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Association between Single Nucleotide Polymorphisms in  Interleukin-6 Gene and Periodontal Disease:  A Systematic Review and Meta-analysis

Association between Single Nucleotide Polymorphisms in Interleukin-6 Gene and Periodontal Disease: A Systematic Review and Meta-analysis

The Cochrane Library, Medline-PubMed, ISI Web of Knowledge, EMBASE, VHL (Virtual Health Library), and gray literature (SIGLE) databases were searched for articles published in English. The main meSH headings and keywords used were: ‘periodontitis’ or ‘periodontal disease’ or ‘aggressive periodontitis’ or ‘chronic periodon- titis’ combined with ‘SNP’ or ‘interleukin-6’ or ‘genotype’ or ‘cytokines’. Suitable modiications in the keywords were done to follow the syntax rules of each database. If the abstract contained insuficient information to allow decision making with regard to inclusion or exclusion, the full article was obtained and reviewed before deciding. Any disagreement regarding article selection was solved by discussion. The selected articles were then carefully read for quality assessment and control of bias and for data extraction. In addiction, the reference lists of the included articles, recent reviews and meta-analyses were manually searched.
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Lee mas

Lack of an association between two BER gene polymorphisms and breast cancer risk: a meta-analysis.

Lack of an association between two BER gene polymorphisms and breast cancer risk: a meta-analysis.

Breast cancer is currently the most common cancer and one of the main causes of cancer-related death in the world, which has become a major public health challenge [1]. It is a multifactorial disease caused by complex genetic and environmental factors [2]. Genetic variation in DNA repair genes can cause altered DNA repair function, resulting in accumulation of DNA damage, followed by cell apoptosis or unregulated cell growth and cancer. Individual variations in DNA damage and repair have been associated with breast cancer susceptibility and highlight the importance of DNA damage/repair in the development of the disease. Among DNA repair systems, the base excision repair (BER), which is an important pathway responsible for the repair of base damage and single strand breaks caused by X-rays, oxygen radicals, and alkylating agents, has been associated with risk of cancers [3–6].
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Association of three common single nucleotide polymorphisms of ATP binding cassette G8 gene with gallstone disease: a meta-analysis.

Association of three common single nucleotide polymorphisms of ATP binding cassette G8 gene with gallstone disease: a meta-analysis.

The associations between genotypes/alleles of Apo E polymor- phism with GSD were evaluated by using the software Stata/SE 11.0(StataCorp LP, College Station, USA). In the meta-analysis, we used the random-effects model with the method of DerSimo- nian & Laird to bring the individual effect-size estimates together. The estimate of heterogeneity was taken from the Mantel- Haenszel model [25]. Heterogeneity was assessed by the I 2 statistic, which was documented for the percentage of the observed between-study variability due to heterogeneity rather than chance with the ranges of 0 to 100% [I 2 = 0–25%, no heterogeneity; I 2 = 25–50%, moderate heterogeneity; I 2 = 50–75%, large hetero- geneity; I 2 = 75–100%, extreme heterogeneity] [26]. Publication bias was evaluated by using funnel plots and the Egger test [27]. The biochemical and gene expression data were expressed as means 6 SEM and compared by t-test between genotypes with and without minor allele. Statistical significance level was set as P,0.05.
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Association of endothelial nitric oxide synthase gene polymorphisms with coronary artery disease: an updated meta-analysis and systematic review.

Association of endothelial nitric oxide synthase gene polymorphisms with coronary artery disease: an updated meta-analysis and systematic review.

