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Desmosomal Component Expression in Normal, Dysplastic, and Oral Squamous Cell Carcinoma
Author(s) -
Nagamani Narayana,
Julie Gist,
Tyler S. Smith,
Daniel Tylka,
Gavin Trogdon,
James K. Wahl
Publication year - 2010
Publication title -
dermatology research and practice
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.456
H-Index - 29
eISSN - 1687-6113
pISSN - 1687-6105
DOI - 10.1155/2010/649731
Subject(s) - desmoplakin , medicine , pathology , dysplasia , desmosome , epithelial dysplasia , epithelium , oral mucosa , cancer , carcinoma , cell , biology , genetics
Squamous cell carcinoma (oral SCC) is the most common oral cancer in the U.S., affecting nearly 30,000 Americans each year. Despite recent advances in detection and treatment, there has been little improvement in the five-year survival rate for this devastating disease. Oral cancer may be preceded by premalignant disease that appears histologically as dysplasia. Identification of molecular markers for cellular change would assist in determining the risk of dysplasia progressing to oral squamous cell carcinoma. The goal of this study was to determine if any correlation exists between histological diagnosed dysplasia and OSCC lesions and altered expression of desmosomal cell-cell adhesion molecules in the oral epithelium. Our data showed that oral SCC tissue samples showed decreased immunoreactivity of both desmoplakin and plakophilin-1 proteins compared to normal oral epithelium. Furthermore, significant decrease in desmoplakin immunoreactivity was observed in dysplastic tissue compared to normal oral epithelium. In contrast, the level of desmoglein-1 staining was unchanged between samples however desmoglein-1 was found localized to cell borders in oral SCC samples. These data suggest that changes in expression of desmoplakin and plakophilin-1 may prove to be a useful marker for changes in tissue morphology and provide a tool for identifying pre-neoplastic lesions of the oral cavity.

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