Objectives: A cross-sectional study has shown a higher rate of TP53 mutation in lichen planus than in hyperkeratosis (Ögmundsdóttir et al., Eur J Oral Sci 2002;110: 192-198). By performing analysis for TP53 mutations in serial samples from a small group of patients it was hoped to determine if these mutations were related to disease progression. Methods: Nine patients presenting with lesions resembling oral leukoplakia or lichen planus were followed from 1 –11y (mean 4y). From 1-5 samples of biopsy tissue were available for analysis from these patients. Mutation analysis was performed on archival samples and mutations were detected by constant denaturant gradient gel electrophoresis (CDGE) analysis for hotspots A, B, C, D and exon 6. Results: Five patients were diagnosed clinically with lichen planus: 3 were confirmed by histopathology; 2 were diagnosed as hyperkeratosis. Four patients had leukoplakia with a histological diagnosis of hyperkeratosis. Six patients subsequently developed squamous carcinoma: 2/6 patients had TP53 mutations in the premalignant lesion; 1/6 only at the time of malignancy (after 11 years without mutation); 1/6 at the time of recurrent malignancy; 1/6 post-irradiation; and 1/6 had a mutation in the cancer (no premalignant sample available). One cancer-free patient had no mutation from 5 serial samples, the remaining 2 had mutations associated with a worsening of disease, clinically or histologically. Conclusions: This study indicates a role for TP53 mutation in malignant progression of oral lesions.

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