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1.
Both transforming growth factor-β receptor I (TGFBR1) and receptor II (TGFBR2) are serine/threonine kinases and play important
roles in TGF-β/Smads signal pathway. The case–control study was performed to evaluate the possible association of Int7G24A
and *6A polymorphisms of TGFBR1 and G-875A polymorphism of TGFBR2 with susceptibility to gastric cardia adenocarcinoma (GCA)
in a population of North China. Polymerase-chain reaction (PCR)-restriction fragment length polymorphism (RFLP) and PCR methods
were used respectively to detect the genotype of Int7G24A, *6A and G-875A in 468 GCA and 584 healthy controls. Immunohistochemistry
method was used to determine the protein expression of TGFBR1 and TGFBR2. Family history of upper gastrointestinal cancer
(UGIC) significantly increased the risk of developing GCA. There were no differences in the genotype distribution of TGFBR1
*6A polymorphism among cases and controls. However, A allele of Int7G24A significantly elevated the risk of developing GCA
(adjusted OR = 1.34, 95% CI 1.03–1.87) and A allele of G-875A significantly decreased the risk of developing GCA (adjusted
OR = 0.73, 95% CI 0.49–0.92). When stratified for TNM stage, A allele of Int7G24A and G-875A allele carriers had a 1.41-fold
(95% CI 1.05–1.98) increased and a 0.70-fold (95% CI 0.47–0.92) decreased risk of stage III and IV gastric cardia adenocarcinoma.
The protein expression of TGFBR1 and TGFBR2 in GCA was not correlated with genotypes of them. In conclusions, TGFBR1 Int7G24A
and TGFBR2 G-875A polymorphisms may play important roles in the risk of GCA in North China. 相似文献
2.
Ru-Yan Liao Chen Mao Li-Xin Qiu Hong Ding Qing Chen Hai-Feng Pan 《Molecular biology reports》2010,37(7):3227-3232
Published data on the association between TGFBR1*6A/9A polymorphism and cancer risk are inconclusive. To derive a more precise estimation of the relationship, a meta-analysis
was performed. A total of 32 studies including 13,662 cases and 14,147 controls were involved in this meta-analysis. Overall,
significantly elevated cancer risks were associated with TGFBR1*6A in all genetic models (for allelic effect: OR = 1.11; 95% CI = 1.03–1.21; for 6A/6A vs. 9A/9A: OR = 1.30; 95% CI = 1.01–1.69;
for 9A/6A vs. 9A/9A: OR = 1.08; 95% CI = 1.01–1.15; for dominant model: OR = 1.08; 95% CI = 1.02–1.15; for recessive model:
OR = 1.29; 95% CI = 1.00–1.68). In the subgroup analysis by cancer types, significant associations were found in breast cancer
(for allelic effect: OR = 1.16; 95% CI = 1.01–1.34) and ovarian cancer (for allelic effect: OR = 1.24; 95% CI = 1.00–1.54;
for 6A/6A vs. 9A/9A: OR = 2.34; 95% CI = 1.03–5.33). However, no significant associations were found in colorectal cancer,
bladder cancer, prostate cancer and lung cancer for all genetic models. In summary, this meta-analysis suggests that the TGFBR1*6A/9A polymorphism is associated with cancer susceptibility, increasing the risk of breast and ovarian cancer. 相似文献
3.
Epidemiological studies have evaluated the association between ATM 5557G>A (p.D1853N) polymorphism and breast cancer risk. However, the results remain conflicting rather than conclusive. To
derive a more precise estimation of the relationship, we performed this meta-analysis. Systematic searches of PubMed and Medline
databases were performed. A total of nine studies included 3155 cases and 2752 controls were identified. When all nine studies
were pooled into the meta-analysis, there was no evidence for significant association between 5557G>A mutation and breast
cancer risk(for G/A vs. G/G: OR = 1.05, 95% CI = 0.83–1.34; for A/A vs. G/G: OR = 0.77, 95% CI = 0.58–1.03; for dominant model:
OR = 1.04, 95% CI = 0.82–1.31; for recessive model: OR = 0.87, 95% CI = 0.69–1.09). In the subgroup analyses by family history
and ethnicity, significant associations were found among Amerindians (for G/A vs. G/G: OR = 2.19, 95% CI = 1.38–3.47; for
dominant model: OR = 2.15, 95% CI = 1.37–3.38). In summary, the meta-analysis suggest that ATM 5557G>A polymorphism is associated with increased breast cancer risk among Amerindians. However, due to the small subjects
included in analysis and the selection bias existed in some studies, the results for Amerindians should be interpreted with
caution. 相似文献
4.
