P53 Codon 72 polymorphisms: A case-control study of gastric cancer and potential interactions

Sul, James; Yu, Guo-Pei; Lu, Qing-Yi; Lu, Ming-Lan; Setiawan, Veronica Wendy; Wang, Ming-Rong; Guo, Chun Hua; Yu, Shun-Zhang; Mu, Lina; Cai, Lin; Kurtz, Robert C; Zhang, Zuo-Feng

doi:10.1016/j.canlet.2005.07.004

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Volume 238, Issue 2 , Pages 210-223, 18 July 2006

P53 Codon 72 polymorphisms: A case-control study of gastric cancer and potential interactions

James Sul
- Clinical Instructor, Division of Digestive Diseases, David Geffen School of Medicine at UCLA, 10833 Le Conte Avenue, 44-138 CHS, Los Angeles, CA 90095-1684, USA
- Corresponding author. Tel.: +1 (310) 206 0517; fax: +1 (310) 825 1700.
Guo-Pei Yu
- Biostatistics and Epidemiology Service, New York Eye and Ear Infirmary, New York, NY 10003
Qing-Yi Lu
- Center for Human Nutrition, UCLA School of Medicine, Los Angeles, CA 90095, USA
Ming-Lan Lu
- Department of Pathology, Memorial Sloan-Kettering Cancer Center, New York, NY 10021, USA
Veronica Wendy Setiawan
- Department of Preventive Medicine, University of Southern California, Los Angeles, CA, USA
Ming-Rong Wang
- Yangzhong County Anti-Epidemic Station, Yangzhong County, P.R. of China
Chun Hua Guo
- Yangzhong County Anti-Epidemic Station, Yangzhong County, P.R. of China
Shun-Zhang Yu
- Department of Epidemiology, School of Public Health, Fudan University, Shanghai, China
Lina Mu
- Department of Epidemiology, School of Public Health, Fudan University, Shanghai, China
Lin Cai
- Department of Epidemiology and Biostatistics, School of Public Health, Fijian Medical University, Fuzhou, Fujian, China
Robert C Kurtz
- Gastroenterology and Nutrition Service, Department of Medicine, Memorial Sloan-Kettering Cancer Center, New York, NY 10021
Zuo-Feng Zhang
- Department of Epidemiology, UCLA School of Public Health, and Jonsson Comprehensive Cancer Center, Los Angeles, CA 90095, USA

Received 20 November 2004; received in revised form 6 July 2005; accepted 8 July 2005.

Abstract

P53 codon 72 polymorphisms have been reported to be associated with cancers of the lung, esophagus and cervix. However, there have been no reports on the interaction of select risk factors and p53 codon 72 polymorphisms in gastric cancer susceptibility. 155 gastric cancer cases and 134 cancer-free controls were enrolled at the Memorial Sloan Kettering Cancer Center (MSKCC) from November 1992 to November 1994. The crude odds ratio (OR1) associated with the (Pro/Pro) polymorphism and the risk of gastric cancer was 1.27 (0.70–2.33). Adjusting for age, sex, race and education (OR2) and further adjusting for BMI, calories, sodium, smoking, vitamin C, fiber, alcohol, fat, and H. pylori status (OR3) did not yield significant results. Significant joint effects were associated with high fat consumption (OR1=2.61 (95% CI:1.13–6.06); OR2=2.85 (95% CI:1.14–7.15) for total cancers and for proximal tumors (OR1=2.56 (95%CI:1.00–6.54)). The low vitamin C intake/high-risk polymorphism group (Pro/Pro) had an OR1 of 4.82 (95% CI: 1.72–13.45) and the OR2 was 6.19 (95% CI: 2.08–18.40) for distal tumors. The point estimates were increased for interaction odds ratios but not statistically significant (OR1=4.25 (95% CI: 0.66–27.50); OR2=4.73 (95% CI: 0.67–33.43); OR3=5.55 (95% CI: 0.66–46.47)). Further studies specifically looking at proximal and distal tumors are required to confirm any potential interaction between the p53 codon 72 polymorphisms and environmental risk, in particular low dietary vitamin C and high fat consumption.

Keywords: Gastric cancer, p53 codon 72 polymorphism, gene-environment interaction