Skip Navigation


Carcinogenesis Advance Access originally published online on June 12, 2008
Carcinogenesis 2008 29(8):1467-1474; doi:10.1093/carcin/bgn062
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow All Versions of this Article:
29/8/1467    most recent
bgn062v2
bgn062v1
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 arrowRequest Permissions
Google Scholar
Right arrow Articles by Taioli, E.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Taioli, E.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© The Author 2008. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Gene–environment interaction in tobacco-related cancers

Emanuela Taioli*

Department of Epidemiology, University of Pittsburgh Cancer Institute, UPMC Cancer Pavilion, 5150 Center Avenue, Pittsburgh, PA 15232, USA

* To whom correspondence should be addressed. Tel: +412 623 2217; Fax: +412 623 3878; Email: taiolien{at}upmc.edu

This review summarizes the carcinogenic effects of tobacco smoke and the basis for interaction between tobacco smoke and genetic factors. Examples of published papers on gene–tobacco interaction and cancer risk are presented. The assessment of gene–environment interaction in tobacco-related cancers has been more complex than originally expected for several reasons, including the multiplicity of genes involved in tobacco metabolism, the numerous substrates metabolized by the relevant genes and the interaction of smoking with other metabolic pathways. Future studies on gene–environment interaction and cancer risk should include biomarkers of smoking dose, along with markers of quantitative historical exposure to tobacco. Epigenetic studies should be added to classic genetic analyses, in order to better understand gene–environmental interaction and individual susceptibility. Other metabolic pathways in competition with tobacco genetic metabolism/repair should be incorporated in epidemiological studies to generate a more complete picture of individual cancer risk associated with environmental exposure to carcinogens.

Abbreviations: GSTM1, glutathione S-transferase µ; GSTT1, glutathione S-transferase {theta}; GSTP1, glutathione S-transferase {phi}; PAH, polycyclic aromatic hydrocarbon

Received October 22, 2007; revised February 27, 2008; accepted February 27, 2008.


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
M. Gwinn, I. Guessous, and M. J. Khoury
Invited Commentary: Genes, Environment, and Hybrid Vigor
Am. J. Epidemiol., September 15, 2009; 170(6): 703 - 707.
[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.