Published data on the association between lymphocyte-specific protein 1 (LSP1) rs3817198T>C polymorphism and breast cancer
risk are inconclusive. Hence, we conducted a meta-analysis of the LSP1 gene and risk of breast cancer to obtain the most reliable
estimate of the association. PubMed, Embase and Web of Science databases were searched. Crude odds ratios (ORs) with 95% confidence
intervals (CIs) were extracted and pooled to assess the strength of the association between the LSP1 rs3817198T>C polymorphism
and risk of breast cancer. A total of seven eligible studies including 33,920 cases and 35,671 controls based on the search
criteria were involved in this meta-analysis. The distributions of genotypes in the controls were all in agreement with Hardy–Weinberg
equilibrium. We observed that the LSP1 rs3817198T>C polymorphism was significantly correlated with breast cancer risk when
all studies were pooled into the meta-analysis (the allele contrast model: OR = 1.06, 95% CI = 1.04–1.08; the homozygote codominant:
OR = 1.14, 95% CI = 1.01–1.28). In the stratified analysis by ethnicity, significant association was observed in Caucasians
for CC versus TT homozygote codominant model (OR = 1.25; 95% CI = 1.03–1.52) and for the recessive model (OR = 1.22; 95% CI = 1.02–1.47).
There was significant association observed in Africans for CC versus TT homozygote codominant model (OR = 0.45; 95% CI = 0.22–0.92)
and for the recessive model (OR = 0.43; 95% CI=0.22–0.88). Also, significant association was observed in mixed ethnicities
for CC versus TT homozygote codominant model (OR = 1.12; 95% CI = 1.05–1.19). When stratified by study design, statistically
significantly elevated risk was found in nested case–control studies (CC vs. TT: OR = 1.12, 95% CI = 1.05–1.19). But no significant
association was observed for all comparison models between LSP1 rs3817198T>C polymorphism and breast cancer risk in hospital-based
and people-based studies. When stratified by BRCA1 mutation carriers status, statistically significantly elevated risk was
found in this meta-analysis (the allele contrast model: OR = 1.07, 95% CI = 1.01–1.14; the dominant model: OR = 1.09, 95%
CI = 1.00–1.18). And significant association was found in the BRCA2 mutation carriers in the allele contrast (OR = 1.11, 95%
CI = 1.03–1.20), the homozygote codominant (OR = 1.23, 95% CI = 1.04–1.47), the heterozygote codominant (OR = 1.12, 95% CI = 1.00–1.25)
and the dominant models (OR = 1.14, 95% CI = 1.03–1.27). There was significant association between LSP1 rs3817198T>C polymorphism
and breast cancer risk in BRCA1 and BRCA2 positive cohort in all comparison models (the allele contrast model: OR = 1.08,
95% CI = 1.03–1.13; CC vs. TT: OR = 1.16, 95% CI = 1.05–1.29; TC vs. TT: OR = 1.09, 95% CI = 1.01–1.16; the dominant model:
OR = 1.10, 95% CI = 1.03–1.17; the recessive model: OR = 1.12, 95% CI = 1.01–1.23). In conclusion, this meta-analysis suggests
that the LSP1 rs3817198T>C polymorphism is a low-penetrant risk factor for developing breast cancer but may not be in Africans. 相似文献
5.
Xeroderma pigmentosum group A (XPA) participates in modulating recognition of DNA damage during the DNA nucleotide excision
repair process. The XPA A23G polymorphism has been investigated in case–control studies to evaluate the cancer risk attributed to the variant, but
the results were conflicting. To clarify the effect of XPA A23G polymorphism in cancer risk, we conducted a meta-analysis that included 30 published case–control studies. Overall,
no significant association of XPA A23G variant with cancer susceptibility was observed for any genetic model. However, significant
association was observed for colorectal cancer (GG vs. AA: OR = 1.68, 95% CI = 1.15–2.44; dominant genetic model GG + AG vs.
