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1.
Zhang X Wu L Sheng Y Zhou W Huang Z Qu J Gao G Cai D Zhang M 《Molecular biology reports》2012,39(3):2567-2574
Epidemiological studies found inconsistent results on the association of two variants on TGFBR1 (TGFBR1*6A and Int7G24A) with colorectal cancer (CRC) risk. The present study was aimed to evaluate the association of these
two variants with CRC susceptibility via the meta-analysis methods. For variant TGFBR1*6A, nine reports including 6,765 CRC
patients and 8,496 unrelated controls were identified. The heterozygotes *6A/*9A showed a significant increased risk of CRC
with the pooled OR was 1.12 (95% CI = 1.02–1.23), and the pooled OR for the homozygotes *6A/*6A was 1.13 (95% CI = 0.80–1.58)
compared to the homozygotes *9A/*9A. However, under the dominant effect model, the TGFBR1*6A carriers showed a significantly
increased CRC risk (pooled OR = 1.12, 95% CI = 1.03–1.23, *6A/*6A and *6A/*9A vs. *9A/*9A). For variant Int7G24A, three case–control
studies with 1,074 cases and 1,945 controls were found. Although no significant association was found for heterozygosity Int7G24A
carriers with CRC risk (pooled OR = 0.97, 95% CI = 0.67–1.42), the homozygosity A/A carriers showed a significant elevated
risk of CRC (pooled OR = 1.68, 95% CI = 1.14–2.47) compared to G/G homozygotes. Under the recessive effect model, homozygotes
A/A showed a 71% increase of CRC risk compared to the A/G and G/G genotype carriers (pooled OR = 1.71, 95% CI = 1.17–2.51).
These data strongly suggested that the two polymorphisms of TGFBR1 may confer low-penetrance susceptibility of CRC risk. 相似文献
2.
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
3.
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
4.
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
5.
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
6.
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
7.
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
8.
The relationship of stomach cancer susceptibility and the presence of E-cadherin (CDH1) promoter −160 C/A polymorphism had been reported with conflicting results. To further explore the association of this polymorphism
with stomach cancer susceptibility, we performed an extensive search of relevant studies and carried out a meta-analysis to
obtain a more precise estimate. A total of 16 studies including 2,611 cases and 3,788 controls were involved in this meta-analysis.
When all studies involved, the meta-analysis results suggest no statistically significant association between CDH1 −160 C/A polymorphism and stomach cancer risk (CA vs. CC: OR = 1.01, 95% CI: 0.85–1.19; AA vs. CC: OR = 1.05, 95% CI: 0.75–1.46;
dominant model: OR = 1.02, 95% CI: 0.86–1.20; recessive model: OR = 1.04, 95% CI: 0.76–1.41). When subgroup analyses were
performed by ethnicity, the A-allele carriers conferred a decreased stomach cancer risk in Asians (AA vs. CC: OR = 0.67, 95%
CI: 0.47–0.96; dominant model: OR = 0.85, 95% CI: 0.72–0.99), but no statistically significant association was found in Caucasians.
In conclusion, this meta-analysis suggests that CDH1 −160 A-allele may play a protective role of stomach cancer development in Asians but not in Caucasians. 相似文献
9.
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
10.
Wang JJ Zheng Y Sun L Wang L Yu PB Dong JH Zhang L Xu J Shi W Ren YC 《Molecular biology reports》2011,38(8):4847-4853
Colorectal cancer constitutes a significant proportion of the global burden of cancer morbidity and mortality. A number of
studies have been conducted to explore whether TP53 codon 72 polymorphism is associated with colorectal cancer susceptibility. However, controversial results were obtained.
In order to derive a more precise estimation of the relationship, we systematically searched Medline, Google scholar, and
Ovid database for studies reported before May 2010. A total of 3603 colorectal cancer cases and 5524 controls were included.
TP53 codon 72 polymorphism was not associated with colorectal cancer risk in all genetic models (for dominant model: OR = 0.99,
95% CI: 0.86–1.15; for recessive model: OR = 1.00, 95% CI: 0.81–1.23; for Arg/Pro vs. Arg/Arg: OR = 1.00, 95% CI: 0.87–1.15;
for Pro/Pro vs. Arg/Arg: OR = 0.97, 95% CI: 0.76–1.25). In the subgroup analyses by ethnic groups and sources of controls,
no significant associations were found in all models. Taken together, this meta-analysis suggested that the biologically usefulness
of TP53 codon 72 polymorphism as a selection marker in colorectal cancer susceptibility may be very limited. 相似文献
11.
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
12.
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
13.
