Publications (7)16.76 Total impact
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Article: CYP1A2 rs762551 polymorphism contributes to cancer susceptibility: a meta-analysis from 19 case-control studies.
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ABSTRACT: BACKGROUND: Genetic polymorphism (rs762551A>C) in gene encoding cytochrome P450 1A2 (CYP1A2) has been shown to influence the inducibility of CYP1A2 expression and thus might be associated with risk of several types of human cancer. However, the results of previous studies on the associations of this polymorphism with risk of cancer are not all consistent. To clarify the potential contribution of CYP1A2 rs762551 to cancer risk, we performed a meta-analysis of the published case--control studies. METHODS: We used PubMed, Embase, OVID, ScienceDirect, and Chinese National Knowledge Infrastructure databases to identify the related publications for this meta-analysis. The pooled odds ratio (OR) and 95% confidence interval (CI) were calculated using random effect model to evaluate the association of rs762551 with cancer risk. A chi2-based Q-test was used to examine the heterogeneity assumption and the funnel plot and Egger's test were used to examine the potential publication bias. The leave-one-out sensitivity analysis was conducted to determine whether our assumptions or decisions have a major effect on the results of the review. RESULTS: Our analysis of 19 eligible case--control studies showed a significant association between rs762551C variant with risk of cancer in the genetic model of CC versus AA (OR = 1.30, 95% CI = 1.02-1.64) and the dominant model (OR = 1.19, 95% CI = 1.04-1.36). In subgroup analysis based on ethnicity, the rs762551CC genotype was associated with increased cancer risk (OR = 1.29, 95% CI = 1.27-1.63 in co-dominate model and OR = 1.17, 95% CI = 1.02-1.34 in dominant model in Caucasians, but not in Asians and the mixed population. CONCLUSION: These results suggested that CYP1A2 rs762551 polymorphism is likely to be associated with susceptibility to cancer in Caucasians.BMC Cancer 11/2012; 12(1):528. · 3.01 Impact Factor -
Article: Cigarette smoking strongly modifies the association of complement factor H variant and the risk of lung cancer.
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ABSTRACT: The complement system is an important immunosurveillance mechanism against tumors, and complement factor H (CFH) is a key regulator for activation of the complement system. Expression of complement factor H has been demonstrated in cell lines from several malignancies. In this study we examined the contribution of the single-nucleotide polymorphism (SNP) Try402His (Y402H) (rs1061170) in the CFH gene to the risk of lung cancer in a case-control study with 1000 cases and 1000 controls. Odds ratios (ORs) and 95% confidence intervals (CIs) were computed by logistic regression. The frequencies for CFH Y402H genotypes among the cases were statistically significantly different from those among controls (χ(2)=8.66, P=0.003), with 402His/His or 402His/Try genotypes being over-represented among patients compared with controls (13.6% versus 9.4%, P<0.004). A multivariate regression analysis showed that a significantly increased risk of lung cancer for the 402His/His or 402His/Try carriers with OR (95% CI), 1.50 (1.12-2.00). When stratified by smoking status, the elevated risk of the cancer associated with variant CFH genotypes was observed among smokers, but not among non-smokers. When analyzed with cumulative smoking dose (pack-years), a super-multiplicative interaction was observed at different smoking levels. Among carriers with the 402Tyr/His or His/His genotype, the ORs of developing lung cancer for smoking<16, 16-28, or >28 pack-years were 0.98 (0.49-1.94), 2.36 (1.14-4.90), and 6.39 (3.49-11.68), respectively. These findings suggest that CFH Y402H polymorphism may interact with cigarette smoking to effect the development of lung cancer in the Chinese population.Cancer epidemiology. 12/2011; 36(2):e111-5. -
Article: Genetic variant in CASP3 affects promoter activity and risk of esophageal squamous cell carcinoma.