AA: OR = 1.54, 95% CI = 1.08–1.17), for breast cancer an increased but non-significant risk was found (GG vs. AA: OR = 1.27,
95% CI = 0.98–1.66; dominant genetic model GG + AG vs. AA: OR = 1.27, 95% CI = 0.99–1.63), and for head and neck cancer an
increased risk was observed in recessive model (OR = 1.19, 95% CI = 1.02–1.38), whereas for lung cancer a significant reduced
risk was observed (GG vs. AA: OR = 0.77, 95% CI = 0.66–0.90; dominant genetic model GG + AG vs. AA: OR = 0.76, 95% CI = 0.66–0.87),
it’s noting that in Asian population the inverse association was more apparent. In addition, in Asian population for esophageal
cancer a significant decreased risk was also found in dominant genetic model (OR = 0.55; 95% CI = 0.43–0.70) and for head
and neck cancer an increased risk was observed in dominant genetic model (OR = 1.51, 95% CI = 1.03–2.23). The meta-analysis
suggested that the XPA A23G G allele is a low-penetrant risk factor for cancer development. 相似文献
6.
The G801A polymorphism in the CXCL12 gene has been implicated in breast cancer risk. However, the published findings are inconsistent.
We therefore performed a meta-analysis to investigate this relationship. Odds ratios (ORs) and 95% confidence intervals (CIs)
were used to assess the strength of the association. The pooled ORs were performed for codominant model, dominant model, and
recessive model, respectively. Five published case–control studies, including 1,058 breast cancer cases and 1,023 controls
were identified. No study had a deviation from the Hardy–Weinberg equilibrium (HWE) in controls. We found that the CXCL12
G801A (rs1801157) polymorphism was associated with a significantly increased risk of breast cancer risk when all studies were
pooled into the meta-analysis (codomiant model: AA versus GG, OR = 1.64, 95% CI = 1.16–2.33; GA versus GG, OR = 1.42, 95%
CI = 1.18–1.71; dominant model: AA/GA versus GG, OR = 1.44, 95% CI = 1.21–1.72). Furthermore, Egger’s test did not show any
evidence of publication bias (P > 0.05 for the dominant model). In conclusion, the results suggest that the CXCL12 G801A polymorphism may be a low-penetrant
risk factor for developing breast cancer. 相似文献
7.
Evidence suggested that interleukin-10 (IL-10) may be involved in the etiology of gastric cancer (GC). However, epidemiological
studies on the association between IL-10-1082 promoter polymorphism and GC risk are still ambiguous. To quantitatively summarize
the evidence for such a relationship, we performed a meta-analysis. Systemic searches of the PubMed and Medline databases
were performed, with the last report up to July 2011. Crude odds ratios (ORs) with 95% confidence intervals (CIs) were used
to assess the strength of association. 22 independent studies including 4,289 cases and 5,965 controls were involved in this
meta-analysis. Obvious association was found when all studies were pooled into the meta-analysis (A vs. G: OR = 0.489, 95%
CI = 0.335–0.713, P < 0.001). In the subgroup analysis by ethnicity, we observed significant associations in Asians (A vs. G: OR = 0.651, 95%
CI = 0.506–0.838, P = 0.001; AA vs. GG: OR = 0.482, 95% CI = 0.328–0.709, P < 0.001; AA/AG vs. GG: OR = 0.711, 95% CI = 0.527–0.959, P = 0.025; AA vs. AG/GG: OR = 0.701, 95% CI = 0.520–0.944, P = 0.019) and Caucasians (A vs. G: OR = 0.365, 95% CI = 0.140–0.949, P = 0.039), but not in Latino population. When stratified analysis by control sources, our results indicated that A allele
decreased approximately 48% risk among population-based studies (A vs. G: OR = 0.524, 95% CI = 0.374–0.733, P < 0.001). Taken together, this meta-analysis suggests that IL-10-1082 polymorphism is associated with GC risk. 相似文献
8.
