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http://dx.doi.org/10.7314/APJCP.2012.13.3.945

Association Between the FAS/FASL Polymorphisms and Gastric Cancer Risk: A Meta-Analysis  

Tian, Jing (Department of Epidemiology and Biostatistics, School of Public Health, Anhui Medical University)
Pan, Feng (Department of Oncology, The First Affiliated Hospital of Anhui Medical University)
Li, Jing (Department of Epidemiology and Biostatistics, School of Public Health, Anhui Medical University)
Ma, Yan (Department of Epidemiology and Biostatistics, School of Public Health, Anhui Medical University)
Cen, Han (Department of Epidemiology and Biostatistics, School of Public Health, Anhui Medical University)
Pan, Hai-Feng (Department of Epidemiology and Biostatistics, School of Public Health, Anhui Medical University)
Pan, Yue-Yin (Department of Oncology, The First Affiliated Hospital of Anhui Medical University)
Ye, Dong-Qing (Department of Epidemiology and Biostatistics, School of Public Health, Anhui Medical University)
Publication Information
Asian Pacific Journal of Cancer Prevention / v.13, no.3, 2012 , pp. 945-951 More about this Journal
Abstract
Objective: FAS/FASL gene promoter polymorphisms have been repeatedly associated with gastric cancer risk, but findings are inconclusive across studies. To address a more precise estimation of the relationship, a meta-analysis was performed. Methods: Data were collected from the Pubmed, Medline and EMBASE databases, with the last report up to 1 December, 2011. Crude ORs with 95% CIs were used to assess the strength of the association by (1) the additive, (2) the codominant, (3) the dominant, and (4) the recessive models. Results: A total of seven studies, including six studies on FAS -1377G>A polymorphism, five studies on FAS -670A>G polymorphism, and six studies on FASL -844T>C polymorphism, were identified in the current meta-analysis. Overall, an association of FAS -1377G>A (AA versus GG: OR = 1.313, 95% CI = 1.045-1.650, Ph = 0.347, $I^2$ = 10.8) and FASL -844T>C (CC versus TT: OR = 1.352, 95% CI = 1.043-1.752, Ph = 0.461, $I^2$ = 0.0) polymorphisms with gastric cancer was found in the codominant model. However, we did not detect any association between gastric cancer and the FAS -670A>G polymorphism. In the subgroup analysis by ethnicity, similar elevated risks were also observed in Asian population for FAS -1377G>A (AA versus GG: OR = 1.309, 95% CI = 1.041-1.646, Ph = 0.240, $I^2$ = 27.3) and FASL -844T>C (CC versus TT: OR = 1.420, 95% CI = 1.081-1.865, Ph = 0.524, $I^2$ = 0.0) polymorphisms. Conclusions: This meta-analysis indicated that FAS -1377G>A and FASL -844T>C polymorphisms might be associated with gastric cancer risk.
Keywords
Gastric cancer; FAS; FASL; polymorphism; meta-analysis;
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1 Ashkenazi A, Dixit VM (1999). Apoptosis control by death and decoy receptors. Curr Opin Cell Biol, 11, 255-60.   DOI   ScienceOn
2 Budihardjo I, Oliver H, Lutter M, et al (1999). Biochemical pathways of caspase activation during apoptosis. Annu Rev Cell Dev Biol, 15, 269-90.   DOI   ScienceOn
3 Chappell DB, Restifo NP (1998). T cell-tumor cell: a fatal interaction? Cancer Immunol Immunother, 47, 65-71.   DOI
4 Cochran WG (1954). The combination of estimates from different experiments. Biometrics, 10, 101-29.   DOI
5 DerSimonian R, Laird N (1986). Meta-analysis in clinical trials. Control Clin Trials, 7, 177-88.   DOI
6 Duell EJ, Travier N, Lujan-Barroso L, et al (2011). Alcohol consumption and gastric cancer risk in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort. Am J Clin Nutr, 94, 1266-75.   DOI   ScienceOn
