共查询到20条相似文献,搜索用时 31 毫秒
1.
Han CZ Du LL Jing JX Zhao XW Tian FG Shi J Tian BG Liu XY Zhang LJ 《Biological trace element research》2008,126(1-3):38-48
We evaluated the relationship among the leptin receptor (LEPR) gene Gln223Arg polymorphism, body mass index (BMI), waist and hip circumference ratio (WHR), dietary structure, lifestyle, and other biomarkers with breast cancer and determined whether they could be effective for the prevention and treatment of breast cancer. The Gln223Arg polymorphisms in the LEPR gene were investigated in blood deoxyribonucleic acid (DNA) available for 240 breast cancer cases and 500 controls. Genotyping was performed by polymerase chain reaction-restriction fragment length polymorphism. Leptin, insulin were determined by enzyme-linked immunosorbent assays. We found that the serum levels of leptin, insulin, triglyceride (TG), free cholesterol (FCH), apolipoprotain (APO) A1, and BMI were significantly higher in breast cancer cases than the controls, while physical activity was clearly less in breast cancer cases (P < 0.02 approximately P < 0.001, respectively). Moreover, there were significant association between the Gln223Arg genotype and breast cancer risk; homozygotes for AA and heterozygotes for AG,AG + GG genotypes had been proved to increase the risk of breast cancer, and their corresponding odds ratio were 7.14 (95% confidence interval [CI] = 1.92-25.64), 1.33(95% CI = 1.03-2.70), and 2.04 (95% CI = 1.09-3.82). Interestingly, logistic regression analysis showed that LEPR gene Gln223Arg polymorphism and elevated leptin, insulin, TG, FCH, APOA1, WHR, and reduced APOB increased the risk of developing breast cancer, respectively. And, it also suggested that LEPR gene Gln223Arg polymorphisms, elevated leptin, insulin, TG, FCH, APOA1, WHR, and reduced APOB should play a major role in the development of breast cancer. 相似文献
2.
Growing bodies of studies have been conducted on the association of TP53 Arg72Pro polymorphism with susceptibility to ovarian cancer and have yielded conflicting results. Thus, a meta-analysis was
performed to summarize the possible association. 18 case–control studies, including 2,193 ovarian cancer cases and 5,175 controls
were identified. The quality of the studies was assessed according to a predefined scale. The strength of the associations
between TP53 Arg72Pro polymorphism and ovarian cancer was measured by crude odds ratios (ORs) with 95% confidence intervals (CIs). Overall,
no significant association was found between TP53 Arg72Pro polymorphism and ovarian cancer risk when all studies pooled into the meta-analysis in all genetic model. In the
subgroup analysis by ethnicity, still no association of this polymorphism with ovarian cancer risk was obtained for all comparison
models. However, significantly decreased risks of ovarian cancer were found for Arg/Arg versus Arg/Pro+Pro/Pro (OR 0.84, 95%
CI 0.74–0.96) when the analysis was restricted to high quality studies. Conversely, when it was restricted to low quality
studies, significantly increased risks were observed for Arg/Arg versus Pro/Pro (OR 1.58, 95% CI 1.09–2.28) and Arg/Arg+Arg/Pro
versus Pro/Pro: (OR 1.50, 95% CI 1.10–2.06), which might be spurious due to the poor design of these studies. In conclusion,
this meta-analysis suggests that the Arg allele is at a moderately reduced risk for ovarian cancer and this polymorphism might
protect against ovarian carcinogenesis. 相似文献
3.
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
4.
Methionine synthase reductase (MTRR) gene is involved in tumorigenesis by regulating DNA methylation through activation of methionine synthase (MTR). MTRR is polymorphic at nucleotide 66 (A-to-G) and the resulting variant enzyme has a lower affinity for MTR. The reported associations of MTRR A66G polymorphism with cancer risk are contradictory. Therefore, we performed a meta-analysis to better assess the associations,
including 18,661 cases and 27,678 controls from 35 studies. Crude ORs with 95% CIs were used to assess the strength of association
between the MTRR
A66G polymorphism and cancer risk. The pooled ORs were performed for homozygote model (GG vs. AA), heterozygote model (GG vs.