Lucia Klimčáková Viera Habalová Monika Sivoňová Vincent Nagy Ján Šalagovič Jozef Židzik 《Molecular biology reports》2011,38(2):1287-1293
N-acetyltransferase 2 (NAT2) is phase II enzyme with major roles in catalyzing the detoxification of aromatic amines, which
are known risk factors for bladder cancer, and are ubiquitously present in the environment. We assessed the association between
common polymorphisms in NAT2 gene and the risk of bladder cancer in 90 Slovak patients and 274 ethnicity-matched healthy controls.
Effect modifications by smoking, age and gender were also evaluated. Overall, NAT2 slow acetylation was associated with significantly
increased risk of bladder cancer (OR = 1.90; 95% CI, 1.15–3.16). In stratified analyses by age and gender, the elevated risk
conferred by slow acetylator genotype was evident in older individuals (OR = 3.55; 95% CI, 1.77–7.35) and males (OR = 4.65;
95% CI, 1.68–16.10), with further increasing in NAT2*5B/*6A genotype carriers. Smoking was confirmed to be important risk
factor, moreover, the risk was markedly increased in smokers with NAT2 slow acetylator genotype, and NAT2*5B/*6A carriers
especially. In summary, these findings are consistent with previous literature suggesting that individual susceptibility to
bladder cancer may be modulated by NAT2 polymorphisms, particularly in interaction with relevant environmental exposures such
as smoking. 相似文献
9.
He XF Wei W Su J Yang ZX Liu Y Zhang Y Ding DP Wang W 《Molecular biology reports》2012,39(5):5125-5134
The previous published data on the association between X-ray repair cross-complementing group 3 (XRCC3) T241M, A4541G, and
A17893G polymorphisms and breast cancer risk remained controversial. Hence, we performed a meta-analysis to investigate the
association between breast cancer and XRCC3 T241M (21,910 cases and 23,961 controls), A4541G (9,633 cases and 10,994 controls),
and A17893G polymorphisms (10,761 cases and 12,235 controls) in different inheritance models. When all the eligible studies
were pooled into the meta-analysis of XRCC3 T241M polymorphism, significantly increased risk of breast cancer was observed
in recessive model (odds' ratio [OR] = 1.10, 95% confidence interval [CI] = 1.04–1.16) and in additive model (OR = 1.10, 95% CI = 1.03–1.16). No significant association was found between A4541G polymorphism and breast cancer risk. When all the eligible studies
were pooled into the meta-analysis of XRCC3 A17893G polymorphism, no significant association was found in any genetic model.
Additionally, when one study was deleted in the sensitive analysis, the results of XRCC3 A17893G were changed in the additive
model (OR = 0.90, 95% CI = 0.82–0.99) and dominant model (OR = 0.94, 95% CI = 0.89–0.99). In summary, this meta-analysis indicates
that T241M polymorphism show an increased breast cancer risk and A17893G polymorphism may be associated with decreased breast
cancer risk. A study with the larger sample size is needed to further evaluated gene-environment interaction on XRCC3 T241M,
A4541G, and A17893G polymorphisms and breast cancer risk. 相似文献
10.
Zhang Y Chen GQ Ji Y Huang B Shen WS Deng LC Xi L Cao XM 《Molecular biology reports》2012,39(5):6203-6211
Published studies on the relationships between 5,10-methylenetetrahydrofolate reductase (MTHFR) polymorphisms and lung cancer
risk have been conflicting. To derive a more precise estimation of the relationship, a meta-analysis was performed. Odds ratios
(ORs) with 95% confidence intervals (CIs) were estimated to assess the association between MTHFR C677T and A1298C polymorphisms
and lung cancer risk. A total of 15 studies including 10,753 cases and 11,275 controls described C677T genotypes, among which
11 articles totalling 6,161 cases and 7,684 controls described A1298C genotypes, were also involved in this meta-analysis.
