BACKGROUND: The expression of tumour suppressor p53 and oncogene c-myc was investigated in an experimental model of chemically induced carcinogenesis in normal and diabetic (type I) Sprague-Dawley rats. MATERIALS AND METHODS: Tissue sections ranging from normal mucosa to moderately differentiated oral squamous cell carcinoma were studied using monoclonal antibodies against mutant p53 and c-myc proteins. RESULTS: From hyperplasia to later stages of oral oncogenesis, mutant p53 expression was at higher levels in diabetic rats in comparison to normal animals, although the pattern of expression was similar. In contrast, c-myc expression was significantly higher in diabetic than in normal rats only in normal mucosa and hyperplasia. CONCLUSION: It seems that diabetes contributed to increased accumulation of mutations in the p53 gene, contributing to increased proliferation of tumour cells during oral oncogenesis. Additionally, diabetes appeared to enhance c-myc expression only in the initial stages of oral oncogenesis.
BACKGROUND: The expression of tumour suppressor p53 and oncogene c-myc was investigated in an experimental model of chemically induced carcinogenesis in normal and diabetic (type I) Sprague-Dawley rats. MATERIALS AND METHODS: Tissue sections ranging from normal mucosa to moderately differentiated oral squamous cell carcinoma were studied using monoclonal antibodies against mutant p53 and c-myc proteins. RESULTS: From hyperplasia to later stages of oral oncogenesis, mutant p53 expression was at higher levels in diabeticrats in comparison to normal animals, although the pattern of expression was similar. In contrast, c-myc expression was significantly higher in diabetic than in normal rats only in normal mucosa and hyperplasia. CONCLUSION: It seems that diabetes contributed to increased accumulation of mutations in the p53 gene, contributing to increased proliferation of tumour cells during oral oncogenesis. Additionally, diabetes appeared to enhance c-myc expression only in the initial stages of oral oncogenesis.