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KMID : 1140120080130020085
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Cancer Prevention Research
2008 Volume.13 No. 2 p.85 ~ p.90
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p16INK4a Promoter Methylation and Immunohistochemical Expression in Breast Carcinoma and Association with Pathological Features
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Lee Jong-Sil
Yang Jung-Wook
Kim Dong-Chool
Lee Jeong-Hee
Ko Gyung-Hyuck
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Abstract
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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)
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KEYWORD
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p16INK4a, Methylation, Immunohistochemistry, Breast cancer
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