BACKGROUND: The aim of the current study was to examine the possible association of the p53 tumor suppressor gene with the development of oral cancer. We examined biopsy material from patients with oral squamous cell carcinoma for p53 protein expression and p53 mutations. METHODS: Eighteen samples were analyzed. These comprised oral squamous cell carcinoma biopsy samples and oral dysplastic biopsy material taken from nine patients. An immunohistochemical technique was used to determine p53 protein expression. A direct sequencing technique was used to detect mutations in the p53 gene itself. RESULTS: Overall seven of nine (77%) oral squamous cell carcinomas and seven of nine (77%) oral dysplastic lesions analyzed showed evidence of p53 protein over-expression. Mutations in exons 5 and 6 of the p53 gene were detected in five of nine (55%) oral squamous cell carcinomas and four of nine (44%) dysplastic lesions analyzed. CONCLUSIONS: Both p53 protein over-expression and p53 mutations were noted in dysplastic oral lesions. Over-expression of the p53 protein and p53 gene mutations were not always coexistent, however, suggesting that gene mutation may be only one of the mechanisms responsible for stabilization of the p53 protein.
BACKGROUND: The aim of the current study was to examine the possible association of the p53tumor suppressor gene with the development of oral cancer. We examined biopsy material from patients with oral squamous cell carcinoma for p53 protein expression and p53 mutations. METHODS: Eighteen samples were analyzed. These comprised oral squamous cell carcinoma biopsy samples and oral dysplastic biopsy material taken from nine patients. An immunohistochemical technique was used to determine p53 protein expression. A direct sequencing technique was used to detect mutations in the p53 gene itself. RESULTS: Overall seven of nine (77%) oral squamous cell carcinomas and seven of nine (77%) oral dysplastic lesions analyzed showed evidence of p53 protein over-expression. Mutations in exons 5 and 6 of the p53 gene were detected in five of nine (55%) oral squamous cell carcinomas and four of nine (44%) dysplastic lesions analyzed. CONCLUSIONS: Both p53 protein over-expression and p53 mutations were noted in dysplastic oral lesions. Over-expression of the p53 protein and p53 gene mutations were not always coexistent, however, suggesting that gene mutation may be only one of the mechanisms responsible for stabilization of the p53 protein.