Skip Navigation



Carcinogenesis Advance Access published online on June 10, 2004

Carcinogenesis, doi:10.1093/carcin/bgh203
© 2004 by Oxford University Press
This Article
Right arrow Advance Access manuscript (PDF) Freely available
Right arrow All Versions of this Article:
25/10/1935    most recent
bgh203v1
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 arrowRequest Permissions
Google Scholar
Right arrow Articles by Yang, P.
Right arrow Articles by de Andrade, M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Yang, P.
Right arrow Articles by de Andrade, M.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Received March 9, 2004
Revised April 26, 2004
Accepted May 27, 2004

MOLECULAR EPIDEMIOLOGY AND CANCER PREVENTION

Glutathione pathway genes and lung cancer risk in young and old age populations

P. Yang 1*, W. R. Bamlet 2, J. O. Ebbert 3, W. R. Taylor 4, M. de Andrade 2

1 Division of Epidemiology, Mayo Clinic College of Medicine, 200 First Street SW, Rochester, Minnesota, 55905, USA
2 Division of Biostatistics, Mayo Clinic College of Medicine, 200 First Street SW, Rochester, Minnesota, 55905, USA
3 Nicotine Research Center, Mayo Clinic College of Medicine, 200 First Street SW, Rochester, Minnesota, 55905, USA
4 Department of Laboratory Medicine and Cancer Genotyping Facility, Mayo Clinic College of Medicine, 200 First Street SW, Rochester, Minnesota, 55905, USA

* To whom correspondence should be addressed. E-mail: yang.ping{at}mayo.edu.


   Abstract

Objective: Multiple enzymes with overlapping functions and shared substrates in the glutathione (GSH) metabolic pathway have been associated with host susceptibility to tobacco smoke carcinogens and in lung cancer etiology. However, few studies have investigated the differing and interacting roles of GSH-pathway enzymes with tobacco smoke exposure on lung cancer risk in young (< 50 years of age) and old (> 80 years of age) populations. Method: Between 1997 and 2001, 237 primary lung cancer patients (170 young, 67 old) and 234 controls (165 young, 69 old) were consecutively enrolled at the Mayo Clinic. Using PCR amplification of genomic DNA, polymorphic markers for {gamma}GCS, GPX1, GSTP1 (I105V and A114V), GSTM1 and GSTT1 were genotyped. Recursive partitioning and logistic regression models were used to build binary classification trees and to estimate an odds ratio (OR) and 95% confidence intervals for each splitting factor. Results: Young age group: Cigarette smoking had the greatest association with lung cancer (OR=3.3). For never smokers, the dividing factors of recursive partitioning were GSTT1 (OR=1.7), GPX1 (OR=0.6), and then GSTM1 (OR=4.3). Old age group: Smoking had the greatest association with lung cancer (OR=3.6). For smokers, the dividing factors were GPX1 (OR=3.3) and GSTP1 (I105V, OR=4.1). Results from logistic regression analysis supported the results from RPART models. Conclusion: GSH-pathway genes are associated with lung cancer development in young and old populations through differing interactions with cigarette smoking and family history. Carefully evaluating multiple levels of gene-environment and gene-gene interactions is critical in assessing lung cancer risk.

Key Words: lung neoplasms, glutathione, glutathione transferases, smoking, genetics


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
Am J EpidemiolHome page
C. Carlsten, G. S. Sagoo, A. J. Frodsham, W. Burke, and J. P. T. Higgins
Glutathione S-Transferase M1 (GSTM1) Polymorphisms and Lung Cancer: A Literature-based Systematic HuGE Review and Meta-Analysis
Am. J. Epidemiol., April 1, 2008; 167(7): 759 - 774.
[Abstract] [Full Text] [PDF]


Home page
Am J EpidemiolHome page
S Raimondi, V Paracchini, H Autrup, J. Barros-Dios, S Benhamou, P Boffetta, M. Cote, I. Dialyna, V Dolzan, R Filiberti, et al.
Meta- and Pooled Analysis of GSTT1 and Lung Cancer: A HuGE-GSEC Review
Am. J. Epidemiol., December 1, 2006; 164(11): 1027 - 1042.
[Abstract] [Full Text] [PDF]


Home page
Cancer Res.Home page
S. Landi, F. Gemignani, F. Canzian, V. Gaborieau, R. Barale, D. Landi, N. Szeszenia-Dabrowska, D. Zaridze, J. Lissowska, P. Rudnai, et al.
DNA Repair and Cell Cycle Control Genes and the Risk of Young-Onset Lung Cancer.
Cancer Res., November 15, 2006; 66(22): 11062 - 11069.
[Abstract] [Full Text] [PDF]


Home page
JCOHome page
P. Yang, J. O. Ebbert, Z. Sun, and R. M. Weinshilboum
Role of the Glutathione Metabolic Pathway in Lung Cancer Treatment and Prognosis: A Review
J. Clin. Oncol., April 10, 2006; 24(11): 1761 - 1769.
[Abstract] [Full Text] [PDF]


Home page
HypertensionHome page
M. W. McBride, M. J. Brosnan, J. Mathers, L. I. McLellan, W. H. Miller, D. Graham, N. Hanlon, C. A. Hamilton, J. M. Polke, W. K. Lee, et al.
Reduction of Gstm1 Expression in the Stroke-Prone Spontaneously Hypertension Rat Contributes to Increased Oxidative Stress
Hypertension, April 1, 2005; 45(4): 786 - 792.
[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.