Apoptosis Gene Polymorphisms, Age, Smoking and the Risk of Non-Small Cell Lung Cancer
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2008/11/01
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Details
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Personal Author:Asomaning K ; Christiani, David C. ; Devivo I ; Heist RS ; Lin X ; Liu G ; Lynch TJ ; Su L ; Ter-Minassian M ; Wain JC ; Zhai R ; Zhou W
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Description:Apoptosis is important for targeting cancer cells for destruction. Various single-nucleotide polymorphisms (SNPs) in apoptotic genes have been associated with increased risks in lung cancer, particularly FAS -1377 G>A (rs2234767), FASLG -844 C>T (rs763110), IL1B +3954 C>T Phe105Phe (rs1143634) and BAT3 Ser625Pro (rs1052486). We studied the association of these SNPs with non-small cell lung cancer (NSCLC) in a large case-control study (N = 4263: 2644 cases and 1619 controls). No associations with NSCLC were observed in the main effects analysis for all four SNPs, adjusting for age, gender, smoking status, pack-years and years since smoking cessation. In subjects under age 60, for FASLG -844 C>T polymorphism, CT compared with the CC genotype, was significantly associated with increased risk of NSCLC, adjusted odds ratio (aOR) = 1.58 (1.22, 2.05), P = 0.0006 and TT aOR = 1.45 (1.01, 2.04), P = 0.04. In contrast, for those over age 60, the CT aOR = 0.91 (0.73, 1.13), P = 0.37 and TT aOR = 0.86 (0.64, 1.16), P = 0.32. The P-value for the age-genotype interaction was 0.004. For the IL1B +3954 C>T polymorphism, compared with the CC genotype, TT showed significant associations in former smokers and in men but tests of interaction were not significant (P(smoking) = 0.24, P(gender) = 0.17). No interactions were observed for FAS -1377 G>A and BAT3 Ser625Pro polymorphisms. Our findings indicate that age and smoking may modify the association of the FASLG -844 and IL1B + 3954 SNPs with the risk of NSCLC. [Description provided by NIOSH]
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ISSN:0143-3334
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Volume:29
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Issue:11
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NIOSHTIC Number:nn:20034811
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Citation:Carcinogenesis 2008 Nov; 29(11):2147-2152
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Contact Point Address:Monica Ter-Minassian, Department of Environmental Health, Harvard School of Public Health, 665 Huntington Avenue, Boston, MA 02115
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Email:mtermina@hsph.harvard.edu
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Federal Fiscal Year:2009
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Performing Organization:Harvard School of Public Health
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Peer Reviewed:True
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Start Date:20050701
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Source Full Name:Carcinogenesis
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End Date:20280630
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Main Document Checksum:urn:sha-512:fb4a33f6340da023039d49ec86aa9b608eb01013fe8db0e1126cbbf9a7f3fd3a86adc8a1f32bd83993ea672c4243e7473270e3c000636f2355b3091977a11716
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