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1.
Zeynep Ermis Karaali Seyma Sozen Melis Yurdum Canan Cacina Bahar Toptas Ozlem Gok Bedia Agachan 《Molecular biology reports》2010,37(7):3615-3619
Inflammation is a crucial component of coronary atherosclerosis and myocardial infarction (MI). Chemokine receptors are important
modulators of inflammation. Polymorphisms in genes coding for chemokine receptors, CCR2 and CCR5, have been studied as genetic markers of coronary artery
disease. In the present study, we investigated whether genetic variants of CCR2-V64I and CCR5-delta32 chemokine receptors
have any effect on the development of myocardial infarction. A total of 146 MI patients and 202 control subjects were genotyped
for CCR2 and CCR5. CCR2-V64I genotypes were not significantly different between patients with MI and controls (P > 0.05). CCR5-delta32 genotype distribution in cases was significantly different from that of controls (P = 0.042). The CCR5-delta32 wt/deletion genotype frequencies for controls and cases were 0.10 and 0.19, respectively and individuals
with CCR5-delta32 wt/deletion genotype had a 2.13-fold increased risk of myocardial infarction (P = 0.0013). Individuals carrying the CCR5-delta32 heterozygote or homozygous variant genotype (deletion/deletion + wt/deletion)
had a 1.96-fold increased risk of myocardial infarction compared with the wild-type genotype (wt/wt) (p: 0.016). In conclusion,
our data have suggested that genetic variant of CCR5 might be associated with the development of MI. Further larger sample
size studies are required to confirm our findings. 相似文献
2.
Rahimi Z Ahmadian Z Akramipour R Vaisi-Raygani A Rahimi Z Parsian A 《Molecular biology reports》2012,39(3):2195-2200
In order to determine the influence of polymorphism in thymidylate synthase (TS 28-bp repeat) and methionine synthase (MS
A2756G) genes on the susceptibility to acute lymphoblastic leukemia (ALL), 73 children with ALL and 128 age and sex matched
unrelated healthy individuals from the Kermanshah Province of Iran were screened. The genotyping of TS 28-bp repeat and MS
A2756G polymorphisms were performed by polymerase chain reaction (PCR) and PCR–RFLP, respectively. The frequency of TS 2R
allele in patients and controls were 41.5 and 38%, respectively (Odds ratios (OR) = 1.13, 95%CI 0.73–1.74, P = 0.56). The allelic frequency of G allele of MS was higher (25%) in patients compared with healthy subjects (23%) (OR = 1.09,
95%CI 0.67–1.75, P = 0.71). Considering MS AA and TS 3R3R genotypes as reference indicated that individuals with MS GG + TS 2R2R genotypes have
1.3-fold increase in the risk of ALL (OR = 1.3, 95%CI 0.6–2.7, P = 0.5). Our results showed that neither TS 28-bp repeat nor MS A2756G polymorphisms are risk factors for susceptibility to
ALL in Western Iran. 相似文献
3.
The aim of this study was to determine whether the protein tyrosine phosphatase nonreceptor 22 (PTPN22) C1858T polymorphism
confers susceptibility to rheumatoid arthritis (RA) in populations with different ethnicities. A meta-analysis was conducted
on the PTPN22 C1858T polymorphism involving eighteen studies, which in total contained 20344 RA patients and 21828 controls.
Meta-analysis revealed an association between the PTPN22 C1858T polymorphism T allele and RA in all subjects (odds ratio [OR] = 1.637,
95% confidence interval [CI] = 1.514–1.770, P < 0.001). After stratification by ethnicity, analysis indicated that the PTPN22 C1858T polymorphism T allele was significantly
associated with RA in Europeans and Non-Europeans (OR = 1.587, 95% CI = 1.486–1.696, P < 0.001; OR = 1.748, 95% CI = 1.274–2.398, P < 0.001). Meta-analysis of the CT + TT genotype showed the same result patterns as that shown by the PTPN22 C1858T polymorphism
T allele. Furthermore, a direct comparison between rheumatoid factor (RF)-positive and -negative subjects revealed a significant
association with the T allele in RA patients with RF, but not in subjects without RF. In conclusion, this meta-analysis confirms
that the PTPN22 C1858T polymorphism is associated with RA susceptibility in different ethnic groups, especially in Europeans,
and the PTPN22 C1858T polymorphism T allele is significantly more prevalent in RF-positive patents than in RF-negative patients. 相似文献
4.
