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Nuclear localization of beta-catenin involved in precancerous change in oral leukoplakia

BACKGROUND: Oral leukoplakia is a precancerous change developed in the oral mucosa, and the mechanism that oral leukoplakia becomes malignant through atypical epithelium is not known. Here we compared the β-catenin expression detected by immunohistochemical staining in the normal oral epithelium and...

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Detalles Bibliográficos
Autores principales: Ishida, Kosei, Ito, Satoshi, Wada, Naoyuki, Deguchi, Hiroyo, Hata, Tsuyoshi, Hosoda, Masaru, Nohno, Tsutomu
Formato: Texto
Lenguaje:English
Publicado: BioMed Central 2007
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2140063/
https://www.ncbi.nlm.nih.gov/pubmed/17922924
http://dx.doi.org/10.1186/1476-4598-6-62
Descripción
Sumario:BACKGROUND: Oral leukoplakia is a precancerous change developed in the oral mucosa, and the mechanism that oral leukoplakia becomes malignant through atypical epithelium is not known. Here we compared the β-catenin expression detected by immunohistochemical staining in the normal oral epithelium and in the oral leukoplakia with or without dysplasia. RESULTS: The normal oral epithelium showed β-catenin expression only in the cell membrane, but not in the nuclei. In the oral leukoplakia without dysplasia, 7 out of 17 samples (41%) showed β-catenin expression in the cell membrane, and 5 samples (29%) showed expression in the nuclei. In the oral leukoplakia with dysplasia, nuclear expression of β-catenin was shown in 11 out of 12 samples (92%). Incidence of nuclear β-catenin expression was significantly different between dysplasia and normal oral epithelium (P < 0.01), and also between oral leukoplakia with dysplasia and those without dysplasia (P < 0.01). Wnt3 expression was detected in the epithelial cell membrane or cytoplasm in oral leukoplakia where nuclear expression of β-catenin was evident, but not in epithelial cells without nuclear expression of β-catenin. CONCLUSION: The components of canonical Wnt pathway, such as Wnt3, β-catenin, and cyclin D1, were detected, implying that this pathway is potentially involved in the progression of dysplasia in oral leukoplakia.