Skip Navigation



Japanese Journal of Clinical Oncology Advance Access published online on June 27, 2006

Japanese Journal of Clinical Oncology, doi:10.1093/jjco/hyl055
This Article
Right arrow FREE Full Text (PDF) Freely available
Right arrow All Versions of this Article:
36/8/483    most recent
hyl055v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Request Permissions
Google Scholar
Right arrow Articles by Shin, M. C.
Right arrow Articles by Park, J. Y.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Shin, M. C.
Right arrow Articles by Park, J. Y.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© 2006 Foundation for Promotion of Cancer Research
Received February 1, 2006
Accepted April 15, 2006

Original Article

Glu346lys Polymorphism in the Methyl-Cpg Binding Domain 4 Gene and the Risk of Primary Lung Cancer

Moo Chul Shin 1, Su Jeong Lee 2, Jin Eun Choi 2, Sung Ick Cha 1, Chang Ho Kim 1, Won Kee Lee 3, Sin Kam 3, Young Mo Kang 1, Tae Hoon Jung 1, and Jae Yong Park 4 *

1 Department of Internal Medicine, Kyungpook National University, Daegu, Korea
2 Cancer Research Institute, Kyungpook National University, Daegu, Korea
3 Department of Preventive Medicine, School of Medicine, Kyungpook National University, Daegu, Korea
4 Department of Internal Medicine, Kyungpook National University, Daegu, Korea; Cancer Research Institute, Kyungpook National University, Daegu, Korea

* To whom correspondence should be addressed.
Jae Yong Park, E-mail: jaeyong{at}knu.ac.kr


   Abstract

Background: Methyl-CpG binding domain 4 (MBD4) protein functions as a DNA repair enzyme and minimizes mutations at 5-methylcytosine. Polymorphisms in the DNA repair gene MBD4 may be associated with differences in DNA repair capacity and thereby influence an individual's susceptibility to lung cancer. To test this hypothesis, we examined the potential association between the MBD4 Glu346Lys polymorphism and the risk of lung cancer in a Korean population.

Methods: The MBD4 Glu346Lys genotypes were determined in 432 lung cancer patients and 432 healthy age- and gender-matched control subjects.

Results: The distribution of the MBD4 Glu346Lys genotypes was not significantly different between the overall lung cancer cases and the controls. However, when the cases were categorized by tumor histology, the Lys346Lys genotype was associated with a significantly decreased risk of adenocarcinoma (AC) as compared with the Glu346Glu genotype [adjusted odds ratio (OR) = 0.50, 95% confidence interval (CI) = 0.26-0.97, P = 0.04]. On the stratification analysis, the protective effect of the Lys346Lys genotype against AC was statistically significant in older individuals and heavier smokers (adjusted OR = 0.08, 95% CI = 0.01-0.64, P = 0.02; and adjusted OR = 0.09, 95% CI = 0.01-0.72, P = 0.02, respectively).

Conclusions: Our findings suggest that the MBD4 Glu346Lys polymorphism could be used as a marker for genetic susceptibility to AC of the lung.

Keywords: MBD4; polymorphism; genetic susceptibility; lung cancer.
Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
Hum Mol GenetHome page
A. Miremadi, M. Z. Oestergaard, P. D.P. Pharoah, and C. Caldas
Cancer genetics of epigenetic genes
Hum. Mol. Genet., April 15, 2007; 16(R1): R28 - R49.
[Abstract] [Full Text] [PDF]



Disclaimer:
Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.