Skip Navigation



Carcinogenesis Advance Access published online on November 2, 2005
Carcinogenesis, doi:10.1093/carcin/bgi258
This Article
Right arrow Advance Access manuscript (PDF) Freely available
Right arrow All Versions of this Article:
27/4/798    most recent
bgi258v1
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 Li, Y.
Right arrow Articles by Lu, S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Li, Y.
Right arrow Articles by Lu, S.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© The Author 2005. Published by Oxford University Press. All rights reserved. For permissions, please email: journals.permissions@oxfordjournals.org
Received August 5, 2005
Revised October 18, 2005
Accepted October 26, 2005

MOLECULAR EPIDEMIOLOGY AND CANCER PREVENTION

Identification of a novel polymorphism Arg290Gln of esophageal cancer related gene 1 (ECRG1) and it related risk to esophageal squamous cell carcinoma

Yuanyuan Li 1, Xuemei Zhang 1, Ge Huang 1, Xiaoping Miao 1, Liping Guo 1, Dongxin Lin 1, and Shixin Lu 1*

1 Department of Etiology and Carcinogenesis, Cancer Institute & Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100021, R.P. China

* To whom correspondence should be addressed.
Shixin Lu, E-mail: shlu{at}public.bta.net.cn


  Abstract

We previously cloned and identified the esophageal cancer related gene 1 (ECRG1), a novel candidate tumor suppressor gene, from human esophageal cells. A single nucleotide polymorphism (Arg290Gln) was identified in the coding region of ECRG1 and might play a role in susceptibility to esophageal squamous cell carcinoma (ESCC). To examine this hypothesis, we analyzed 998 ESCC patients and 1252 controls in a hospital-based, case-control study among Chinese population for this polymorphism. We observed a statistically significantly increased risk of ESCC associated with the ECRG1 290Arg/Gln and 290Gln/Gln genotypes compared with the 290Arg/Arg [odds ratio (OR) = 1.23, 95% confidence interval (CI) =1.03-1.46; P < 0.05]. A greater than multiplicative joint effect between the ECRG1 polymorphism and tobacco smoking exposure was also observed (OR = 1.95, 95% CI = 1.48-2.56; P < 0.001). Furthermore, the elevated risk of ESCC associated with the ECRG1 polymorphism was increased consistently with cumulative smoking dose. ORs (95% CI) for 290Arg/Gln and 290Gln/Gln genotypes among nonsmokers and smokers who smoked ≤27 and >27 pack-years were 1.03 (0.78-1.35), 1.91 (1.36-2.67) and 2.08 (1.48-2.92), respectively (P trend test < 0.001). Taken together, our results indicate that the ECRG1 290Gln variant allele might be a genetic susceptibility factor for developing ESCC, especially in the smoking population.

Keywords: ECRG1; esophageal squamous cell carcinoma; SNP; genetic susceptibility.
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
 CarcinogenesisHome page
W. Yueying, W. Jianbo, L. Hailin, T. Huaijing, G. Liping, and L. Shih-Hsin
ECRG1, a novel esophageal gene, cloned and identified from human esophagus and its inhibition effect on tumors
Carcinogenesis, January 1, 2008; 29(1): 157 - 160.
[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.