, F. N. et al. Evaluation of the p-AKT, p-JNK and FoxO3a function in the oral epithelial dysplasia malignance. Oral Diseases, Houndmills, p. 1-27, 2016.
Abstract: OBJECTIVES: To evaluate the expression of p-AKT, p-JNK, FoxO3a and KI-67 in samples of Oral Squamous Cell Carcinoma (OSCC) and Oral Epithelial Dysplasias (OEDs) to understand their possible involvement in the malignant transformation process of oral lesions. MATERIALS AND METHODS: Tissue samples of 20 cases of OSCCs, 20 OEDs and normal oral mucosa were subjected to immunohistochemistry reactions for anti-p-Akt, anti-p-JNK, anti-FoxO3a and anti-Ki-67 antibodies. It was analyzed quantitative (number of immunostained cells) and qualitative (immunostaining intensity) parameters in different cell immunostaining sublocations. RESULTS: Nuclear p-AKT was observed significantly greater immunostaining in OSCC (21.2 ± 19.0) than in dysplasias (7.9 ± 8.1) and control (1.8 ± 4.7) (p = 0.002). Immunostaining of strong nuclear p-JNK was greater in controls (48.3 ± 13.7) than in OEDs (11.0 ± 10.3) and OSCCs (1.1 ± 1.3) (p<0.001). Strong nuclear immunostaining of FoxO3a proved to be absent in OSCCs (0.0 ± 0.1) with little staining on dysplasias (3.2 ± 5.4) and increased expression in controls (13.5 ± 4.8) (p<0.001). Immunostaining of strong nuclear ki-67 was grater in OSCCs (48.1±49.6) than in OED (11.8±10.6) and controls (1.9±2.0) (p<0.001). CONCLUSIONS: Malignant process of OEDs in this research may involve the same mechanisms of established malignant lesions.
URI: http://www.repositorio.ufc.br/handle/riufc/21487
ISSN: 1354-523X
Appears in Collections:DCOD - Artigos publicados em revistas científicas

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