Overall, no significantly elevated lung cancer risk was found in any genetic models when all studies were pooled. For C677T
polymorphism: (TT vs. CC: OR = 1.17, 95% CI = 0.97–1.42; TC vs. CC: OR = 1.06, 95% CI = 0.94–1.20; dominant model: OR = 1.09,
95% CI = 0.96–1.24; and recessive model: OR = 1.08, 95% CI = 0.95–1.24); for A1298C polymorphism: (CC vs. AA: OR = 1.04, 95%
CI = 0.91–1.19; AC vs. AA: OR = 0.98, 95% CI = 0.91–1.06; dominant model: OR = 0.99, 95% CI = 0.92–1.06; and recessive model:
OR = 1.05, 95% CI = 0.92–1.20). In the subgroup analyses, the results showed that 677T varients could decrease lung cancer
risk in female (OR = 0.63, 95% CI = 0.41–0.95, P-value = 0.03, 677CC as reference). No evidence of any associations of MTHFR A1298C polymorphism with lung cancer was found
in overall or subgroup analyses. Our meta-analysis supports that the common polymorphisms of C677T and A1298C in MTHFR gene
are not susceptibility gene for lung cancer from currently available evidence. 相似文献
11.
P73 is a structural and functional homologue of p53, and plays an important role in regulating cell cycle and apoptosis. A
potentially functional polymorphism (designated as p73 G4C14-to-A4T14) has been identified in a region in exon 2 of the p73 gene, which may theoretically form a stem-loop structure and thereby affect p73 expression. Several investigations have reported the correlation between p73 G4C14-to-A4T14 polymorphism and cancer risk.
However, the results are inconclusive. To further assess the association between p73 polymorphism and cancer risk, we performed
meta-analysis of the data sets obtained from 26 individual studies involving 8,148 cancer patients and 8,150 controls. The
association between p73 G4C14-to-A4T14 polymorphism and cancer risk was determined by crude odd ratios (OR) with 95% CI (confidential
interval). AT-allele carriers were found to have a significantly increased risk of cervical cancer (AT/GC vs. GC/GC, OR = 1.63,
95% CI = 1.14–2.33; AT/AT + AT/GC vs. GC/GC, OR = 1.49, 95% CI = 1.05–2.10), colorectal cancer (AT/AT vs. AT/GC + GC/GC, OR = 1.98,
95% CI = 1.25–3.12), head and neck cancer (AT/AT + AT/GC vs. GC/GC, OR = 1.44, 95% CI = 1.06–1.96) and other cancers (AT/AT
vs. GC/GC, OR = 1.78, 95% CI = 1.24–2.57; AT/AT vs. AT/GC + GC/GC, OR = 1.80, 95% CI = 1.26–2.56). In the stratified analysis
of ethnicity, a significantly elevated cancer risk was found in Caucasians (AT/AT + AT/GC vs. GC/GC, OR = 1.18, 95% CI = 1.08–1.30;
allele AT vs. allele GC, OR = 1.15, 95% CI = 1.06–1.24). No significant association of p73 polymorphism with the cancer risk
of smoking was detected by stratified analysis by smoking status. Together, our data suggest that the p73 G4C14-to-A4T14 may
be a risk factor of cancer especially in Caucasians. 相似文献
12.
This study aimed to perform a meta-analysis to assess the association of survivin −31 G/C promoter polymorphism and cancer
risk. Thirteen case–control studies identified through PubMed and published between 2007 and 2011 with a total of 3329 cancer
cases and 3979 controls were included in this meta-analysis. Odds ratio (OR) and 95% confidence interval (95% CI) were used
to investigate the strength of the association. Overall, the pooled analysis showed that survivin −31C allele was associated
with 1.27 fold increased risk of cancer compared with the −31G allele (95% CI = 1.091–1.479; random model). Subgroup analyses
based on type of cancer and ethnicity were also performed, and results indicated that survivin −31G/C polymorphism was not
associated with risk of gastric cancer [OR = 2.879; 95% CI = 0.553–15.004) for CC vs.GG] and esophageal cancer [OR = 1.352;
95% CI = 0.494–3.699) for CC vs.GG]. Stratification on the basis of ethnicity showed that the risk due to −31C allele was
significant only in Asian population [OR = 1.894; 95% CI = 1.206–2.974 for CC vs.GG]. The present meta-analysis suggests an
important role of survivin −31 G/C polymorphism with cancer risk especially in Asian population. However, further studies
with larger sample size are required to draw more comprehensive conclusions and provide more precise evidence in individual
cancers. 相似文献
13.