The databases of the US National Institutes of Health (PubMed), EMBASE and a MEDLINE Scopus and Web of Knowledge were systematically searched for relevant articles published online by March 2014. Both medical search headings and open text fields were used to identify articles. We systemat- ically searched various databases and the reference lists of the relevant publications using the combination of terms like ‘NOS3’ OR ‘eNOS’ OR ‘constitutive endothelial NOS’ OR ‘ecNOS’ OR ‘endothelial nitric oxide synthase’ OR ‘endothelial NO synthase’ paired with ‘atherosclerotic heart disease’ OR ‘coronary artery disease’ OR ‘CAD’ OR ‘MI’ OR ‘Myocardial Infarction’ OR ‘AMI’ OR Acute Myocardial Infarction OR ‘ACS’ OR ‘Acute Coronary Syndrome’ AND ‘polymorphism’ OR ‘mutation’ OR ‘gene polymorphism’ Or ‘SNP’ OR ‘Single Nucleotide Polymor- phism’. The search in these databases was restricted to articles relating to humans, covering all relevant English language publications published up to March 2014. All references cited in the resulting studies and in previously published reviews on this topic were examined to identify additional work not indexed in internet databases. Papers without sufficient information were identified and their corresponding authors were contacted via at least three emails (spaced one week apart) requesting needed information. Publications whose corresponding authors did not respond were thenceforth not included. Since data from unpub- lished studies is unlikely to be trustworthy, we chose not to include it into this present meta-analysis. The decision to include studies was hierarchical; initially study titles, then abstracts and finally the full body of the text were assessed. The following information was recorded from the retrieved studies: author’s names, publication year, country where the study was conducted, study design, inclusion criteria for CAD patients and normal controls, methods used for genotyping and the distribution of polymorphic genotypes and alleles in each group.
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Lymphotoxin-alpha gene and risk of myocardial infarction in 6,928 cases and 2,712 controls in the ISIS case-control study.

Lymphotoxin-alpha gene and risk of myocardial infarction in 6,928 cases and 2,712 controls in the ISIS case-control study.

Lymphotoxin-a (LTA) is a pro-inflammatory cytokine that plays an important role in the immune system and local inflammatory response. LTA is expressed in atherosclerotic plaques and has been implicated in the pathogenesis of atherosclerosis and coronary heart disease (CHD). Polymorphisms in the gene encoding lymphotoxin-a (LTA) on Chromosome 6p21 have been associated with susceptibility to CHD, but results in different studies appear to be conflicting. We examined the association of seven single nucleotide polymorphisms (SNPs) across the LTA gene, and their related haplotypes, with risk of myocardial infarction (MI) in the International Study of Infarct Survival (ISIS) case- control study involving 6,928 non-fatal MI cases and 2,712 unrelated controls. The seven SNPs (including the rs909253 and rs1041981 SNPs previously implicated in the risk of CHD) were in strong linkage disequilibrium with each other and contributed to six common haplotypes. Some of the haplotypes for LTA were associated with higher plasma concentrations of C-reactive protein (p ¼ 0.004) and lower concentrations of albumin (p ¼ 0.023). However, none of the SNPs or related haplotypes were significantly associated with risk of MI. The results of the ISIS study were considered in the context of six previously published studies that had assessed this association, and this meta-analysis found no significant association with CHD risk using a recessive model and only a modest association using a dominant model (with narrow confidence intervals around these risk estimates). Overall, these studies provide reliable evidence that these common polymorphisms for the LTA gene are not strongly associated with susceptibility to coronary disease.
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Lee mas

Toll-like receptor -1, -2, and -6 polymorphisms and pulmonary tuberculosis susceptibility: a systematic review and meta-analysis.

Toll-like receptor -1, -2, and -6 polymorphisms and pulmonary tuberculosis susceptibility: a systematic review and meta-analysis.

We searched the PubMed, EMBASE, Medline (Ovid), ISI Web of Knowledge and Chinese National Knowledge Infrastructure (CNKI) to identify studies of the association between TB susceptibility and TLRs polymorphisms until 1 st January 2013. The key words were: ‘Mycobacterium tuberculosis’ or ‘tubercu- losis’ in combination with ‘polymorphism’ or ‘variant’ or ‘genotype’ or ‘allele’ or ‘mutation’, and in combination with ‘toll’ or ‘TLR’ or ‘Toll-like receptor’ or ‘Toll like receptor’. The search results were limited to English and Chinese language articles. All retrieved titles and abstracts were examined for relevant studies on the association between TB and TLR gene polymorphisms. Studies were selected if they met the following criteria: 1) case- control studies of unrelated individuals; 2) evaluation of polymor- phisms TLR1 G1805T, TLR2 T597C, T1350C, G2258A, TLR6 C745T and TB susceptibility; 3) genotype distribution in both cases and controls were available. Exclusion criteria were: 1) study design based on family or sibling pairs; 2) genotype frequencies not reported; and 3) data from reviews and abstracts. Additional studies were also identified by hand searching reference lists of
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Association between the ENPP1 K121Q polymorphism and risk of diabetic kidney disease: a systematic review and meta-analysis.

Association between the ENPP1 K121Q polymorphism and risk of diabetic kidney disease: a systematic review and meta-analysis.