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
5.
Munshi A Sharma V Kaul S Al-Hazzani A Alshatwi AA Shafi G Koppula R Mallemoggala SB Jyothy A 《Molecular biology reports》2012,39(2):1677-1682
Genetic variants of cytochrome P450 4F2 (CYP4F2) gene have been suggested to be risk factors for hypertension, cardiovascular
diseases and stroke. In the present case–control study we investigated the association of 1347 G/A polymorphism (rs2108622)
in the 11th exon region of CYP4F2 gene with hypertension, ischemic stroke and stroke subtypes classified according to TOAST
(Trial of Org 10172 in Acute Stroke Treatment) classification. Five hundred and seven stroke patients (hypertensives: normotensives = 279:228)
and four hundred and eighty seven, age and sex matched controls (males: females = 356:131) (hypertensives: normotensives = 148:339)
were involved in the study. The genotypes were determined by PCR-RFLP technique. Genotypes were confirmed by subjecting the
PCR products to sequencing. Significant difference was observed in the genotypic distribution and allelic frequency between
the stroke patients and healthy controls. AA genotype and A allele associated significantly with stroke and hypertension [P = 0.009; OR = 1.59 (95% CI = 1.119–2.283) and P = 0.010; OR = 1.26 (95% CI = 1.056–1.502); P = 0.01; OR = 1.58 (95% CI = 1.11–2.272) and P = 0.010; OR = 1.25(95% CI = 1.054–1.504) respectively]. A stepwise logistic regression analysis confirmed these findings.
To establish that this polymorphism is associated with stroke independent of hypertension; we compared stroke patients without
hypertension with normotensive controls. Significant difference was observed in genotypic distribution and allelic frequency
between the two groups (P = 0.001 and 0.002 respectively). Evaluating the association of this polymorphism with stroke subtypes we found significant
associations with cardioembolic stroke (P < 0.001). In conclusion our study suggests that 1347A allele of CYP4F2 gene is an important risk factor for hypertension
and ischemic stroke. 相似文献
6.
Zhang R Duan L Jiang Y Zhang X Sun P Li J Zhang M Tang G Wang X Li X 《Molecular biology reports》2011,38(8):5079-5084
Previously published analyses of the association between the interleukin 7 receptor (IL7R) T244I polymorphism (rs6897932) and multiple sclerosis (MS) have yielded conflicting results. We performed a meta-analysis
to assess whether the combined data showed this association, and to investigate its effect size. We analyzed 10 studies identified
from PubMed (12,185 MS patients and 15,855 controls) and calculated the odds ratios (ORs) and 95% confidence intervals (CIs)
for the C-allele, the C/C genotype (recessive effect) and the C/C + C/T (dominant effect) genotype. Heterogeneity within and
between studies was observed: allele C: Q = 30.86, P = 0.002; genotype C/C: Q = 30.28, P = 0.003. Using a random-effects model, the C-allele and the C/C genotype were associated with MS (OR = 1.11, 95% CI = 1.04–1.19,
P = 0.001 for the C-allele; OR = 1.15, 95% CI = 1.06–1.24, P = 0.0009 for the C/C genotype). The C/C + C/T genotype was also associated with MS using a fixed-effects model (OR = 1.15,
95% CI = 1.05–1.26, P = 0.003). There was no significant publication bias among the selected studies according to the funnel plot. We also performed
the analysis on a European subgroup. This revealed an association between IL7R T244I and MS (P < 0.00001 for the C-allele and the C/C genotype; P = 0.0004 for the C/C + C/T genotype), no heterogeneity was observed (allele C: P = 0.07; genotype C/C: P = 0.10). In conclusion, the meta-analysis demonstrated that the IL7R T244I polymorphism was associated with susceptibility to MS. 相似文献
7.