GA), recessive genetic model (GG vs. GA + AA), and dominant genetic model (GG + GA vs. AA), respectively. Overall, results
indicated that the G allele and GG variant genotypes were associated with a significantly increased cancer risk (G vs. A:
OR, 1.039; 95% CI, 1.009–1.078; homozygote model: OR, 1.094; 95% CI, 1.006–1.191). In subgroup analysis by ethnicity, significant
increased risks were found among Asians with G allele (G vs. A: OR, 1.063; 95% CI, 1.011–1.119; homozygote model: OR, 1.189;
95% CI, 1.055–1.341; recessive model: OR, 1.197; 95% CI, 1.068–1.341). For stratification analysis, the cancer types with
fewer than three studies were categorized into “other cancers”, and the results indicated that there was a significant elevated
cancer risk in “other cancers” in all genetic models, not in colorectal cancer, lymphoid leukemia or breast cancer. In summary,
our study suggests that the MTRR A66G polymorphism is a potential biomarker for cancer risk. 相似文献
5.
The published data on the association between xeroderma pigmentosum group D (XPD) Lys751Gln polymorphism and esophageal cancer
(EC) remained controversial. The present meta-analysis of literatures was performed to derive a more precise estimation of
the relationship. A comprehensive literature search was conducted to identify all case–control studies of Lys751Gln polymorphism
and risk for two main types of EC: esophageal adenocarcinoma (EADC) and esophageal squamous cell carcinoma (ESCC). A total
of 12 studies were identified to the meta-analysis, including 2,575 cases (1,294 ESCC and 1,281 EADC) and 4,951 controls (1,891
ESCC and 3,060 EADC). Random-effects or fix-effects model was used according to between-study heterogeneity. The odds ratio
(OR) for the variant homozygous genotype Gln/Gln of the Lys751Gln polymorphism, compared with the wild type homozygote Lys/Lys,
was 1.26, with 95% confidence interval (95% CI) 1.02–1.56, for EADC risk without between-study heterogeneity. When stratified
by ethnicity, statistically significantly elevated risk was found among Chinese (Gln/Gln vs. Lys/Lys: OR 2.45, 95% CI = 1.10–5.44).
However, no significant associations were found between XPD Lys751Gln polymorphism and EC risk when all studies pooled into
the meta-analysis (Lys/Gln vs. Lys/Lys: OR 1.07, 95% CI = 0.88–1.28; Gln/Gln vs.us Lys/Lys: OR 1.25, 95% CI = 0.92–1.71; dominant
model: OR 1.09, 95% CI = 0.90–1.33). In conclusion, this meta-analysis suggests that the Lys751Gln genetic polymorphism may
be a potential biomarker of EC susceptibility in Chinese populations. And a study with the larger sample size is needed to
further evaluate gene–environment interaction on XPD Lys751Gln polymorphism and EC risk. 相似文献
6.
Two leptin receptor single nucleotide polymorphisms, Lys109Arg and Gln223Arg, have been shown to associate with several risk factors for cardiovascular disease. In addition, we have previously shown that Arg109 and Arg223 homozygotes displayed lower intima-media thickness in our well-defined OPERA (Oulu Project Elucidating Risk of Atherosclerosis) study. This current research investigated the impact of these LEPR polymorphisms on cardiovascular events and related death as well as to total mortality in the 19-year follow-up of OPERA. Subjects were randomly selected, middle-aged drug-treated hypertensives and their age- and sex-matched control subjects recruited to the OPERA study between 1990 and 1993. Mortality and hospital events of 1045 subjects were followed up until 2009. A total of 151 coronary heart disease (CHD) and 211 cardiovascular disease (CVD) events or deaths including 58 CHD and 69 CVD deaths occurred. Furthermore, during this follow-up, a total of 165 subjects died. Logistic regression analysis was performed to assess the impact of Lys109Arg and Gln223Arg on the events and death. Further modeling was performed with Cox regression for Lys109Arg. The logistic regression analysis revealed a significant protective impact of Arg109Arg genotype on CHD (OR 0.433; CI 95% 0.217–0.863) and CVD (OR 0.540; CI 95% 0.309–0.942) events or death as well as on total mortality (OR 0.390; CI 95% 0.196–0.775) when adjusted with age, sex and study group. Even after further adjustment with BMI, smoking status, systolic blood pressure and low-density lipoprotein cholesterol, the protective effect of Arg109Arg on CHD events or death and total mortality still remained statistically significant (OR 0.463; CI 95% 0.230–0.931 and OR 0.442; CI 95% 0.218–0.896, respectively). Arg109Arg was also shown to confer protection against CHD mortality (HR 0.224; CI95% 0.055–0.919) and overall mortality (HR 0.413; CI95% 0.218–0.783) also in Cox regression analysis. In conclusion, the Arg109Arg genotype of LEPR seems to be protective from cardiovascular events and death and this phenomenon seems to be independent of the traditional risk factors for atherosclerosis. 相似文献
7.