The potential association between the K121Q (A/C, rs1044498) polymorphism in the ecto- nucleotide pyrophosphatase/phosphodiesterase (ENPP1) gene and risk of diabetic kidney disease (DKD) has been investigated. Nevertheless, the effect of this variant on DKD risk is still under debate, and conflicting results have been reported. To this date, no meta-analysis has evaluated the association of the K121Q polymorphism with DKD. This paper describes the first meta-analysis conducted to evaluate whether the ENPP1K121Q polymorphism is associated with DKD. A literature search was conducted to identify all case-control or cross- sectional studies that evaluated associations between the ENPP1K121Q polymorphism and DKD. Pooled odds ratios (OR) and 95% confidence intervals (95% CI) were calculated for allele contrast, additive, dominant and recessive inheritance models. Seven studies were eligible for inclusion in the meta-analysis, providing data on 3571 type 1 or type 2 dia- betic patients (1606 cases with DKD and 1965 diabetic controls without this complication). No significant heterogeneity was observed among the studies included in the meta-analysis when assuming different inheritance models (I ²
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Lee mas

Association between adiponectin concentrations and cardiovascular disease in diabetic patients: a systematic review and meta-analysis.

Association between adiponectin concentrations and cardiovascular disease in diabetic patients: a systematic review and meta-analysis.

Adiponectin, a 244 amino acid collagen-like protein encoded by the AdipoQ gene in humans [1], is decreased in obesity [2], type 2 diabetes mellitus (DM), and those with coronary heart disease (CHD) [3], and thus have been hypothesized to have insulin sensitizing, anti-inflammatory and anti-atherogenic activities [4]. Meanwhile, atherosclerosis is one of the most common causes of cardiovascular disease, which remains the biggest cause of deaths in the world [5]. Most previous studies have accessed the association between adiponectin concentrations and risk of cardiovascular disease (CVD), and several meta-analyses reported positive [6] or inversed [7,8] association or no statistically significant [6,9,10]. One reason for explaining these controversial results may be the pre-existing disease in study population [9], such as diabetics, patients on hemodialysis, and CHD patients. Diabetes can not only cause CVD, one of its long-term complications, but also doubles the risk of CVD [11]. So, it is interestingly to investigate the relationship between adiponectin concentration and the risk of CVD in diabetic patients. Rare data on the association between adiponectin concentration and risk of CVD in diabetic patients have been reported and the results are
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ASSOCIATION OF INTERLEUKIN-10 -592A>C AND -819T>C POLYMORPHISMS WITH GASTRIC CANCER RISK: A SYSTEMATIC REVIEW AND META-ANALYSIS OF 44 CASE-CONTROL STUDIES

ASSOCIATION OF INTERLEUKIN-10 -592A>C AND -819T>C POLYMORPHISMS WITH GASTRIC CANCER RISK: A SYSTEMATIC REVIEW AND META-ANALYSIS OF 44 CASE-CONTROL STUDIES

The electronic databases of the US National Library of Medicine’s PubMed, EMBASE, Web of Knowledge, Google Scholar, Wanfang, Chinese National Knowledge Infrastructure (CNKI), and Chinese Biomedical Literature Database (CBM) were systematically searched to retrieve potential publications that assessed the association between -592A>C and -819T>C polymorphisms of IL-10 gene and GC risk up to April 10, 2018. Key search terms used were as follows: (gastric cancer OR gastric neoplasm OR stomach neoplasms) AND (Interleukin-10 OR IL-10) AND (-592A>C OR rs1800872) AND (-819T>C OR rs1800871) AND (Polymorphism OR SNP OR single nucleotide polymorphism OR variation OR mutation). This meta-analysis included only publications relating to humans, covering all relevant written in English and Chinese publications with available full-text articles. Reference lists of retrieved articles, review articles, and previous meta-analysis were also manually searched to avoid missing relevant studies.
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Clinics  vol.68 número2

Clinics vol.68 número2

Pearson’s Chi-squared test with simulated p-values was used to compare the genotype distributions between cases and controls. The interactions between the GSK3B, GAB2 and SORL1 SNPs and APOE*4 were tested in two ways: first, each group was stratified into APOE*4-positive and APOE*4-negative subgroups, and the association between each SNP and the diagnosis of AD was assessed separately in each group. In the second step, a binomial logistic regression model was used to compare the interactions between APOE*4 and each of the three SNPs in the entire sample. The statistical analysis was conducted using R software version 2.12.2.
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Genetic association study of UCMA/GRP and OPTN genes (PDB6 locus) with Paget's disease of bone