Until now, there were several studies evaluating the association between the polymorphisms in the IGFBP3 gene and cancer risk in diverse populations and in multiple types of cancer, but their outcomes have been contradictory and
need to be investigated further. Here, we performed a meta-analysis from all eligible case–control studies to address the
association of IGFBP3 A-202C and Gly32Ala polymorphisms to cancer. 20 articles including 41 studies for A-202C variant including 28,322 cancer
patients and 36,772 healthy controls and six articles for Gly32Ala variant including 4,477 cases and 5,443 controls were selected
in our analysis. Overall, A-202C polymorphism was appeared to be a risk factor of cancer (OR = 0.98, P = 0.05). A allele of IGFBP3 A-202C SNP was significantly less common in the cancer patients than in controls and AA genotype significantly decreased
the cancer risk in additive genetic model when comparing to CC genotype (OR = 0.93, P = 0.004). Another SNP, Gly32Ala, seemed to be in linkage equilibrium with A-202C SNP. However, no significance was found
when we analyzed the relation of cancer risk and Gly32Ala polymorphism (OR = 0.93, P = 0.36). Further, we compared the distributions of A-202C SNP in different types of cancer, significant association was found
in additive genetic model in breast cancer (OR = 0.93, P = 0.01) and prostate cancer (OR = 0.88, P = 0.05). In the analysis of the variants in different population, A-202C variant was significantly associated with cancer
risk in Africans (OR = 0.90, P = 0.05), but not in Caucasians (OR = 0.98, P = 0.12) or in Asians (OR = 1.03, P = 0.61). These results indicated that polymorphisms of IGFBP3 might have different effect in different types of cancer and different population. Further large study combining both IGFBP3 A-202C and Gly32Ala SNPs on different types of cancer in different populations were needed to validate former results. 相似文献
8.
Ruiping Hou Bangwei Cao Zhongdong Chen Yong Li Tao Ning Chunhui Li Changqing Xu Ziping Chen 《Molecular biology reports》2010,37(1):515-520
Cytotoxic T lymphocyte-associated antigen-4 (CTLA-4) was widely accepted as a pivotal molecule in downregulating T-cell mediated immune responses. In this study we investigated
the polymorphisms which would impact the CTLA-4 gene expression and function to assess the association with the risk of gastric cancer. 205 gastric cancer patients and 262
healthy controls were included in the case-control study. PCR and restriction fragment length polymorphism (RFLP) methods
were performed to identify the +49A/G and promoter −1661A/G polymorphisms. The promoter −1772T/C polymorphism was detected
by PCR amplification refractory mutation system (ARMS) technique. A significant difference was observed between case and control
groups. The frequency of +49A/G polymorphism AG and −1661A/G polymorphism GG genotype were significantly higher in patients
than in controls (OR = 2.15, OR = 1.88, respectively). No significant difference was found in the allelic frequency of −1772T/C
polymorphism between cases and controls (P = 0.478). By the haplotype analysis, logistic regression showed the frequency of haplotype A (GAT) and D (AGT) in the case
group revealed significant difference compared with in control group(OR = 2.00, P < 0.001; OR = 1.62, P = 0.043, respectively). Our findings implied the genetic variations within CTLA-4 gene would be a critical risk factor to the susceptibility of gastric cancer. 相似文献
9.
Xing Gu Peng Qi Feiguo Zhou Qiang Ji Hao Wang Tonghai Dou Yunpeng Zhao Chunfang Gao 《Human genetics》2010,127(1):75-81
Corticotropin-releasing hormone receptor 2 (CRHR2) plays a role in both the central nervous system (CNS) and the peripheral
nervous system. CRHR2 together with its ligands, urocortins (Ucns) and corticotropin-releasing hormone (CRH), functions as
a mediator of inflammatory response and inhibitor of angiogenesis. Recently, it has been reported to be expressed in many
human cancers. An association between rs2267716 polymorphism in the CRHR2 gene and susceptibility to hepatocellular carcinoma (HCC) was found in patients with chronic hepatitis C virus (HCV) infection.