Published data on the association between β1-adrenergic receptor gene polymorphisms and idiopathic dilated cardiomyopathy (IDCM) risk are inconclusive. To derive a more
precise estimation of the relationship, a meta-analysis was performed. A total of 12 case–control studies including 2642 cases
and 3136 controls provided data on the association between β1-adrenergic receptor gene polymorphisms and susceptibility to IDCM. Overall, no significantly elevated risk was associated
with Arg389Gly polymorphisms for all genetic models. In the subgroup analysis by ethnicity, no statistically increased risk
was found for Gly389Gly versus Arg389Arg (OR 0.73; 95% CI 0.54–0.99; P
h = 0.35) and Gly389Gly versus Arg389Arg + Arg389Gly (OR 0.75; 95% CI 0.55–1.01; P
h = 0.52) among Europeans. Meanwhile, significantly increased risk was found among Asians based on the relatively small sample
size. Further, significantly elevated IDCM risk was associated with Ser49Gly polymorphisms for all genetic models. When stratified
by ethnicity, statistical association was found among Asians for Gly49Gly versus Ser49Ser (OR 4.56; 95% CI 1.36–15.23; P
h = 0.10) and Gly49Gly versus Ser49Ser + Ser49Gly (OR 4.49; 95% CI 1.33–15.15; P
h = 0.12), but not among Europeans. In summary, this meta-analysis suggests that no statistically increased risk was found
between β1-adrenergic receptor gene polymorphisms and susceptibility to IDCM among Europeans. 相似文献
8.
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
9.
To investigate the possible association of P53 codon 72 Arg/Pro polymorphisms with risk of gastric cancer in the high incidence
Hexi area of Gansu province in China. Blood samples from 140 patients with gastric carcinoma and 125 healthy controls were
collected in Hexi area of Gansu province. Polymorphism of P53Arg72Pro was genotyped by PCR-TaqMan. For detection Helicobacter pylori infection, Warhin–Starry staining was used. Three kinds of polymorphisms of P53Arg72Pro were Arg/Arg, Arg/Pro, Pro/Pro. The
frequencies in gastric cancer group were 15.7, 60.0, 24.3%, and the frequencies in healthy controls were 25.6, 54.4, 20.0%,
respectively. P53 codon 72 Pro carrier genotype (Arg/Pro + Pro/Pro) increased risk of gastric carcinoma with an odds ratio
1.840 (95% CI: 1.006–3.387). Helicobacter pylori infection rate was 68.6% in patients group and 50.4% in healthy controls. Helicobacter pylori infection rate in gastric cancer patients was remarkably higher than that in the controls (OR: 2.147, 95% CI: 1.302–3.541,
P = 0.003). Stratification analysis showed that P53 codon 72 Pro carrier genotype with Helicobacter pylori infection was significantly higher in cases than that in the controls (OR: 4.182, 95% CI: 1.850–9.454). P53Arg72Pro polymorphisms
could be a risk factor for gastric cancer in high incidence Hexi area of Gansu Province in China. P53 codon 72 Pro carrier
genotype and Helicobacter pylori positive infection may have a synergistic effect on gastric cancer in high incidence Hexi area of Gansu Province in China. 相似文献
10.