Previous data on association between CYP2E1 Rsa I/Pst I polymorphism and oral cancer risk were controversial. To investigate
the association between CYP2E1 Rsa I/Pst I polymorphism and oral cancer risk. We performed a meta-analysis to assess the relationship
between oral cancer and genotype with English language until June 2010. Twelve published case–control studies of 1259 patients
with oral cancer and 2262 controls were acquired. Odds ratios (ORs) with 95% confidence intervals (CIs) were used to assess
the strength of the association in codominant and dominant models. Overall, the pooled ORs indicated a significant association
between CYP2E1 Rsa I/Pst I polymorphism and oral cancer risk (for c1/c2 vs. c1/c1: OR = 1.30, 95% CI = 1.04–1.62, Pheterogeneity = 0.57; for (c1/c2 + c2/c2) vs. c1/c1: OR = 1.32, 95% CI = 1.07–1.64, Pheterogeneity = 0.57, respectively). In subgroup analysis by race, the same significant risks were found among Asian (for c1/c2 vs. c1/c1:
OR = 1.41, 95% CI = 1.05–1.91, Pheterogeneity = 0.92; for (c1/c2 + c2/c2) vs. c1/c1: OR = 1.43, 95% CI = 1.08–1.88, Pheterogeneity = 0.97, respectively). In conclusion, this meta-analysis demonstrates that CYP2E1 Rsa I/Pst I c2 allele may be a biomarker
for oral cancer, especially among Asian populations. 相似文献
14.
Tumor necrosis factor alpha (TNF-α) is a vital cytokine involved in inflammation, immunity, and cellular organization. The
TNFA-308G/A (rs1800629) and -238G/A (rs361525) polymorphisms are two widely investigated variants for their associations with
risk of cervical cancer, but the results are conflicting. Here, we performed a meta-analysis to pool the data and evaluate
the between-studies heterogeneity. All the case–control studies published from January 1989 to October 2010 on the association
between the two polymorphisms of TNFA and cervical cancer risk were identified by searching the electronic literature Medline. The cervical cancer risk associated
with the two polymorphisms of TNFA gene was estimated for each study by OR together with its 95% CI, respectively, by using the Review Manager 4.2 software. It was showed that the variant homozygote
-308AA was associated with a significantly increased risk of cervical cancer (AA vs. GG: OR = 1.41, 95% CI = 1.03–1.92, P = 0.033; AA vs. GA/GG: OR = 1.39, 95% CI = 1.02–1.90, P = 0.036), and the effect was more evident among Asians (AA vs. GA/GG: OR = 3.67, 95% CI = 1.25–10.81, P = 0.018). We also found that the variant genotypes -238GA/AA was associated with a significantly decreased risk of cervical
cancer (GA/AA vs. GG: OR = 0.55, 95% CI = 0.41–0.74, P < 0.001). The results suggested that TNFA-308G/A and -238G/A may contribute to cervical cancer susceptibility. 相似文献
15.
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
16.
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
17.
The aim of our meta-analysis was to quantitatively summarize the association of TYK2 gene polymorphisms with autoimmune and
inflammatory diseases. 11 studies that included data from 21497 cases and 22647 controls were identified. OR was used as a
measure of the effect of the association in a fixed/random effect model. Meta-analysis was performed for six TYK2 gene polymorphisms
(rs34536443, rs2304256, rs280523, rs280519, rs12720270 and rs12720356). Significant association was found in rs34536443 (C
versus G: OR = 0.76, 95% CI = 0.69–0.84, P < 0.00001; GC + CC versus GG: OR = 0.78, 95% CI = 0.68–0.90, P = 0.0005; CC versus GG + GC: OR = 0.76, 95% CI = 0.28–2.05, P = 0.58; CC versus GG: OR = 0.74, 95% CI = 0.27–2.02, P = 0.56; GC versus GG: OR = 0.78, 95% CI = 0.68–0.90, P = 0.0006) and rs2304256 (A versus C: OR = 0.78, 95% CI = 0.70–0.87, P < 0.0001; CA + AA versus CC: OR = 0.69, 95% CI = 0.59–0.81, P < 0.0001; AA versus CC + CA: OR = 0.75, 95% CI = 0.66–1.00, P = 0.05; AA versus CC: OR = 0.64, 95% CI = 0.47–0.86, P = 0.003; CA versus CC: OR = 0.70, 95% CI = 0.60–0.83, P < 0.0001) in TYK2 gene, but not for the other polymorphisms (rs280523, rs280519, rs12720270, and rs12720356). This meta-analysis
demonstrates that autoimmune and inflammatory diseases is associated with TYK2 gene rs34536443 and rs2304256 polymorphisms,
but not rs280523, rs280519, rs12720270 and rs12720356. 相似文献
18.