In the present study we analyzed, using a polymerase chain reaction–ligation detection reaction (PCR–LDR), the rs2267716 polymorphism
in 364 hepatitis B virus (HBV)-related HCC patients, 196 non-HCC patients with HBV infection, and 404 healthy controls. The
aim was to detect the possible association of this single-nucleotide polymorphism (SNP) with susceptibility to HBV-related
HCC. Significant differences of rs2267716 allele were detected between HBV-related HCC patients and healthy controls (OR = 1.55,
95% CI 1.13–2.15, P = 0.007) or non-HCC patients with HBV infection (OR = 1.61, 95% CI 1.13–2.31, P = 0.009). These results suggest that the rs2267716 polymorphism in the CRHR2 gene might influence the risk of developing HCC in patients with HBV infection in Chinese population. 相似文献
10.
Mohammadnejad Z Ghanbari M Ganjali R Afshari JT Heydarpour M Taghavi SM Fatemi S Rafatpanah H 《Molecular biology reports》2012,39(2):831-837
Type 1 diabetes mellitus (T1DM) is one of the T-cell mediated autoimmune diseases and vitamin D suppresses activation of T-cell
and has immunomodulatory effects. In this study the association between four vitamin D receptor (VDR) gene polymorphisms,
at positions FokI, BsmI, ApaI and TaqI, and susceptibility to T1DM was investigated. We assessed 87 Iranian patients with
T1DM and one hundred healthy controls with no history of diabetes or other autoimmune diseases. Our results demonstrated that
genotypes frequency of the TaqI VDR polymorphism differed significantly between T1DM patients and controls, TT genotype and
T allele was more frequent in healthy controls compared with TIDM patients (P = 0.003; OR = 0.51, 95% CI = 0.31–0.84). Therefore, allele t is the risk-allele for developing TIDM in this study. No significant association was observed
between others VDR SNPs and disease susceptibility. In conclusion, our case-control study indicated that the VDR TaqI polymorphism
is associated with TIDM in Iranian population. 相似文献
11.
Chemokines regulates the trafficking of leukocytes to the site of inflammation hence may be implicated in cardiac events.
Currently no consistent effects have been revealed their role in acute myocardial infarction (MI). The aim of current study
was to investigate the impact of human chemokine receptor genetic variants, CCR5-Δ32 insertion/deletion, CCR5-59029-A/G, CX3CR1-V249I
and CX3CR1-T280 M on acute MI. 230 acute MI and 300 controls were examined. Patients carrying CCR5-Δ32 genotype were at three
times higher risk of developing MI odds ratio (OR, 3.24, CI 1.127–9.356, P = 0.04). Significant association was found with risk of acute MI in recipients who possessed homozygous 59029-A allele (OR
1.47, CI 1.03–2.09, P = 0.03). While CX3CR1-I249 and M280 were found to be protective in MI patients with OR 0.46, CI 0.32–0.66, P < 0.0001 and OR 0.36, CI 0.24–0.55, P < 0.0001, respectively. It might be possible that risk of acute MI is associated with genetic variation in chemokine receptors,
i.e., CCR5 and CX3CR1. 相似文献
12.
Ahmed W Malik M Saeed I Khan AA Sadeque A Kaleem U Ahmed N Ajmal M Azam M Qamar R 《Molecular biology reports》2011,38(4):2541-2548
A case–control association study on 229 Myocardial Infarction (MI) patients and 217 healthy controls was carried out to determine
the role of tissue-plasminogen activator (t-PA) (Alu-repeat insertion (I)/deletion (D)) and plasminogen activator inhibitor
(PAI-1) (4G/5G insertion/deletion) polymorphisms with MI in the Pakistani population. In MI patients the genotype distribution
of the PAI-1 gene was not found to be different when compared with the unaffected controls (P > 0.05, χ2 = 1.03). The risk allele 4G was also not associated with MI (P > 0.05, χ2 = 0.46, odds ratio (OR) = 1.1 (95% confidence interval (CI) = 0.84–1.43), P > 0.05). Similarly, the genotype frequencies of t-PA I/I, I/D and D/D were not different from the unaffected controls (P > 0.05, χ2 = 1.60), and the risk allele “I” was not found to be associated with MI (P > 0.05, χ2 = 1.35, OR = 0.86 (95% CI = 0.66–1.11), P > 0.05). However, when the data were distributed along the lines of gender a significant association of the 4G/4G PAI-1 genotype
was observed with only the female MI patients (P < 0.05, z-test = 2.21). When the combined genotypes of both the polymorphisms were analyzed, a significant association of
MI was observed with the homozygous DD/4G4G genotype (P < 0.01, z-test = 2.61), which was specifically because of the female samples (P = 0.01, z-test = 2.53). In addition smoking (P < 0.001, χ2 = 13.52, OR = 3.45 (95% CI = 1.77–6.94)), diabetes (P < 0.001, χ2 = 22.45, OR = 8.89 (95% CI = 2.96–29.95)), hypertension (OR = 7.76 (95% CI = 2.88–22.68), P < 0.001) family history (P < 0.001, χ2 = 13.72, OR = 3.7 (95% CI = 1.71–8.18)) and lower HDL levels (P < 0.05) were found to be significantly associated with the disease. In conclusion the PAI-1 gene polymorphism was found to
have a gender specific role in the female MI patients. 相似文献
13.
