Background: A tumor suppressor gene, p16, was found to harbor promoter hypermethylation associated with the loss of protein expression in cancer cells, suggesting that p16 inactivation due to promoter methylation was important for colorectal tumorigenesis.
Materials and methods: The methylation status of the p16 gene was examined in primary carcinomas and the corresponding normal tissues derived from 50 patients with colorectal cancer using quantitative methylation-specific PCR (qMSP) and the correlation between the methylation status and the clinicopathological findings was evaluated.
Results: Aberrant methylation of the p16 gene was detected in 20 out of the 50 (40%) primary colon carcinomas, suggesting that the aberrant methylation of p16 was frequently observed in colorectal carcinomas. The clinicopathological data were then correlated with these results. Significant differences were observed with Dukes' stage (p = 0.0495) and lymphatic invasion (p = 0.0277).
Conclusion: p16 might act as a tumor suppressor in colorectal carcinomas and was more frequently methylated in advanced colorectal carcinomas.