Volume 25, Issue 3 pp. 555-561

Polymorphisms in promoter region of FAS and FASL gene and risk of gastric cardiac adenocarcinoma

Rong-Miao Zhou

Rong-Miao Zhou

Department of Molecular Biology, The Fourth Affiliated Hospital of Hebei Medical University, Hebei Province, China

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Na Wang

Na Wang

Department of Molecular Biology, The Fourth Affiliated Hospital of Hebei Medical University, Hebei Province, China

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Zhi-Feng Chen

Zhi-Feng Chen

Divison of Cancer Prevention and Control, The Fourth Affiliated Hospital of Hebei Medical University, Hebei Province, China

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Ya-Nan Duan

Ya-Nan Duan

Department of Molecular Biology, The Fourth Affiliated Hospital of Hebei Medical University, Hebei Province, China

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Dong-Lan Sun

Dong-Lan Sun

Department of Molecular Biology, The Fourth Affiliated Hospital of Hebei Medical University, Hebei Province, China

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Yan Li

Corresponding Author

Yan Li

Department of Molecular Biology, The Fourth Affiliated Hospital of Hebei Medical University, Hebei Province, China

Yan Li, 12 Jiankang Road, Shijiazhuang, 050011, Hebei Province, China. Email: [email protected]Search for more papers by this author
First published: 25 February 2010
Citations: 26

Abstract

Background and Aim: The FAS and FASL system play an important role in regulating apoptotic cell death. This study was designed to investigate the correlation of FAS-1377 G/A, -670 A/G and FASL-844 T/C polymorphisms with susceptibility to gastric cardiac adenocarcinoma in a population of a high-incidence region of Hebei Province.

Methods: FAS-1377 G/A, -670 A/G and FASL-844 T/C polymorphisms were genotyped by polymerase chain reaction–restriction fragment length polymorphism analysis in 262 gastric cardiac carcinoma (GCA) patients and 524 healthy controls.

Results: Family history of upper gastrointestinal cancer (UGIC) might increase the risk of developing GCA (age- and sex-adjusted odds ratio [OR] = 1.38, 95% confidence interval [CI] = 1.02–1.86). The overall allelotype and genotype distributions of FAS-1377 G/A, and FASL-844 T/C polymorphisms in GCA patients did not significantly differ from that in healthy controls (P > 0.05). Compared with individuals with a FAS-670 A/A genotype, individuals with an A/G genotype in a smoker group had a lower risk of developing GCA (age, sex, and family history of UGIC adjusted OR = 0.55, 95% CI = 0.34–0.88). When the genotypes of FAS and FASL single nucleotide polymorphisms (SNP) were combined to analyze, no significant correlation was found between these SNP and the risk for GCA development.

Conclusion: In the high-incidence region of Hebei Province, FAS-1377 G/A and FASL-844 T/C polymorphisms were not associated with the risk of GCA. However, the FAS-670 A/G genotype might decrease the risk of GCA for smoker individuals.

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