Genetic association study of UCMA/GRP and OPTN genes (PDB6 locus) with Paget's disease of bone

We performed a genetic association study of rare variants and single nucleotide polymorphisms (SNPs) of UCMA/GRP and OPTN genes, in French-Canadian patients with Paget’s disease of bone (PDB) and in healthy controls from the same population. We reproduced the variant found in the UCMA/GRP basal promoter and tested its functionality using in vitro transient transfection assays. Interestingly, this SNP rs17152980 appears to affect the transcription level of UCMA/ GRP. In addition, we have identified five rare genetic variants in UCMA/GRP gene, four of them being population-specific, although none were found to be associated with PDB. Six Tag SNPs of UCMA/GRP gene were associated with PDB, particularly the SNP rs17152980 (uncorrected P=3.8 × 10 −3 ), although not significant after Bonferroni’s correction. More importantly, we replicated the strong and statistically significant genetic association of two SNPs of the OPTN gene, the rs1561570 (uncorrected P=5.7 × 10 −7 ) and the rs2095388 (uncorrected P=4.9 × 10 −3 ), with PDB. In addition, we identified a very rare variant found to be located close to the basal promoter of the OPTN gene, at −232 bp from its distal transcription start site. Furthermore, depending on the type of allele present (G or A), the binding of several important nuclear factors such as the vitamin D or the retinoic acid receptors is predicted to be altered at this position, suggesting a significant effect in the regulation of transcription of the OPTN gene. In conclusion, we identified a functional SNP located in the basal promoter of the UCMA/GRP gene which provided a weak genetic association with PDB. In addition, we replicated the strong genetic association of two already known SNPs of the OPTN gene, with PDB in a founder effect population. We also identified a very rare variant in the promoter of OPTN, and through
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Association between CD14 gene C-260T polymorphism and inflammatory bowel disease: a meta-analysis.

Association between CD14 gene C-260T polymorphism and inflammatory bowel disease: a meta-analysis.

location in DSS (dextran sodium sulfate)-induced colitis model [8,9]. CD14 serves as a receptor for lipopolysaccharides (LPS), and the binding of LPS/CD14 complex to TLR4 could activate NF- kB, and further induce an inflammatory response [10]. Soluble CD14 accompanying with serum LPS-binding protein are markers of disease activity in patients with Crohn’s disease [11]. Co- existence of a mutation in either TLR4 or CD14 gene, and in NOD2/CARD15 is associated with an increased susceptibility to developing CD compared to UC, and to developing either CD or UC compared to healthy individuals [12,13]. It is required for the microbe-induced endocytosis of TLR4. In dendritic cells, this CD14-dependent endocytosis pathway is upregulated upon exposure to inflammatory mediators [14]. Meanwhile, human CD14 gene is mapped on chromosome 5q31.1, adjacent to a region reportedly in linkage with IBD [15,16]. From genetic perspective, the substitution of a promoter polymorphism in CD14 gene (C- 260T, also known as CD14. C-159T) results in elevated transcriptional activity and accordingly high serum CD14 levels [17,18]. Therefore, candidacy of CD14 for IBD is well-defined and its C-260T polymorphism has been reported to be associated with IBD by some but not all studies [19,20]. Generally, studies with insufficient sample sizes account for such inconsistency [21].
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Ocular pseudoexfoliation syndrome and vascular disease: a systematic review and meta-analysis.

Ocular pseudoexfoliation syndrome and vascular disease: a systematic review and meta-analysis.

A study was considered relevant if it reported quantitative estimates of the unadjusted and (or) multivariable adjusted (i.e. age, sex, serum cholesterol, blood pressure, current smoking, diabetes, family history, etc.) odds ratio (OR) with a corresponding 95% confidence interval (CI) for the log relative risk for vascular events. As few studies were eligible and as authors employed heterogeneous endpoints related to vascular disease, we defined a composite of major clinical vascular disease s as the primary endpoint for our meta-analysis. Vascular diseases include coronary heart disease (CHD, such as myocardial infarction, angina pectoris, and other ischemic heart disease), cerebrovascular disease (CVD, such as cerebral hemorrhage and stroke), aortic aneurysm, and peripheral vascular disease. Unpublished papers, nonhuman studies, letters/case reports, studies enrolling ,10 subjects or subjects age ,18 years, editorials, reviews, studies lacking raw data, and studies lacking a suitable control group, and studies using inadequate case definition were excluded.
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REPOSITORIO INSTITUCIONAL DA UFOP: Fenótipo da obesidade, ancestralidade genética e polimorfismos em genes candidatos em escolares de uma população miscigenada.