Lu N Yang Y Wang Y Liu Y Fu G Chen D Dai H Fan X Hui R Zheng Y 《Molecular biology reports》2012,39(6):6581-6589
The polymorphisms of angiotensin-converting enzyme 2 (ACE2) gene have been suggested to be linked to increase risk of essential hypertension in multiple populations. However, the
results are still debatable. To assess the association between ACE2 G8970A genetic polymorphism and essential hypertension, we conducted a meta-analysis of case–control studies across different
ethnicity. PubMed, Embase, CBM, Wanfang and VIP databases were searched, and a total of 11 separate studies in females and
nine separate studies in males met the inclusion criteria. Because ACE2 is on the X chromosome, data for each sex were analyzed separately. The selected studies contained 7,251 (4,472 females/2,779
males) hypertensive patients and 3,800 (2,161 females/1,639 males) normotensive controls. A statistically significant association
was observed between the G8970A gene polymorphism and essential hypertension risk in female hypertensive group in the recessive
genetic model (AA vs. GG+GA: P = 0.03, OR = 1.15, 95% CI = 1.02–1.30, P
heterogeneity = 0.40, I
2 = 5%, fixed-effects model). Although no association was shown between the frequency of the A allele and the genetic susceptibility
to essential hypertension in all male patients (A Allele: P = 0.38, OR = 1.10, 95% CI = 0.89–1.38, P
heterogeneity = 0.02, I
2 = 56%, random-effects model), we found that the relationship between carrier of A allele and the essential hypertension risk
in Han-Chinese male patients subgroup (A Allele: P = 0.006, OR = 1.21, 95% CI = 1.06–1.38, P
heterogeneity = 0.10, I
2 = 44%, fixed-effects model). The current meta-analysis provided solid evidence suggesting that ACE2 gene polymorphism G8790A was probably a genetic risk factor for essential hypertension across different ethnic populations
in female subjects and in Han-Chinese male subjects. 相似文献
19.
Rui‐Xi Hua Zhenjian Zhuo Lili Ge Jinhong Zhu Li Yuan Chongfen Chen Jing Liu Jiwen Cheng Haixia Zhou Jiao Zhang Huimin Xia Xianwei Zhang Jing He 《Journal of cellular and molecular medicine》2020,24(1):1059-1066
Neuroblastoma ranks the most common seen solid tumour in childhood. Overexpression of LIN28A gene has been linked to the development of multiple human malignancies, but the relationship between LIN28A single nucleotide polymorphisms (SNPs) and neuroblastoma susceptibility is still under debate. Herein, we evaluated the correlation of four potentially functional LIN28A SNPs (rs3811464 G>A, rs3811463 T>C, rs34787247 G>A, and rs11247957 G>A) and neuroblastoma susceptibility in 505 neuroblastoma patients and 1070 controls from four independent hospitals in China. The correlation strengths were determined by using odds ratios (ORs) and corresponding 95% confidence intervals (CIs). Among these SNPs, rs34787247 G>A exhibited a significant association with increased susceptibility in neuroblastoma (GA vs GG: adjusted OR = 1.30, 95% CI = 1.03‐1.64; AA vs GG: adjusted OR = 2.51, 95% CI = 1.36‐4.64, AA/GA vs GG: adjusted OR = 1.42, 95% CI = 1.12‐1.80, AA vs GG/GA: adjusted OR = 2.39, 95% CI = 1.29‐4.42). Furthermore, the combined analysis of risk genotypes revealed that subjects carrying three risk genotypes (adjusted OR = 1.64, 95% CI = 1.02‐2.63) are more inclined to develop neuroblastoma than those without risk genotype, and so do carriers of 1‐4 risk genotypes (adjusted OR = 1.26, 95% CI = 1.01‐1.56). Stratification analysis further revealed risk effect of rs3811464 G>A, rs34787247 G>A and 1‐4 risk genotypes in some subgroups. Haplotype analysis of these four SNPs yields two haplotypes significantly correlated with increased neuroblastoma susceptibility. Overall, our finding indicated that LIN28A SNPs, especially rs34787247 G>A, may increase neuroblastoma risk. 相似文献
20.
Wei B Xu Z Ruan J Zhu M Jin K Zhou D Xu Z Hu Q Wang Q Wang Z 《Molecular biology reports》2012,39(2):1997-2002
Epidemiological studies have evaluated the association between MTHFR 677C>T and 1298A>C polymorphisms and risk of male infertility.
However, the results from the published studies on the association between these two MTHFR polymorphisms and male infertility
risk are conflicting. To derive a more precise estimation of association between the MTHFR polymorphisms and risk of male
infertility, we performed a meta-analysis. A comprehensive search was conducted to identify all case–control studies of MTHFR
polymorphisms and male infertility risk. We used odds ratios (ORs) with 95% confidence intervals (CIs) to assess the strength
of the association. Overall, we found that both 677C>T and 1298A>C polymorphisms were not significantly associated with male
infertility risk. However, in stratified analysis by ethnicity, we found that the 677C>T polymorphism was significantly associated
with the risk of male infertility in Asian population (TT vs. CC: OR = 1.57, 95% CI: 1.05–2.37, P = 0.03; TT vs. TC + CC: OR = 1.40, 95% CI: 1.05–1.86, P = 0.02; TT + TC vs. CC: OR = 1.34, 95% CI: 1.01–1.77, P = 0.04). Although some modest bias could not be eliminated, this meta-analysis suggested that the MTHFR 677T allele might
be a low-penetrant risk factor for male infertility, especially in Asian population. 相似文献