7 Egger M, Davey Smith G, Schneider M, et al (1997). Bias in meta-analysis detected by a simple, graphical test. BMJ, 315, 629-34.   DOI
8 Faul F, Erdfelder E, Buchner A, et al (2009). Statistical power analyses using G*Power 3.1: tests for correlation and regression analyses. Behav Res Methods, 41, 1149-60.   DOI   ScienceOn
9 Ferlay J, Shin HR, Bray F, et al (2010). Estimates of worldwide burden of cancer in 2008: GLOBOCAN 2008. Int J Cancer, 127, 2893-917.   DOI
10 Green DR, Droin N, Pinkoski M (2003). Activation-induced cell death in T cells. Immunol Rev, 193, 70-81.   DOI   ScienceOn
11 Griffith TS, Brunner T, Fletcher SM, et al (1995). Fas ligandinduced apoptosis as a mechanism of immune privilege. Science, 270, 1189-92.   DOI
12 Gryko M, Guzinska-Ustymowicz K, Pryczynicz A, et al (2011). Correlation between Fas and FasL proteins expression in normal gastric mucosa and gastric cancer. Folia Histochem Cytobiol, 49, 142-7.   DOI
13 Hajra KM, Liu JR (2004). Apoptosome dysfunction in human cancer. Apoptosis, 9, 691-704.   DOI
14 Hartgrink HH, Jansen EP, van Grieken NC, et al (2009). Gastric cancer. Lancet, 374, 477-90.   DOI   ScienceOn
15 Higgins JP, Thompson SG (2002). Quantifying heterogeneity in a meta-analysis. Stat Med, 21, 1539-58.   DOI   ScienceOn
16 Higgins JP, Thompson SG, Deeks JJ, et al (2003). Measuring inconsistency in meta-analyses. BMJ, 327, 557-60.   DOI   ScienceOn
17 Hirschhorn JN, Lohmueller K, Byrne E, et al (2002). A comprehensive review of genetic association studies. Genet Med, 4, 45-61.   DOI
18 Hsu PI, Lu PJ, Wang EM, et al (2008). Polymorphisms of death pathway genes FAS and FASL and risk of premalignant gastric lesions. Anticancer Res, 28, 97-103.
19 Huang QR, Morris D, Manolios N (1997). Identification and characterization of polymorphisms in the promoter region of the human Apo-1/Fas (CD95) gene. Mol Immunol, 34, 577-82.   DOI   ScienceOn
20 Ikehara SK, Ikehara Y, Matsuo K, et al (2006). A polymorphism of C-to-T substitution at -31 IL1B is associated with the risk of advanced gastric adenocarcinoma in a Japanese population. J Hum Genet, 51, 927-33.   DOI
21 Itoh N, Yonehara S, Ishii A, et al (1991). The polypeptide encoded by the cDNA for human cell surface antigen Fas can mediate apoptosis. Cell, 66, 233-43.   DOI   ScienceOn
22 Knottnerus JA (1987). Subject selection in hospital-based casecontrol studies. J Chronic Dis, 40, 183-7.   DOI
23 Kupcinskas J, Wex T, Bornschein J, et al (2011). Lack of association between gene polymorphisms of Angiotensin converting enzyme, Nod-like receptor 1, Toll-like receptor 4, FAS/FASL and the presence of Helicobacter pyloriinduced premalignant gastric lesions and gastric cancer in Caucasians. BMC Med Genet, 12, 112.   DOI
24 Liu L, Wu C, Wang Y, et al (2011). Association of candidate genetic variations with gastric cardia adenocarcinoma in Chinese population: a multiple interaction analysis. Carcinogenesis, 32, 336-42.   DOI
25 Mantel N, Haenszel W (1959). Statistical aspects of the analysis of data from retrospective studies of disease. J Natl Cancer Inst, 22, 719-48.
26 Nagata S, Golstein P (1994). The Fas death factor. Science, 267, 1449-56.
27 Nicholson DW, Thornberry NA (1997). Caspases: killer proteases. Trends Biochem Sci, 22, 299-306.   DOI
28 Nomura AM, Wilkens LR, Henderson BE, et al (2012). The association of cigarette smoking with gastric cancer: the multiethnic cohort study. Cancer Causes Control, 23, 51-8.   DOI
29 Oehm A, Behrmann I, Falk W, et al (1992). Purification and molecular cloning of the APO-1 cell surface antigen, a member of the tumor necrosis factor/nerve growth factor receptor superfamily. Sequence identity with the Fas antigen. J Biol Chem, 267, 10709-15.