Yang Li Kefu Tang Zhao Zhang Ming Zhang Zhen Zeng Zangdong He Lin He Chunling Wan 《Molecular biology reports》2011,38(5):3243-3252
In the past decade, a number of case–control studies have been carried out to investigate the relationship between the ApoE
polymorphism and diabetic nephropathy. However, the results have been inconclusive. To investigate this inconsistency, we
performed a meta-analysis of all available studies dealing with the relationship between the ApoE polymorphism and DN. The
23 studies in the meta- analysis included 6,012 diabetic patients with (n = 2,979) and without (n = 3,033) DN. The ApoE ε2 allele was significantly associated with DN (OR = 1.64, 95% CI: 1.26–2.13; P(Z) = 0.00027), whereas the ε4 allele was non-significantly associated with DN (OR = 0.93, 95% CI: 0.78–1.11; P(Z) = 0.418). However, significant heterogeneity was detected. In further subgroup analyses, genotyping methods, outcome of
cases and duration of diabetes in controls were found to explain some of the heterogeneity. Genotypic analysis also found
a strong association between the ε2 carriers and DN (OR = 1.61, 95% CI: 1.22–2.13; P(Z) = 0.001) and indicated that ε4 tended to have a marginally significant protective effect for DN (OR = 0.82, 95% CI: 0.65–1.03;
P(Z) = 0.085). The results of our meta-analysis support a genetic association between the ApoE polymorphism and DN. ε2 increases
the risk of DN in diabetes patients, while ε4 trends to be protective. These findings may have implications for therapeutic
intervention in diabetic nephropathy. 相似文献
14.
The association of the two ERCC polymorphisms, Asp312Asn and Lys751Gln, with lung cancer risk remains controversial and inconclusive.
To better evaluate the potential role of the two polymorphisms and interaction with tobacco smoking in lung cancer susceptibility
presented in diverse populations, we have conducted a meta-analysis based on 26 studies from 24 publications which included
analyses of Asp312Asn (7121 cases, 8962 controls) and Lys751Gln (8396 cases, 10510 controls) polymorphisms. Overall, significantly
elevated lung cancer risk was associated with ERCC2 312Asn allele(homozygous model: OR = 1.20[1.05–1.36], P = 0.006; recessive model: OR = 1.20[1.06–1.35], P = 0.004) and 751Gln allele(homozygous model: OR = 1.31[1.17–1.46], P < 0.00001; heterozygous model: OR = 1.11[1.04–1.19], P = 0.003; recessive model: OR = 1.23[1.11–1.37], P < 0.0001; dominant model: OR = 1.15[1.08–1.23], P < 0.0001). In ethnic subgroup analyses, significantly increased risk was associated with ERCC2 312Asn allele for both Caucasians
and Asians, and 751Gln allele for both Caucasians and Latino-Americans. When stratified by smoking status, significantly elevated
risk of both polymorphisms for never-smokers was detected (dominant model, OR = 1.46[1.09–1.95] and 1.57[1.19–2.08], P = 0.01 and 0.002, respectively). In conclusion, this meta-analysis suggests that the two ERCC2 polymorphisms may contribute
to lung cancer susceptibility serving as low-penetrance risk factors. Extremely large-scale evidence would be necessary to
confirm the effects on ethnically specific populations and gene-environment interactions. 相似文献
15.
