Skip Navigation


Human Molecular Genetics Advance Access originally published online on February 23, 2006
Human Molecular Genetics 2006 15(7):1181-1186; doi:10.1093/hmg/ddl033
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow Supplementary Material
Right arrow All Versions of this Article:
15/7/1181    most recent
ddl033v1
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 ISI Web of Science
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 Search for citing articles in:
ISI Web of Science (9)
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Kim, J. H.
Right arrow Articles by Hong, Y.-C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Kim, J. H.
Right arrow Articles by Hong, Y.-C.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© The Author 2006. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Genetic polymorphisms of ataxia telangiectasia mutated affect lung cancer risk

Jin Hee Kim1, Heon Kim3, Kye Young Lee5, Kang-Hyeon Choe4, Jeong-Seon Ryu6, Ho Il Yoon1,7, Sook Whan Sung2,8, Keun-Young Yoo1 and Yun-Chul Hong1,9,*

1Department of Preventive Medicine and 2Department of Thoracic and Cardiovascular Surgery, Seoul National University College of Medicine, 28 Yongon-dong, Chongno-gu, Seoul 110-799, Republic of Korea, 3Department of Preventive Medicine and 4Department of Internal Medicine, College of Medicine, Chungbuk National University, 12 Kaeshin-dong, Hungdok-gu, Cheongju-si, Chungbuk 361-763, Republic of Korea, 5Department of Internal Medicine, School of Medicine, Konkuk University, No. 4-12 Hwayang-dong, Gwangjin-gu, Seoul 143-729, Republic of Korea, 6Department of Internal Medicine, College of Medicine, Inha University, 7-206 Shinhung-dong 3ga, Jung-gu, Incheon 400-103, Republic of Korea, 7Department of Internal Medicine and 8Department of Thoracic and Cardiovascular Surgery, National University Bundang Hospital, 300 Gumi-dong, Bundang-gu, Seongnam, Geongi-do 463-707, Republic of Korea and 9Institute of Environmental Medicine, SNUMRC, 28 Yongon-dong, Chongno-gu, Seoul 110-799, Republic of Korea

* To whom correspondence should be addressed. Tel: +82 27408394; Fax: +82 27474830; Email: ychong1{at}snu.ac.kr

Received January 6, 2006; Accepted February 15, 2006

The ataxia telangiectasia mutated (ATM) gene is known to be activated by DNA damage and involved in cell cycle arrest, apoptosis and DNA repair. Therefore, ATM gene polymorphisms may act as important factors predicting individual susceptibility to lung cancer. To evaluate the role of ATM gene polymorphisms in lung cancer development, genotypes of the ATM polymorphisms, –4518A>G, IVS21–77C>T, IVS61–55T>C, and IVS62+60G>A, were determined in 616 lung cancer patients and 616 cancer-free controls. When the effects of selected ATM genotypes were evaluated separately, only one ATM genotype (IVS62+60G>A) showed an association with lung cancer risk. Subjects with the A allele at the site (IVS62+60G>A) have significantly higher risk of lung cancer than those with the G allele [odds ratio (OR)=1.6, 95% confidence interval (CI) 1.1–2.1]. When the haplotypes of four ATM single nucleotide polymorphism sites (–4518A>G, IVS21–77C>T, IVS61–55T>C and IVS62+60G>A) were studied, the ATTA haplotype showed significantly increased risk of lung cancer compared with the GCCA haplotype, the most common haplotype (OR=7.6, 95% CI 1.7–33.5). Furthermore, subjects with the (NN)TA haplotype showed highly significant and increased risk of lung cancer when compared with those without the (NN)TA haplotype (OR=13.2, 95% CI 3.1–56.1). Therefore, our results suggest that polymorphisms or haplotypes of the ATM gene play an important role in the development of 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
 JCOHome page
S. L. Dombernowsky, M. Weischer, K. H. Allin, S. E. Bojesen, A. Tybjjrg-Hansen, and B. G. Nordestgaard
Risk of Cancer by ATM Missense Mutations in the General Population
J. Clin. Oncol., June 20, 2008; 26(18): 3057 - 3062.
[Abstract] [Full Text] [PDF]

Home page
 Clin. Cancer Res.Home page
Z. Hu, H. Liu, H. Wang, R. Miao, W. Sun, G. Jin, Y. Wang, H. Ma, L. Jin, Q. Wei, et al.
Tagging Single Nucleotide Polymorphisms in Phosphoinositide-3-Kinase-Related Protein Kinase Genes Involved in DNA Damage "Checkpoints" and Lung Cancer Susceptibility
Clin. Cancer Res., May 1, 2008; 14(9): 2887 - 2891.
[Abstract] [Full Text] [PDF]

Home page
 Clin. Cancer Res.Home page
T. Okazaki, L. Jiao, P. Chang, D. B. Evans, J. L. Abbruzzese, and D. Li
Single-Nucleotide Polymorphisms of DNA Damage Response Genes Are Associated with Overall Survival in Patients with Pancreatic Cancer
Clin. Cancer Res., April 1, 2008; 14(7): 2042 - 2048.
[Abstract] [Full Text] [PDF]

Home page
 Cancer Epidemiol. Biomarkers Prev.Home page
J. Xing, M. R. Spitz, C. Lu, H. Zhao, H. Yang, W. Wang, D. J. Stewart, and X. Wu
Deficient G2-M and S Checkpoints are Associated with Increased Lung Cancer Risk: A Case-Control Analysis
Cancer Epidemiol. Biomarkers Prev., July 1, 2007; 16(7): 1517 - 1522.
[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.