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KMID : 1134120060090020084
Journal of Breast Cancer
2006 Volume.9 No. 2 p.84 ~ p.90
The Loss of p16(ink4)Expression is Strongly Associated with Hyperme thylation-Related Inactivation in Breast Carcinoma
Gong Gyung-Yub

Ahn Sei-Hyun
Kang Gyeong-Hoon
Abstract
Purpose: The loss of p16 protein has been frequently detected in breast carcinoma, but genetic alterations are infrequent. CpG islands of methylation within the p16 promotor have been identified as a mechanism that inactivates the p16 expression. The object of this study is to investigate the relationship between the loss of p16 protein and methylation as a molecular mechanism of the p16 gene inactivation in mammary tumorigenesis.

Methods: We performed an immunohistochemical assay of p16 protein in 70 cases of mammary carcinomas, and we tested for DNA methylation of p16 using methylation-specific PCR, and we then analyzed its correlation with the histopathologic variables.

Results: Among the 70 cases, the p16 expression was lost in 32 cases (45.7%), which was not significantly correlated with the pathologic variables. Twenty-three cases with and 27 cases without loss of p16 expression were tested for DNA methylation of p16. Twenty-one of the 23 interpretable cases with loss of p16 expression (91%) showed hypermethylation on p16, but there was no hypermethylation in any of the cases that were without the loss of the p16 expression.

Conclusion: These findings suggest that the loss of the p16 expression is one of the common abnormalities observed in breast carcinoma and that methylation on the 5¡¯CpG island of the p16 promoter is a major process for p16 ink4 inactivation in breast carcinoma.
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