A number of studies have investigated the association between TNF-308 (rs1800629 G/A) polymorphisms and the susceptibility
towards tuberculosis (TB) in different populations. However, many of these studies provided inconsistent results. In this
study, a systematic review and meta-analysis of the published studies was performed to gain a clearer understanding of this
association. The PubMed, Embase, Web of Science and CNKI databases were searched for case–control studies published up to
Jan 2011, we used no lower date limit. Data were extracted and pooled odds ratios (OR) with 95% confidence intervals (CI)
were calculated. A total of 18 publications from 2001 to 2010, involving 2584 TB cases and 3817 controls were included. Overall,
for the A allele carriers (G/A + A/A) vs. homozygote GG, the pooled OR was 1.03 (95% CI = 0.89–1.19; P = 0.912 for heterogeneity). For the allele A vs. allele G, the pooled OR was 1.07 (95% CI = 0.93–1.22; P = 0.013 for heterogeneity). In the stratified analysis by ethnicity, among Asians significant risk was found for allele A
vs. allele G (OR = 1.22, 95% CI = 1.02–1.47; P = 0.152 for heterogeneity), no significant risks were found among Caucasians. This meta-analysis indicated that the TNF-308
polymorphism was not associated with the risk of TB in the total population, however the significant risk for TNF-308 A allele
was found among Asians not Caucasians. 相似文献
14.
Ku70 plays an important role in the DSBR (DNA double-strand breaks repair) and maintenance of genomic integrity. Genetic variations
within human Ku70 have been demonstrated to be associated with increased risk of several types of cancers. In this hospital-based
case–control study, we aimed to investigate whether a single nucleotide polymorphism (SNP) in the promoter region (rs2267437)
of Ku70 gene is associated with susceptibility to breast cancer in Chinese Han population. A total of 293 patients with breast
cancer and 301 age-matched healthy controls were enrolled in this study. The Ku70 −1310C/G polymorphism was determined by
polymerase chain reaction-restriction fragment length polymorphism (PCR–RFLP) analysis. A significant difference in genotype
distribution and allele frequency was observed between patients and controls. The CG or GG carries were at higher risk of
breast cancer compared with the CC homozygotes (OR = 1.43, 95% CI = 1.02–2.00, P = 0.038 and OR = 3.53, 95% CI = 1.60–7.80, P = 0.002, respectively). Further stratification analysis revealed that G allele was associated with an increased risk of breast
cancer among premenopausal women (OR = 1.68, 95% CI = 1.21–2.33, P = 0.002), but not in postmenopausal women (OR = 1.33, 5% CI = 0.85–2.10, P = 0.216). Our study suggests that the Ku70 −1310C/G promoter polymorphism may be a susceptibility factor for breast cancer
in Chinese Han population. 相似文献
15.
Qiu LX Wang K Yang S Mao C Zhao L Yao L Zhang J Zhang QL Sun S Xue K 《Molecular biology reports》2011,38(7):4491-4494
Several polymorphisms of vascular endothelial growth factor (VEGF) such as 936 C/T, −2578 C/A, −406 C/T, and −1154 G/A polymorphism
have been identified. Published data on the association between VEGF polymorphisms and breast cancer risk are inconclusive.
To derive a more precise estimation of the relationship, a meta-analysis was performed. Crude OR with 95% CI was used to assess
the strength of association between them. For VEGF 936C/T polymorphism, a total of 10 studies including 7,685 cases and 7,915
controls were involved in this meta-analysis. Overall, no significant associations were found between VEGF 936C/T polymorphism
and breast cancer risk when all studies pooled into the meta-analysis (TC vs. CC: OR = 0.904, 95% CI = 0.797–1.024; TT vs.
CC: OR = 0.974, 95% CI = 0.786–1.205; dominant model: OR = 0.911, 95% CI = 0.811–1.024; and recessive model: OR = 0.991, 95%
CI = 0.801–1.226). In the subgroup analysis by ethnicity, still no significant associations were found for all comparison
models. For −2578 C/A, −406 C/T, and −1154 G/A polymorphism, there were too limited data to perform a meta-analysis. In conclusion,
this meta-analysis suggests that the VEGF 936C/T polymorphism may be not associated with breast cancer development. However,
large sample and representative population-based studies with homogeneous breast cancer patients and well matched controls
are warranted to confirm this finding. 相似文献
16.