Ziping Chen Chuanzhen Zhang Changqing Xu Kun Li Ruiping Hou Danping Li Xiaoli Cheng 《Molecular biology reports》2011,38(3):1507-1513
DNA repair capacity (DRC) can be altered based on sequence variations in DNA repair genes, which may result in cancer susceptibility.
The current study was to evaluate the association between genetic polymorphisms, including associated haplotypes of xeroderma
pigmentosum complementary group D (XPD), and individual susceptibility to gastric cancer. Two-hundred-eight patients with
gastric cancer and 339 healthy controls were enrolled in this study. Their genomic DNA was extracted from peripheral blood
leukocytes. The genotypes at exon 6, 10 and 23 were identified by polymerase chain reaction (PCR). Unconditional logistic
regression model was used to analyze the effects of the polymorphisms, including the corresponding haplotypes, on the susceptibility
to develop gastric cancer. The proportion of genotypes GA or AA at exon 10 in cases was showed to be significantly higher
than that in controls (P < 0.01, P < 0.01, respectively). The risk of genotype GA or AA carriers to develop gastric cancer was simultaneously much higher (OR = 3.38,
95% CI 2.30–4.95; OR = 6.13, 95% CI 2.45–15.31, respectively). The allele A at exon 10 was also observed to manifest a substantially
higher frequency in cases compared to controls (P < 0.01), which might indicate an increased tendency to gastric cancer (OR = 2.40, 95% CI 1.81–3.17). No significant differences
were found in the distribution of genotypes at exon 6 or 23 between the two groups (P = 0.23, P = 0.52; P = 0.44, P = 0.56, respectively). By haplotype analysis, haplotype AAA could individually increase incidence of gastric cancer (P < 0.01, OR = 3.39, 95% CI 2.21–5.21). In contrast, haplotypes CGA and AGA were showed a decline in gastric cancer susceptibility
(OR = 0.67, 95% CI 0.46–0.97; OR = 0.58, 95% CI 0.41–0.83, respectively). The rest of haplotypes made no statistically significant
difference between cases and controls. Taken together, this study demonstrates that the genetic variation at exon 10 and haplotype
AAA may be contributing factors in developing gastric cancer. 相似文献
16.
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
17.
Saedi M Vaisi-Raygani A Khaghani S Shariftabrizi A Rezaie M Pasalar P Rahimi Z Pourmotabbed T 《Molecular biology reports》2012,39(1):555-562
The Matrix metalloproteinas-9 functional promoter polymorphism 1562C>T may be considered an important genetic determinant
of early-onset coronary artery disease (ECAD). In this study, association between MMP-9 1562C>T allele with plasma MMP-9 activity,
homocysteine and lipid–lipoproteins level and ECAD in Iranian subjects was investigated. This case–control study consisted
of 53 ECAD patients (age < 55 years) and unrelated late-onsets CAD (age > 70 years) who angiographically had at least 50%
stenosis. MMP-9 1562C>T polymorphism was detected by PCRRFLP, plasma MMP-9 activity, serum lipid and homocysteine levels were
determined by gelatin gel zymography, enzyme assay and by HPLC, respectively. The presence of MMP-9 1562C>T allele was found
to be associated with ECAD (OR = 3.2, P = 0.001). The ECAD patients with MMP-9 1562C>T allele had higher MMP-9 activity (P = 0.001), LDL-C (P = 0.045), TC (P = 0.02) and homocysteine (P = 0.01) levels than the LCAD subjects. MMP-9 1562C>T allele is a risk factor for ECAD. The carriers of this allele have high
levels of MMP-9 activity, LDL-C, TC and homocysteine (P = 0.01), thus, are more likely to develop myocardial infarction and CAD at young age (less than 55 years). 相似文献
18.