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ABSTRACT: Caspase-3 (CASP3) is the main executioner of apoptosis, mediating both extrinsic and intrinsic cell death signaling pathways, and is involved in tumor behaviors. In this study, we investigated the association of two regulatory variants in CASP3 and the risk of esophageal squamous cell carcinoma (ESCC) in 1026 cases and 1270 healthy controls. Odds ratios (OR) and 95% confidence intervals (CI) were computed by logistic regression. The function of the CASP3 829 A>C polymorphism was examined by luciferase reporter assay and real-time PCR. A significant increased risk of ESCC was found for the CASP3 829 AC and CC genotypes with OR (95% CI), 1.53 (1.26-1.89) and 1.42 (1.11-1.82), respectively. When stratified by age and gender, the risk of ESCC was more significant in younger (≤57 years) and male individuals. No significantly changed risk of ESCC was related to 20541 C>T variant. Luciferase reporter assay showed 829 A>C variant dramatically reduced the transcriptional activity of luciferase reporter gene by over 95% in both KYSE30 and KYSE450 esophageal cancer cells. Remarkably, the transcriptional activity of the 829C-containing construct was much lower than the activity of the pGL3-basic construct, with over 85% reduction in both cell lines. Real-time PCR analyses showed that 829 AA genotype carriers had significantly higher RNA levels (0.015 ± 0.00216, n = 24) than the 829 AC genotype carriers (0.00969 ± 0.00136, n = 36), and 829 CC genotype carriers (0.00663 ± 0.00097, n = 20). These findings suggest that CASP3 829 A>C polymorphism may highly affect the function of caspase-3 and play an important role in the development of ESCC in Chinese populations.Cancer Science 12/2011; 103(3):555-60. · 3.33 Impact Factor -
Article: Interaction of cyclooxygenase-2 promoter polymorphisms with Helicobacter pylori infection and risk of gastric cancer.
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ABSTRACT: Overexpression of cyclooxygenase (COX)-2 has been implicated in the development of cancer. This study aimed to evaluate the relationship between genetic variants in COX-2 promoter interacting with Helicobacter pylori and the susceptibility to gastric cancer (GC). Three COX-2 polymorphisms -1290A>G (rs689465), -1195G>A (rs689466), and -765G>C (rs20417) were genotyped in 323 GC patients and 944 controls. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated by logistic regression model. In GC patients, the ORs were 2.33 (95% CI = 1.50-3.63) and 2.70 (95% CI = 1.68-4.33) for -1195AA and -765CG genotype carriers, respectively. Haplotype analysis showed all -1195A allele-containing haplotypes, except G(-1290)-A(-1195)-G(-765), were associated with increased risk for GC, compared with the A(-1290)-G(-1195)-G(-765) haplotype. Moreover, significant multiplicative and additive interactions were observed between H. pylori infection and all these three polymorphisms, and H. pylori-infected subjects carrying the variant allele of -1290A>G, -1195G>A, or -765G>C had increased risk of GC compared with non-H. pylori-infected subjects with wild-type allele (OR = 4.10, 95% CI = 1.90-8.83; OR = 3.46, 95% CI = 1.31-9.11; and OR = 3.32, 95% = 1.27-8.73, respectively). Our results suggested that the COX-2 promoter polymorphisms were associated with increased risk of GC, especially interacting with H. pylori infection.Molecular Carcinogenesis 05/2011; 50(11):876-83. · 3.16 Impact Factor -
Article: Interaction of Cyclooxygenase‐2 promoter polymorphisms with Helicobacter pylori infection and risk of gastric cancer
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ABSTRACT: Overexpression of cyclooxygenase (COX)-2 has been implicated in the development of cancer. This study aimed to evaluate the relationship between genetic variants in COX-2 promoter interacting with Helicobacter pylori and the susceptibility to gastric cancer (GC). Three COX-2 polymorphisms −1290A>G (rs689465), −1195G>A (rs689466), and −765G>C (rs20417) were genotyped in 323 GC patients and 944 controls. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated by logistic regression model. In GC patients, the ORs were 2.33 (95% CI = 1.50–3.63) and 2.70 (95% CI = 1.68–4.33) for −1195AA and −765CG genotype carriers, respectively. Haplotype analysis showed all −1195A allele-containing haplotypes, except G−1290–A−1195–G−765, were associated with increased risk for GC, compared with the A−1290–G−1195–G−765 haplotype. Moreover, significant multiplicative and additive interactions were observed between H. pylori infection and all these three polymorphisms, and H. pylori-infected subjects carrying the variant allele of −1290A>G, −1195G>A, or −765G>C had increased risk of GC compared with non-H. pylori-infected subjects with wild-type allele (OR = 4.10, 95% CI = 1.90–8.83; OR = 3.46, 95% CI = 1.31–9.11; and OR = 3.32, 95% = 1.27–8.73, respectively). Our results suggested that the COX-2 promoter polymorphisms were associated with increased risk of GC, especially interacting with H. pylori infection. © 2011 Wiley Periodicals, Inc.Molecular Carcinogenesis 05/2011; 50(11):876 - 883. · 3.16 Impact Factor -
Article: Smoking and COX-2 functional polymorphisms interact to increase the risk of gastric cardia adenocarcinoma in Chinese population.
