Evaluation of the p‐AKT, p‐JNK and FoxO3a function in oral epithelial dysplasia

Chaves, Filipe Nobre; Bezerra, Tmm; Silva, PG de Barros; Oliveira, Faf; Sousa, FB; Costa, F M S; Alves, Apnn; Pereira, Karuza Maria Alves

doi:10.1111/odi.12623

Cited by 2 publications

(3 citation statements)

References 73 publications

(121 reference statements)

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“…In addition, Akt expression was shown to be a prognostic determinant for patients affected by OSCC . In this regard, in our work the increase in PTEN expression observed in the evolution of dysplastic lesions can be understood as an attempt to control the increased expression of Akt described in several studies of oral dysplastic lesions . In addition, a decrease in PTEN expression was observed in OSCC.…”

Section: Discussionsupporting

confidence: 59%

“…Recently, Chaves et al . studied p‐Akt function in oral epithelial dysplasia and in OSCC, observing that p‐Akt immunostaining was significantly higher in the malignancy group than in dysplasias and controls . Other studies investigated p‐Akt in the process of malignant transformation of oral epithelium, suggesting that activation of the PI3K‐AKT signal pathway is involved in the malignant phenotype acquisition process from its early stages .…”

Section: Discussionmentioning

confidence: 99%

“…Recent studies have proposed that activation of Akt has been shown to be associated with advanced stages and poor prognosis in OSCC; furthermore, studies using OSCC cell lines have shown that induced PTEN overexpression down‐regulated Akt phosphorylation significantly and induced apoptosis . Regarding oral potentially malignant lesions, several studies have shown that p‐Akt may play an important role in the conversion of these lesions to its malignant counterpart …”

Section: Introductionmentioning

confidence: 99%

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PTEN allelic loss is an important mechanism in the late stage of development of oral leucoplakia into oral squamous cell carcinoma

et al. 2017

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PTEN allelic loss is an important mechanism in the late stage of development of oral leucoplakia into oral squamous cell carcinomaAim: The aim of this study was to analyse allelic loss of the phosphatase and tensin homologue deleted on chromosome 10 (PTEN) gene and its protein immuno-expression in dysplastic oral lesions and oral squamous cell carcinomas (OSCCs). Methods and results: Samples were collected from 153 patients [20 ranulas used as a control (C); 30 leucoplakias with mild dysplasia (MD); 30 leucoplakias with moderate to severe dysplasia (MSD); 73 oral squamous cell carcinoma (OSCC)]. PTEN protein expression was investigated using immunohistochemistry, and PTEN allelic loss was analysed by fluorescence in-situ hybridisation (FISH). Differences among groups were evaluated using the v 2 test.PTEN expression was higher in MSD (P = 0.002) and OSCC (P = 0.0259) compared with the C group; additionally, a higher expression was observed in MSD (P = 0.0035) and OSCC (P = 0.049) than MD. Regarding FISH analysis, a higher hemizygous (single copy) loss was observed in OSCC than in C (P = 0.0467) and in OSCC than in MD (P = 0.0175), as well as a higher homozygous deletion in OSCC compared with C (P = 0.0159) and OSCC than MD (P = 0.0145). Conclusion:The results of this work suggest that PTEN allelic loss is an important mechanism in the late stage of the development of oral potentially malignant lesions into oral cancer.

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Section: Discussionsupporting

confidence: 59%

Section: Discussionmentioning

confidence: 99%