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Carcinogenesis Advance Access published online on December 6, 2006
Carcinogenesis, doi:10.1093/carcin/bgl242
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© The Author 2006. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Associations of functional polymorphisms in cyclooxygenase-2 and platelet 12-lipoxygenase with risk of occurrence and advanced disease status of colorectal cancer

Wen Tan1, Jianxiong Wu2, Xuemei Zhang1, Yongli Guo1, Junniao Liu1, Tong Sun1, Bailin Zhang2, Dan Zhao1, Ming Yang1, Dianke Yu1 and Dongxin Lin1,*

1 Department of Etiology & Carcinogenesis, Cancer Institute & Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China
2 Department of Abdominal Surgery, Cancer Institute & Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China

* To whom correspondence should be addressed. Fax: +86 1067722460. E-mail: dlin{at}public.bta.net.cn

Aberrant arachidonic acid metabolism by cyclooxygenase-2 (COX-2) and 12-lipoxygenase (12-LOX) has implicated in carcinogenesis. Genetic polymorphisms in COX-2 and 12-LOX might therefore affect susceptibility to colorectal cancer (CRC). To examine this hypothesis, genotypes of COX-2 –1290A>G, –1195G>A, –765G>C, and 12-LOX 261Arg>Gln polymorphisms were determined in 1000 CRC patients and 1300 controls. Increased risk of developing CRC was associated with the COX-2 –1195GA [adjusted odds ratio (OR) = 1.24, 95% confidence interval (CI) = 1.00–1.54] and –1195AA (adjusted OR = 1.77, 95% CI = 1.38–2.25) genotypes compared with the –1195GG genotype. Similarly, the increased risk for CRC was also associated with the COX-2 –765GC genotype (adjusted OR = 1.73, 95% CI = 1.23–2.43) compared with the –765GG genotype. Consistent with the results of genotype analyses, the ORs for the A–1195–C–765-containing haplotypes were significantly higher than those for the G–1195–G–765-containing haplotypes (P < 0.01). Furthermore, the –1195A allele was further associated with advanced CRC, with adjusted ORs of Dukes D CRC against Dukes A CRC being 2.43 (95% CI = 1.15–4.97) and 2.66 (95% CI = 1.23–5.74) for the –1195GA and –1195AA genotypes, respectively. The increased risk of CRC was also associated with the 12-LOX 261Gln/Gln genotype compared with the Arg/Arg genotype (adjusted OR = 1.38, 95% CI = 1.09–1.74). Together, these observations indicate that inherited polymorphisms in arachidonic acid-metabolizing enzymes may confer susceptibility to CRC.


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