Ligia A N Miyahara1, Flávia S C Pontes2, Rommel M R Burbano2, Nicolau Conte Neto2, Douglas M Guimarães2, Felipe P Fonseca3, Hélder A R Pontes1,2. 1. Oral Diagnosis Department, Semiology and Oral Pathology Areas, Piracicaba Dental School, University of Campinas (UNICAMP), São Paulo, Brazil. 2. João de Barros, Barreto University Hospital (HUJBB), Federal University of Pará (UFPA), Pará, Brazil. 3. Department of Oral Surgery and Pathology, School of Dentistry, Federal University of Minas Gerais (UFMG), Minas Gerais, Brazil.
Abstract
AIM: 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 χ2 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.
AIM: 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 χ2 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.