Ping Zhan Jing Wang Shu-Zhen Wei Qian Qian Li-Xin Qiu Li-Ke Yu Yong Song 《Molecular biology reports》2011,38(1):219-227
Chronic obstructive pulmonary disease (COPD) is a complex polygenic disease in which gene–environment interactions play a
critical role in disease onset and progression. The gene encoding tumor necrosis factor (TNF) is one of several candidate
loci for the pathogenesis of COPD and is highly polymorphic. A number of studies have investigated the association between
the TNF-308 polymorphisms and COPD risk in different populations, and resulted in inconsistent results. A systematic review
and meta-analysis of the published studies were performed to gain a clearer understanding of this association. The PubMed,
Embase, Web of Science, and CNKI databases were searched for case–control studies published from 1966 to April 2009. Data
were extracted and pooled odds ratios (OR) with 95% confidence intervals (CI) were calculated. Twenty-four eligible studies,
comprising 2,380 COPD cases and 3,738 controls, were included in the meta-analysis. The pooled result showed that the TNF-308
polymorphisms were significantly associated with an increased risk of COPD (OR = 1.335, 95% CI: 1.172–1.522, for allele A
carriers versus G/G; OR = 1.330, 95% CI = 1.174–1.505, for allele A versus allele G). Subgroup analysis supported the results
in the Asian populations, but not in the Caucasian populations. When the analysis was limited to only those studies in which
the COPD cases and controls were smokers/ex-smokers, the pooled results supported the conclusion. This meta-analysis suggested
that the TNF-308 A allele is a more significant risk factor for developing COPD among Asian populations, but not among Caucasians. 相似文献
17.
Li-Xin Qiu Jian Shi Hui Yuan Xin Jiang Kai Xue Hai-Feng Pan Jin Li Ming-Hua Zheng 《Human genetics》2009,125(4):431-435
Published data on the association between FAS −1,377 G/A polymorphism and cancer risk are inconclusive. To derive a more precise estimation of the relationship, a meta-analysis
was performed. A total of 17 studies including 10,564 cases and 12,075 controls were involved in this meta-analysis. Overall,
significantly elevated cancer risk was associated with AA variant genotype when all the eligible studies were pooled into
the meta-analysis (for AA vs GG: OR = 1.19; 95% CI = 1.01–1.40; P
heterogeneity = 0.05; for recessive model: OR = 1.21; 95% CI = 1.04–1.41; P
heterogeneity = 0.05). In the subgroup analysis by ethnicity, borderline statistically significantly increased risks were found among Asians
for recessive model (OR = 1.20; 95% CI = 1.00–1.45; P
heterogeneity = 0.01). In the subgroup analysis by population-based controls or hospital-based controls, statistically significantly increased
risks were found among groups with population-based controls for AA versus GG (OR = 1.27; 95% CI = 1.02–1.58; P
heterogeneity = 0.05) and recessive model (OR = 1.25; 95% CI = 1.00–1.59; P
heterogeneity = 0.01). For breast cancer, borderline statistically significantly increased risks were found for AA versus GG (OR = 1.29;
95% CI = 1.00–1.67; P
heterogeneity = 0.41). In summary, this meta-analysis suggests that the FAS −1,377 G/A polymorphism is associated with cancer susceptibility.
L. X. Qiu, J. Shi and H. Yuan contributed equally to this work and should be considered as co-first authors. 相似文献
18.
Li BH Zhang LL Yin YW Pi Y Yang QW Gao CY Fang CQ Wang JZ Li JC 《Molecular biology reports》2012,39(5):5623-5630
Epidemiological studies have evaluated the association between paraoxonase 2 (PON2) Ser311Cys polymorphism and ischemic stroke
risk which developed inconsistent conclusions. The aim of this study was to perform a meta-analysis to investigate a more
authentic association between PON2 Ser311Cys polymorphism and ischemic stroke. Systematic searches in PUBMED, EMBASE, CBM,
and CNKI databases were performed. Data analyses were carried out by Review Manager 5.1.2 and Stata 11.0. The pooled odds
ratios (ORs) with 95% confidence intervals (CIs) were used for additive model (Cys/Cys vs. Ser/Ser), dominant model (Ser/Cys+Cys/Cys
vs. Ser/Ser), recessive model (Cys/Cys vs. Ser/Cys+Ser/Ser), and allelic model (Cys allele vs. Ser allele), respectively.
