Skip Navigation


Carcinogenesis Advance Access originally published online on April 16, 2009
Carcinogenesis 2009 30(7):1155-1160; doi:10.1093/carcin/bgp077
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
30/7/1155    most recent
bgp077v1
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 Mason, R. A.
Right arrow Articles by Andrew, A. S.
PubMed
Right arrow PubMed Citation
Right arrow Articles by Mason, R. A.
Right arrow Articles by Andrew, A. S.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© The Author 2009. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

EGFR pathway polymorphisms and bladder cancer susceptibility and prognosis

Rebecca A. Mason, Elaine V. Morlock, Margaret R. Karagas, Karl T. Kelsey1,2, Carmen J. Marsit1,2, Alan R. Schned3 and Angeline S. Andrew*

Section of Biostatistics and Epidemiology, Department of Community and Family Medicine, Dartmouth Medical School, One Medical Center Drive, Lebanon, NH 03756, USA
1 Department of Community Health/Epidemiology
2 Department of Pathology and Laboratory Medicine, Center for Environmental Health and Technology, Brown University, Providence, RI 02912, USA
3 Department of Pathology, Dartmouth Medical School, One Medical Center Drive, Lebanon, NH 03756, USA

* To whom correspondence should be addressed. Dartmouth Medical School, 7927 Rubin 860, One Medical Center Drive, Lebanon, NH 03756, USA. Tel: +1 603 653 9019; Fax: +1 603 653 9093; Email: angeline.andrew{at}dartmouth.edu

The epidermal growth factor receptor (EGFR) pathway has recently been appreciated as a central mediator of tumorigenesis and an important drug target; however, the influence of genetic variation in this pathway on bladder cancer is not understood. Pathway activation leads to cell proliferation, angiogenesis and is antiapoptotic. We sought to test the hypothesis that bladder cancer susceptibility and survival are modified by inherited variations in the sequence of the EGFR and its pathway members. We tested associations using a population-based study of 857 bladder cancer cases and 1191 controls from New Hampshire. Multifactor dimensionality reduction software was used to predict gene–gene interactions. We detected an increased risk of bladder cancer associated with variant genotypes for the single nucleotide polymorphisms EGFR_03 [adjusted odds ratio (OR) 1.7 (95% confidence interval (CI) 1.0–2.8)] and EGFR_05 [adjusted OR 1.5 (95% CI 1.0–2.1)] compared with wild-type. EGFR variants experienced longer survival than those with wild-type alleles [e.g. adjusted hazard ratio EGFR_1808 0.3 (95% CI 0.1–0.9)]. In contrast, the variant form of the ligand, EGF_04, had worse survival [adjusted hazard ratio 1.5 (95% CI 1.0–2.3)] compared with wild-type. Our findings suggest modified bladder cancer risk and survival associated with genetic variation in the EGFR pathway. Understanding these genetic influences on increased bladder cancer susceptibility and survival may help in cancer prevention, drug development and choice of therapeutic regimen.

Abbreviations: CCND1, cyclin D1; CI, confidence interval; EGF, epidermal growth factor; EGFR, epidermal growth factor receptor; LD, linkage disequilibruim; MDR, multifactor dimensionality reduction; OR, odds ratio; SNP, single nucleotide polymorphism; VEGF, vascular endothelial growth factor

Received October 27, 2008; revised March 26, 2009; accepted March 28, 2009.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?




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.