Objectives: Alteration of DNA methylation patterns are common changes in human cancer. Hypermethylation of CpG island promoter is associated with silencing of various tumor suppressor genes. Hypermethylations of p15 and p16, tumor suppressor genes, have been identified in oral squamous cell carcinoma (SCC). However, the DNA methylation in oral precancerous lesion remains incompletely investigated and poorly understood. Oral SCC, epithelial dysplasia and submucous fibrosis appear to be related to habit of betel quid chewing. The present study investigated the DNA hypermethylation of p15 and p16 in oral epithelial dysplasia in betel quid chewers. Methods: We used 26, 22, 25 and 25 cases diagnosed as mild dysplasia (MD), severe dysplasia (SD), SCC and normal epithelium, respectively. In order to analyze the CpG island methylation of p15 and p16 genes, DNA was extracted from the paraffin sections. The methylation profiles of the p15 and p16 were assessed using CpG WIZTM amplification kits (Sreologicals Corp,GA). The association between DNA-methylation and the histological features were analyzed using Fisher's exact tests. Results: The frequency of hypermethylation for p15 was 12% in the MD, 14% in the SD and 16% in the SCC. The frequency of hypermethylation for p16 was 57% in the MD, 59% in the SD and 56% in the SCC. No hypermethylation of the gene was detected in the normal epithelium. Although the frequency for p16 was significantly higher than that for p15 in each lesion (p<0.001), no significant difference of the frequency between the lesions was observed. Conclusion: The results indicate that hypermethylation of p15 and p16 may be involved in the development of epithelial dysplasia and in the malignant transformation of oral epithelium in betel quid chewers.

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