The transmembrane transport of anticancer drugs is mainly regulated by P-glycoprotein encoded by the human multidrug resistance
gene 1 gene (MDR1). Since there were controversies regarding the association between MDR1 C3435T polymorphism and response to chemotherapy among patients with advanced breast cancer, a meta-analysis of the link
was conducted. A total of 7 studies consist of 464 advanced breast cancer patients relating MDR1 C3435T polymorphism to the response of chemotherapy were included in this meta-analysis. The main analysis revealed a lack
of association between the MDR1 C3435T and response to chemotherapy, with odds ratios (ORs) and their corresponding 95% confidence intervals (CIs) of 1.37
(95% CI: 0.78–2.40), 1.17 (95% CI: 0.69–2.01), 1.18 (95% CI: 0.76–1.84) and 1.61 (95% CI: 0.70–3.68) for homozygous comparison,
heterozygous comparison, dominant model and recessive model, respectively. The subgroup analysis by ethnicity did not change
the pattern of results, with ORs of 0.99 (95% CI: 0.11–9.07), 0.68 (95% CI: 0.29–1.60), 0.81 (95% CI: 0.36–1.85) and 1.51
(95% CI: 0.77–2.96), in homozygous comparison, heterozygous comparison, dominant model and recessive model, respectively in
Caucasian, and 1.50 (95% CI: 0.75–3.03), 1.72 (95% CI: 0.85–3.47), 1.59 (95% CI: 0.90–2.80) and 2.29 (95% CI: 0.51–10.35),
respectively in Asian. The available evidence indicates that MDR1 C3435T polymorphism cannot be considered as a reliable predictor of response to chemotherapy in patients with advanced breast
cancer. 相似文献
11.
The common genetic polymorphism for SULT1A1 is Arg213His polymorphism, which may affect the sulfation process of various environmental
carcinogens and thus is suggested to be related to susceptibility of several cancers. However, studies on the association
between SULT1A1 Arg213His polymorphism and cancer susceptibility are inconsistent. To assess the relationship between Arg213His
polymorphism and environmental-related cancers systematically, we performed a meta analysis from 20 case–control studies including
5,915 cases and 7,900 controls. The odds ratios (ORs) and 95% confidence intervals (CIs) were used to estimate the strength
of risk, we found a significant association between SULT1A1 Arg213His polymorphism and environment-related cancers (for dominant
model: OR 1.22, 95% CI 1.07–1.39, P = 0.003). When stratified by ethnicity, a significant risk was observed in Asian cases, compared with controls (for dominant
model: OR 1.69, 95% CI 1.17–2.43, P = 0.005). When we chose only smokers in our analysis, we also found a significantly increased risk between Arg213His polymorphism
and susceptibility of environment-related cancers for participants exposed to a smoking environment. In conclusion, SULT1A1
Arg213His polymorphism, ethnicity, smoking may modulate environment-related cancer risk. Studies on gene–gene interactions
in the sequential or concurrent metabolic pathway and gene-environment interactions need to be further conducted to explore
the susceptibility of cancer occurrence. 相似文献
12.
Many studies have reported the role of COMT Val158Met with breast cancer risk, but the results remained controversial. In
addition, previous meta-analysis on COMT Val158Met showed conflicting results. Hence, we performed a meta-analysis to investigate
the association between breast cancer and COMT Val158Met (30,199 cases and 38,922 controls) in different inheritance models.
When all the eligible studies were pooled into this meta-analysis, there was no evidence of significant association between
breast cancer risk and COMT Val158Met polymorphism in any genetic model (dominant model: odds ratio [OR] = 0.99, 95% confidence
interval [CI] = 0.94–1.04, P value of heterogeneity test [P
h] = 0.009, I
2 = 36.9%; recessive model: OR = 0.97, 95% CI = 0.92–1.02, P
h = 0.044, I
2 = 28.6%; additive model: OR = 0.98, 95% CI = 0.91–1.05, P
h = 0.004, I
2 = 40.4%). However, significant between-study heterogeneity was detected in any genetic model. Hence, we performed the stratified
analysis according to ethnicity, source of controls, menopausal status, and family history. In the stratified analysis by
ethnicity significantly decreased breast cancer risk was observed in Caucasian population (recessive model: OR = 0.96, 95%
CI = 0.92–1.00, P
h = 0.419, I
2 = 3.1%). In conclusion, this meta-analysis indicates that COMT Val158Met polymorphism may be associated with decreased breast
cancer risk in Caucasian population. However, a study with the larger sample size is needed to further evaluated gene-environment
interaction on COMT Val158Met polymorphisms and breast cancer risk. 相似文献
13.