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ABSTRACT: Over-expression and increased activity of cyclooxygenase (COX)-2 induced by smoking has been implicated in the development of cancer. This study aimed to explore the interaction between smoking and functional polymorphisms of COX-2 in modulation of gastric cardia adenocarcinoma (GCA) risk. Three COX-2 polymorphisms, including -1195G>A (rs689466), -765G>C (rs20417), and 587Gly>Arg (rs3218625), were genotyped in 357 GCA patients and 985 controls. In the multivariate logistic regression analysis, we found that the -1195AA, -765GC, and 587Arg/Arg genotypes were associated with increased risk of GCA (OR = 1.50, 95% CI = 1.05-2.13; OR = 2.06, 95% CI = 1.29-3.29 and OR = 1.67, 95% CI = 1.04-2.66, respectively). Haplotype association analysis showed that compared with G(-1195)-G(-765)- G(Gly587Arg), the A(-1195)-C(-765)-A(Gly587Arg) conferred an increased risk of GCA (OR = 2.49, 95% CI = 1.54-4.01). Moreover, significant multiplicative interactions were observed between smoking and these three polymorphisms of -1195G>A, -765G>C, and 587Gly>Arg, even after correction by false discovery rate (FDR) method for multiple comparisons (FDR-P(interaction) = 0.006, 5.239×10(-4) and 0.017, respectively). Similarly, haplotypes incorporating these three polymorphisms also showed significant interaction with smoking in the development of GCA (P for multiplicative interaction = 2.65×10(-6)). These findings indicated that the functional polymorphisms of COX-2, in interaction with smoking, may play a substantial role in the development of GCA.PLoS ONE 01/2011; 6(7):e21894. · 4.09 Impact Factor -
Article: [Correlation of genetic polymorphisms in DNA repair genes ADPRT and XRCC1 to risk of gastric cancer].
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ABSTRACT: Adenosine diphosphate ribosyl transferase (ADPRT) and X-ray repair cross-complementing 1 (XRCC1) are 2 major DNA base excision repair (BER) proteins and act interactively in stimulating and executing BER processes. Polymorphisms of ADPRT 762Val-->Ala and XRCC1 399Arg-->Gln have been verified to associate with altered protein function and BER activity. This study was to examine the contribution of these 2 polymorphisms, alone or in combination, to the risk of developing gastric cancer. A total of 236 patients with gastric cancer and 708 cancer-free controls were genotyped for the 2 polymorphisms by polymerase chain reaction-restrictive fragment length polymorphism (PCR-RFLP) method. Odds ratio (OR) and 95% confidence interval (CI) were calculated using unconditional logistic regression model to evaluate the impact of these 2 polymorphisms on the risk of developing gastric cancer. The subjects having the ADPRT Ala/Ala genotype had an OR of 2.07 (95% CI=1.33-3.21; P=0.001) compared with those having the Val/Val genotype. Gene-gene interaction of ADPRT and XRCC1 polymorphisms increased the risk of gastric cancer in a super-multiplicative manner, with an OR of 5.32 (95% CI=1.12-28.57) for the presence of both ADPRT 762Ala/Ala and XRCC1 399Gln/Gln genotypes, although the XRCC1 polymorphism itself was not associated with the risk of gastric cancer. The ADPRT 762Val-->Ala polymorphism plays an important role in the development of gastric cancer, and the XRCC1 399Arg-->Gln polymorphism may serve as a risk modifier.Ai zheng = Aizheng = Chinese journal of cancer 01/2006; 25(1):7-10.