30 Reed JC (2000). Mechanisms of apoptosis. Am J Pathol, 157, 1415-30.   DOI
31 Reichmann E (2002). The biological role of the Fas/FasL system during tumor formation and progression. Semin Cancer Biol, 12, 309-15.   DOI
32 Sibley K, Rollinson S, Allan JM, et al (2003). Functional FAS promoter polymorphisms are associated with increased risk of acute myeloid leukemia. Cancer Res, 63, 4327-30.
33 Sivachandran N, Dawson CW, Young LS, et al (2012). Contributions of the Epstein-Barr Virus EBNA1 Protein to Gastric Carcinoma. J Virol, 86, 60-8.   DOI
34 Strand S, Hofmann WJ, Hug H, et al (1996). Lymphocyte apoptosis induced by CD95 (APO-1/Fas) ligand-expressing tumor cells--a mechanism of immune evasion? Nat Med, 2, 1361-6.   DOI   ScienceOn
35 Suda T, Takahashi T, Golstein P, et al (1993). Molecular cloning and expression of the Fas ligand, a novel member of the tumor necrosis factor family. Cell, 75, 1169-78.   DOI   ScienceOn
36 Sun T, Zhou Y, Li H, et al (2005). FASL -844C polymorphism is associated with increased activation-induced T cell death and risk of cervical cancer. J Exp Med, 202, 967-74.   DOI
37 Takahama Y, Yamada Y, Emoto K, et al (2002). The prognostic significance of overexpression of the decoy receptor for Fas ligand (DcR3) in patients with gastric carcinomas. Gastric Cancer, 5, 61-8.   DOI
38 Thompson CB (1995). Apoptosis in the pathogenesis and treatment of disease. Science, 267, 1456-62.   DOI   ScienceOn
39 Viard-Leveugle I, Veyrenc S, French LE, et al (2003). Frequent loss of Fas expression and function in human lung tumours with overexpression of FasL in small cell lung carcinoma. J Pathol, 201, 268-77.   DOI
40 Walboomers JM, Jacobs MV, Manos MM, et al (1999). Human papillomavirus is a necessary cause of invasive cervical cancer worldwide. J Pathol, 189, 12-9.   DOI   ScienceOn
41 Wang M, Wu D, Tan M, et al (2009). FAS and FAS ligand polymorphisms in the promoter regions and risk of gastric cancer in Southern China. Biochem Genet, 47, 59-68.
42 Wu J, Metz C, Xu X, et al (2003). A novel polymorphic CAAT/enhancer-binding protein beta element in the FasL gene promoter alters Fas ligand expression: a candidate background gene in African American systemic lupus erythematosus patients. J Immunol, 170, 132-8.   DOI
43 Yang CS (2000). Vitamin nutrition and gastroesophageal cancer. J Nutr, 130, S338-9.   DOI
44 Yang KC, Chu A, Liao CS, et al (2006). Evaluation of the role of H pylori infection in pathogenesis of gastric cancer by immunoblot assay. World J Gastroenterol, 12, 7029-32.   DOI
45 Yang WG, Chen CB, Wang ZX, et al (2011). A case-control study on the relationship between salt intake and salty taste and risk of gastric cancer. World J Gastroenterol, 17, 2049-53.   DOI   ScienceOn
46 Zhang W, Li C, Wang J, He C (2011). Functional polymorphisms in FAS/FASL system contribute to the risk of occurrence but not progression of gastric cardiac adenocarcinoma. Hepatogastroenterology, 59. doi: 10.5754/hge11300.
47 Zhou RM, Wang N, Chen ZF, et al (2010). Polymorphisms in promoter region of FAS and FASL gene and risk of cardia gastric adenocarcinoma. J Gastroenterol Hepatol, 25, 555-61.   DOI
48 Zou YF, Wang F, Feng XL, et al (2011). Association of NFKB1 -94ins/delATTG promoter polymorphism with susceptibility to autoimmune and inflammatory diseases: a meta-analysis. Tissue Antigens, 77, 9-17.   DOI