Publication bias was analyzed by Begg’s funnel plot and Egger’s test. A total of 7 studies including 2,046 cases and 2,962
controls were involved. Overall, no significant association was found between PON2 Ser311Cys polymorphism and ischemic stroke
risk when all studies were pooled into the meta-analysis (for additive model: OR = 0.87, 95% CI = 0.67–1.14; for dominant
model: OR = 1.05, 95% CI = 0.91–1.22; for recessive model: OR = 0.90, 95% CI = 0.77–1.05; and for allelic model: OR = 1.17,
95% CI = 0.86–1.59). In the subgroup analysis by ethnicity, significant association was found among Europeans (for recessive
model: OR = 0.83, 95% CI = 0.69–0.99). However, due to the small number of studies included in subgroup analysis, the result
for European population should be interpreted cautiously. 相似文献
19.
Oxidative damage promotes atherosclerosis. SOD2 is an important antioxidant enzyme. A case–control study and a meta-analysis
were performed to assess the association of C47T polymorphism in SOD2 gene with premature, late-onset and overall coronary artery disease (CAD) risk. A hospital-based case–control study was conducted
with 269 premature CAD cases, 278 late-onset CAD cases and 299 healthy controls. Polymerase chain reaction (PCR) and Pyrosequencing
were used to detect the polymorphism. Multinomial logistic regression model was performed to estimate odds ratio (OR) with
95% confidence intervals (CIs) and adjust potential confounders. A meta-analysis was performed using eight outcomes including
our result. Fixed or random effect pooled measure was selected on the basis of homogeneity test among studies. Heterogeneity
among studies was evaluated using I
2. Meta-regression was used to explore potential sources of between-study heterogeneity. Publication bias was estimated using
Peters’s linear regression test. In our case–control study, compared with the TT as the reference, the mutant genotype of
CC + TC was significantly associated with a reduced premature CAD risk both in univariate (OR = 0.60, 95% CI = 0.41–0.87)
and multivariate (OR = 0.59, 95% CI = 0.40–0.87) logistic regressions, but not with late-onset CAD risk. After excluding one
article that deviated from Hardy–Weinberg equilibrium in controls, this meta-analysis showed a significant association of
the C allele with reduced risk of CAD in dominant (FEM: OR = 0.69, 95% CI = 0.61–0.78), recessive (OR = 0.64, 95% CI = 0.50–0.82),
and codominant (FEM: OR = 0.73, 95% CI = 0.65–0.80) models. Our study suggested that the mutant genotype of CC + TC was significantly
associated with a reduced CAD risk. 相似文献
20.
The mouse double minute 2 (MDM2) gene encodes a phosphoprotein that interacts with P53 and negatively regulates its activity.
SNP309 polymorphism (T-G) in the promoter of MDM2 gene has been reported to be associated with enhanced MDM2 expression and
tumor development. Many published studies have evaluated the association between MDM2 SNP309 polymorphism and breast cancer
risk. However, the results were inconsistent. We combined and analyzed the data from 19 case–control studies including 14,450
cases and 13,382 controls. Crude odds ratios (ORs) with 95% confidence intervals (CIs) were used to assess the strength of
the association between MDM2 SNP309 polymorphism and breast cancer risk. No significant association was found in all genetic
models in overall population. However, in subgroup analysis by ethnicity (4 studies in Asian group, 13 studies in European
group, 2 studies of mixed population which were separated into 2 European population group and 2 African population group),
we found an increased breast cancer susceptibility for GT versus TT (OR = 1.31, 95% CI = 1.03–1.67) in Asian population and
for GT versus TT (OR = 1.31, 95% CI = 1.03–1.66) in African population. When stratified by family history status (5 studies
in familial breast cancer group, 5 studies in sporadic breast cancer group), homozygous subjects of sporadic breast cases
carrying the T309G G allele exhibited elevated breast cancer risk (OR = 1.35, 95% CI = 1.00–1.82), whereas heterozygous carriers
did not show significant association with breast cancer risk for GT vs. TT (OR = 1.26, 95% CI = 0.84–1.87). Our meta–analysis
suggests that MDM2 SNP309 polymorphism may increase the risk to breast cancer in Asian and African population. 相似文献