Isabelle Morard Sophie Clément Alexandra Calmy Alessandra Mangia Andrea Cerny Andrea De Gottardi Meri Gorgievski Markus Heim Raffaele Malinverni Darius Moradpour Beat Müllhaupt David Semela Stéphanie Pascarella Pierre-Yves Bochud Franco Negro 《PloS one》2014,9(9)
Background
The CCR5 receptor, expressed on Th1 cells, may influence clinical outcomes of HCV infection. We explored a possible link between a CCR5 32-base deletion (CCR5delta32), resulting in the expression of a non-functioning receptor, and clinical outcomes of HCV infection.Methods
CCR5 and HCV-related phenotypes were analysed in 1,290 chronically infected patients and 160 patients with spontaneous clearance.Results
Carriage of the CCR5delta32 allele was observed in 11% of spontaneous clearers compared to 17% of chronically infected patients (OR = 0.59, 95% CI interval 0.35–0.99, P = 0.047). Carriage of this allele also tended to be observed more frequently among patients with liver inflammation (19%) compared to those without inflammation (15%, OR = 1.38, 95% CI interval 0.99–1.95, P = 0.06). The CCR5delta32 was not associated with sustained virological response (P = 0.6), fibrosis stage (P = 0.8), or fibrosis progression rate (P = 0.4).Conclusions
The CCR5delta32 allele appears to be associated with a decreased rate of spontaneous HCV eradication, but not with hepatitis progression or response to antiviral therapy. 相似文献19.
Kordi-Tamandani DM Hashemi M Sharifi N Kaykhaei MA Torkamanzehi A 《Molecular biology reports》2012,39(2):937-943
Paraoxonase-1 (PON1), a high-density lipoprotein (HDL) associated enzyme, is involved in the metabolism and detoxification
of insecticides and pesticides. Three polymorphisms within the PON1 gene affect the enzyme activity. Two of these (L55M and Q192R) are located at the coding region and the third (–107C/T) is
in promoter region. We performed a case–control study in order to elucidate the possible contribution of variability within
PON1 at three mentioned positions to the risk of MS in a South-East Iranian population. DNA was isolated from peripheral blood
of patients (N = 119) with MS and healthy controls (N = 201). Allelic polymorphisms at positions Q192R, L55M and –107C/T in the PON1 gene were studied by Amplification Refractory Mutation System (ARMS)-PCR. It was observed that genotypes RR and QR + RR of Q192R locus significantly increased the risk of MS (OR = 2; 95% CI: 1.17–3.40, P = 0.0001 and OR = 1.62; 95% CI: 1.0–2.63; P = 0.05, respectively). The risk in patients with MM and LM + MM genotypes at the L55M locus was marginal (OR = 1.33; 95% CI: 0.68–1.85; P = 0.34 and OR = 1.12; 95% CI: 0.68–1.85; P = 0.73 respectively). The CC genotype at –107C/T locus also increased the risk of metabolic syndrome, but was not significant.
This association was somewhat stronger when combined genotypes at Q192R and L55M loci were analyzed (OR = 3.30; 95% CI: 1.34–8.24;
P = 0.007). Our results, in this first study, provide evidence for association of PON1 gene polymorphisms with the risk for metabolic syndrome. 相似文献
20.
Umar M Upadhyay R Khurana R Kumar S Ghoshal UC Mittal B 《Molecular biology reports》2012,39(2):1153-1162
Genetic variants in p53 and in its homologue p73 may modulate Esophageal Cancer (EC) risk because they are supposed to influence cell cycle progression, apoptosis and DNA
repair. Therefore, we aimed to evaluate the association of p53 intron3 16 bp duplication and p73 G4C14-to-A4T14 polymorphisms with susceptibility to EC in a northern Indian population in 255 EC patients and 255 age and sex matched healthy
controls. We found that p53 intron3 16 bp duplication polymorphism was not associated with EC and its clinical characteristics. However, p73 G4C14-to-A4T14 polymorphism was associated with significant higher risk of EC (OR = 1.74, 95% CI = 1.16–2.60, P = 0.007) in an allele dose-dependent manner (Ptrend = 0.0047). Stratification of subjects on the basis of clinical characteristics showed that p73 AT genotype carriers were at significant increased risk of developing esophageal squamous cell carcinoma (OR = 1.78, 95% CI = 1.18–2.67,
P = 0.006) at middle third tumor location (OR = 1.87, 95% CI = 1.18–2.97, P = 0.007) with lymph node metastasis (OR = 1.77, 95% CI = 1.04–3.02, P = 0.035). No interaction with environmental risk factors was observed with any of the studied polymorphisms. In summary,
p73 G4C14-to-A4T14 polymorphism but not the p53 intron3 16 bp duplication polymorphism is associated with EC and its clinical characteristics in northern Indian population. 相似文献