The X-ray repair cross-complementing group 1 (XRCC1) gene, one of over 20 genes that participate in the base excision repair pathway, is thought to account for differences in susceptibility to hepatocellular carcinoma. To assess the relationship between the XRCC1 Arg399Gln polymorphism and the risk of hepatocellular carcinoma (HCC), we performed a meta-analysis. All the relevant studies were extracted from PubMed, Embase, the Chinese biomedicine databases, the Chinese national knowledge infrastructure, and the Wanfang databases (prior to August 2012). The meta-analysis was performed using all eligible studies, which covered a total of 2,554 cases and 3,320 controls, to examine the association between XRCC1 Arg399Gln polymorphism and the risk of HCC. Our analysis suggested that the variant genotypes of the XRCC1 Arg399Gln gene were associated with a significantly increased risk of HCC in a co-dominant model (Arg/Gln vs. Arg/Arg, odd ratios [OR] 1.39, 95 % confidence interval [CI] 1.08–1.79; Gln/Gln vs. Arg/Arg, OR 1.26, 95 % CI 1.04–1.52) and a dominant model (Arg/Gln + Gln/Gln vs. Arg/Arg OR 1.36, 95 % CI 1.07–1.72), whereas no association was observed in the recessive model (Gln/Gln vs. Arg/Gln + Arg/Arg, OR 1.05, 95 % CI 0.91–1.21). The results of the subgroup analysis by ethnicity indicated that the XRCC1 Arg399Gln polymorphism was associated with increased risk of HCC in Asian populations using the co-dominant model (Arg/Gln vs. Arg/Arg, OR 1.41, 95 % CI 1.06–1.87) and the dominant model (Gln/Gln vs. Arg/Gln + Arg/Arg, OR 1.35, 95 % CI 1.03–1.76). Our analysis provides evidence that the XRCC1 Arg399Gln polymorphism may be associated with a higher risk of HCC, especially among Asian populations. 相似文献
14.
Naushad SM Pavani A Digumarti RR Gottumukkala SR Kutala VK 《Molecular biology reports》2011,38(8):4893-4901
In view of growing body of evidence substantiating the role of aberrations in one-carbon metabolism in the pathophysiology
of breast cancer and lack of studies on gene–gene interactions, we investigated the role of dietary micronutrients and eight
functional polymorphisms of one-carbon metabolism in modulating the breast cancer risk in 244 case–control pairs of Indian
women and explored possible gene–gene interactions using Multifactor dimensionality reduction analysis (MDR). Dietary micronutrient
status was assessed using the validated Food Frequency Questionnaire. Genotyping was done for glutamate carboxypeptidase II
(GCPII) C1561T, reduced folate carrier (RFC)1 G80A, cytosolic serine hydroxymethyltransferase (cSHMT) C1420T, thymidylate
synthase (TYMS) 5′-UTR tandem repeat, TYMS 3′-UTR ins6/del6, methylenetetrahydrofolate reductase (MTHFR) C677T, methyltetrahydrofolate-homocysteine
methyltransferase (MTR) A2756G, methyltetrahydrofolate-homocysteine methyltransferase reductase (MTRR) A66G polymorphisms
by using the PCR-RFLP/AFLP methods. Low dietary folate intake (P < 0.001), RFC1 G80A (OR: 1.38, 95% CI 1.06–1.81) and MTHFR C677T (OR: 1.74 (1.11–2.73) were independently associated with
the breast cancer risk whereas cSHMT C1420T conferred protection (OR: 0.72, 95% CI 0.55–0.94). MDR analysis demonstrated a
significant tri-variate interaction among RFC1 80, MTHFR 677 and TYMS 5′-UTR loci (P
trend < 0.02) with high-risk genotype combination showing inflated risk for breast cancer (OR 4.65, 95% CI 1.77–12.24). To conclude,
dietary as well as genetic factors were found to influence susceptibility to breast cancer. Further, the current study highlighted
the importance of multi-loci analyses over the single-locus analysis towards establishing the epistatic interactions between
loci of one-carbon metabolism modulate susceptibility to the breast cancer. 相似文献
15.
