Hypermethylation of p16(INK4a) in Korean Non-small Cell Lung Cancer Patients.
10.3346/jkms.2007.22.S.S32
- Author:
Young Seoub HONG
1
;
Mee Sook ROH
;
Na Young KIM
;
Hye Jung LEE
;
Hee Kyoung KIM
;
Kyung Eun LEE
;
Jong Young KWAK
;
Joon Youn KIM
Author Information
1. Department of Preventive Medicine, College of Medicine, Dong-A University, Busan, Korea. yshong@dau.ac.kr
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- Keywords:
Hypermethylation;
p16(INK4a);
Lung Cancer
- MeSH:
Adult;
Aged;
Base Sequence;
Carcinoma, Non-Small-Cell Lung/*genetics;
*DNA Methylation;
DNA Primers/genetics;
DNA, Neoplasm/chemistry/genetics;
Female;
*Genes, p16;
Humans;
Korea;
Lung Neoplasms/*genetics;
Male;
Middle Aged;
Molecular Sequence Data;
Polymerase Chain Reaction;
Promoter Regions, Genetic;
Smoking/adverse effects/genetics
- From:Journal of Korean Medical Science
2007;22(Suppl):S32-S37
- CountryRepublic of Korea
- Language:English
-
Abstract:
Promoter hypermethylation of the p16(INK4a) gene was investigated in 81 sets of samples of tumor tissue and adjacent normal tissue from Korean patients with primary lung cancer, using the modified real-time polymerase chain reaction (PCR)/ SYBR Green detection method. The results showed hypermethylation of p16(INK4a) in 27.2% of tumor tissues, and in 11.1% of adjacent normal tissue. No significant association was found between the overall aberrant methylation in tumor and corresponding normal specimens (r=0.137, p=0.219). In 22 cases with p16(INK4a) hypermethylation in tumor tissues, only 4 (18.1%) cases were found to have a hypermethylated normal tissue specimen. The findings of this study show that smoking can influence the methylation level of the promoter region of p16(INK4a), and that this occurs in tumor tissues more frequently than in normal tissues. Other clinicopathological characteristics, including age, sex, tumor stage, and histologic type were not found to be correlated with p16(INK4a) methylation.
