Article Search

Journal of Cancer Prevention

Original Article

Cancer prevention research 2008; 13(2): 85-90

Published online June 30, 2008

© Korean Society of Cancer Prevention

p16INK4a Promoter Methylation and Immunohistochemical Expression in Breast Carcinoma and Association with Pathological Features

Jong Sil Lee, Dae Hyun Song, Jung Wook Yang, Dong Chool Kim, Jeong Hee Lee and Gyung Hyuck Ko


A cyclin-dependent kinase (CDK) 4 inhibitor (p16INK4) gene located at 9p21 has been shown to be inactivated in a variety of tumors by homozygous deletions, point mutations, or hypermethylation of its promoter region. The etiologic role of the cdk inhibitor p16INK4a tumor suppressor protein in breast cancer remains unclear. This study attempts to assess the methylation pattern of p16INK4a gene and its correlation with the expression of p16INK4a and to determine, by comparing the correlation between other standard immunohistochemical parameters (Cerb B2, estrogen receptor, progesteron receptor, p53, and Ki-67) and clinicopathological features, the significance of p16INK4a methylation and p16INK4a immunohistochemical expression in breast carcinoma. Immunohistochemical p16INK4a expression was found in 21 (42%) of 50 cases. There was a correlation between loss of p16INK4a expression and advanced stage (p=.016). p16INK4a promoter methylation was found in 72%. Twenty-three (79.3%) of 29 tumors with loss of expression of p16INK4a in immunohistochemistry showed DNA methylation of the p16INK4a gene. Loss of p16INK4a expression was related with high stage breast tumors and p16INK4a promoter hypermethylation was the main mechanism of loss of p16INK4a expression. (Cancer Prev Res 13, 85-90, 2008)

Keywords: p16INK4a, Methylation, Immunohistochemistry, Breast cancer

Share this article on :

Related articles in JCP

Most KeyWord