RNASEL Asp541Glu and Arg462Gln polymorphisms in prostate cancer risk: evidences from a meta-analysis
Wei B Xu Z Ruan J Zhu M Jin K Zhou D Yan Z Xuan F Zhou H Huang X Zhang J Lu P Shao J 《Molecular biology reports》2012,39(3):2347-2353
Epidemiological studies have evaluated the association between RNASEL Asp541Glu and Arg462Gln polymorphisms and prostate cancer (PCa) risk. However, the results remain inconclusive. To derive a more precise estimation of the association between RNASEL polymorphisms and PCa risk, we performed a meta-analysis based on nineteen case?Ccontrol studies. We used odds ratios (ORs) with 95% confidence intervals (CIs) to assess the strength of the association. Overall, we found that both Asp541Glu and Arg462Gln polymorphisms were not associated with PCa risk (for Asp541Glu polymorphism: Glu/Glu vs. Asp/Asp: OR 1.17, 95% CI: 0.95?C1.45, P?=?0.13; Glu/Asp vs. Asp/Asp: OR 1.02, 95% CI: 0.92?C1.14, P?=?0.70; for Arg462Gln polymorphism: Gln/Gln vs. Arg/Arg: OR 0.98, 95% CI: 0.88?C1.08, P?=?0.62; Gln/Arg vs. Arg/Arg: OR 0.97, 95% CI: 0.91?C1.04, P?=?0.53). The insignificant association was maintained in the dominant and the recessive genetic models. In subgroup analyses, the significant association was not detected in Caucasian populations. However, we found the significant association of RNASEL Asp541Glu polymorphism with sporadic PCa (Glu/Glu vs. Asp/Asp: OR 1.29, 95% CI: 1.04?C1.59, P?=?0.02; Glu/Asp vs. Asp/Asp: OR 1.24, 95% CI: 1.03?C1.50, P?=?0.03). In conclusion, we found that these RNASEL polymorphisms were not related to overall PCa risk, especially in Caucasians. However, in subgroup analyses we found a suggestion that RNASEL 541Gln allele might be a low-penetrent risk factor for sporadic PCa. 相似文献
16.
Published data on the association of vascular endothelial growth factor (VEGF) −1154G>A polymorphism with cancer risk is inconclusive.
To derive a more precise estimation of association between VEGF −1154G>A polymorphism and the risk of cancer, we performed
a meta-analysis of 7,071 cancer cases and 7,693 controls from 16 published case–control studies. Our meta-analysis didn’t
reveal an association between VEGF −1154G>A polymorphism and overall cancer risk (GG vs. AA: OR: 1.08, 95% CI: 0.96–1.20;
GA vs. AA: OR: 1.04, 95% CI: 0.93–1.17; recessive model: GG+GA vs. AA: OR: 1.06, 95% CI: 0.95–1.18; dominant model: GG vs.
GA+AA, OR: 1.11, 95% CI: 1.00–1.24). Nevertheless, for non-Caucasians, GG homozygote may have higher cancer risk compared
with either A carriers (OR: 1.58, 95% CI: 1.12–2.23) or AA homozygote (OR: 1.43, 95% CI: 1.17–1.76). No significant heterogeneity
was detected except in the dominant model and “prostate cancer” subgroup analysis. More studies with larger samples are warranted
to confirm these findings. 相似文献
17.
Background
The Arg399Gln polymorphism in the X-ray cross-complementing group 1 (XRCC1) had been implicated in cancer susceptibility. The previous published data on the association between XRCC1 Arg399Gln polymorphism and cancer risk remained controversial.Methodology/Principal Findings
To derive a more precise estimation of the association between the XRCC1 Arg399Gln polymorphism and overall cancer risk, we performed a meta-analysis of 297 case-control studies, in which a total of 93,941 cases and 121,480 controls were included. Overall, significantly increased cancer risk was observed in any genetic model (dominant model: odds ration [OR] = 1.04, 95% confidence interval [CI] = 1.01–1.07; recessive model: OR = 1.08, 95% CI = 1.03–1.13; additive model: OR = 1.09, 95% CI = 1.04–1.14) when all eligible studies were pooled into the meta-analysis. In further stratified and sensitivity analyses, significantly elevated hepatocellular and breast cancers risk were observed in Asians (dominant model: OR = 1.39, 95% CI = 1.06–1.84) and in Indians (dominant model: OR = 1.64, 95% CI = 1.31–2.04; recessive model: OR = 1.94, 95% CI = 1.09–3.47; additive model: OR = 2.06, 95% CI = 1.50–2.84), respectively.Conclusions/Significance
This meta-analysis suggests the participation of XRCC1 Arg399Gln is a genetic susceptibility for hepatocellular cancer in Asians and breast cancer in Indians. Moreover, our work also points out the importance of new studies for Arg399Gln association in some cancer types, such as glioma, gastric cancer, and oral cancer, where at least some of the covariates responsible for heterogeneity could be controlled, to obtain a more conclusive understanding about the function of the XRCC1 Arg399Gln polymorphism in cancer development. 相似文献18.
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
19.
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
20.
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