REPOSITORIO INSTITUCIONAL DA UFOP: Fenótipo da obesidade, ancestralidade genética e polimorfismos em genes candidatos em escolares de uma população miscigenada.

11 por AMP (AMPK) e de PPAR no músculo esquelético e inibe a captação e estocagem da glicose no fígado (Ferrarezi e col., 2007). Atualmente, existem 2589 SNPs descritos para este gene em humanos (disponível no site http://www.ncbi.nlm.nih.gov, acesso em Julho de 2012). Um desses SNPs é o rs17300539 que consiste na troca de guanina para adenina no promotor do gene (-11391). A frequencia do alelo G deste polimorfismo tem sido maior que a do alelo A, tanto em descendetes de africanos (98 %) quanto em europeus (> 92 %), segundo o Projeto International HapMap (http://hapmap.ncbi.nlm.nih.gov, acesso em Maio de 2012). Outro SNP muito estudado é o rs266729 que consiste na troca de citosina para guanina no promotor do gene (-11365). A frequência do alelo C deste polimorfismo tem sido maior que a do alelo G, tanto em descendentes de africanos (70 %) quanto em europeus (92 %), segundo o Projeto International HapMap (http://hapmap.ncbi.nlm.nih.gov, acesso em Maio de 2012). Embora alguns estudos sugiram que a mudança de base em ambos SNPs possa resultar em reduzido nível circulante de adiponectina, os mecanismos envolvidos neste processo são desconhecidos. Em estudo de caracterização do promotor do gene APM1 humano não foram identificados sítios de ligação de fatores de transcrição em ambos SNPs e nem em suas sequências adjacentes (Shaffer e col., 1998). Entretanto, uma análise computacional realizada da sequência abrangendo os nucleotídeos -11435 a -11345 indentificou a sequência [tcctgc], localizada entre os SNPs e adjacente à rs266729, com similaridades à sequência de elemento acentuador (enhancer) do gene receptor do fator de crescimento epidérmico (EGFR), além de múltiplos sítios protegidos por proteínas (Maekawa e col., 1989).
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Association of Polymorphisms in TCF7L2  Gene with Gastric Cancer Risk: A Preliminary Study in Turkish

Association of Polymorphisms in TCF7L2 Gene with Gastric Cancer Risk: A Preliminary Study in Turkish

Aim: The Transcription factor 7-like 2 (TCF7L2) gene, located on chromo- some 10q25.3, encodes a transcription factor, which contains a high mobility group box, demonstrated in association with many cancer types. This factor is a critical part of Wnt/β-catenin signaling pathway that plays key roles in regulation of embryonic development and homeostasis in mature tissues. It is known that the constant activation of Wnt/β-catenin signaling path- way can cause cancer development. In this study, it is aimed to reveal the association between rs7903146C>T and rs12255372G>T single nucleotide polymorphisms in TCF7L2 gene, the key efector of Wnt/β-catenin signaling pathway, and gastric cancer and to determine associated risk alleles. Mate- rial and Method: In our study, polymorphisms in TCF7L2 gene were geno- typed using PCR-PFLP technique in 38 patients with gastric cancer and 48 healthy individuals. The obtained data were statistically analyzed and p<0.05 was accepted signiicant in all assessments. Results: No signiicant associa- tion was determined between rs7903146C>T and disease (p> 0.05) while 12255372G>T polymorphism was associated with the disease under addi- tive model (OR: 0.366 [95% CI: 0.135-0.989] p=0.047). Discussion: This is the irst study to examine the association between TCF7L2 gene and gastric cancer risk in Turkish population and suggests that rs12255372G>T could be a potential indicator for gastric cancer. On the other hand, further studies are required which will be carry out in more increased number of samples in a wider population.
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Estrogen receptor 1 gene polymorphisms in premenopausal women: interaction between genotype and smoking on lipid levels

Estrogen receptor 1 gene polymorphisms in premenopausal women: interaction between genotype and smoking on lipid levels

The action of estrogen is mediated by estrogen recep- tors. Some of the compounds in tobacco smoke may activate estrogen receptor 1, and consequently smoking may modify ESR-regulated gene induction. The +261G>C polymorphism might cause a different ESR1 expression pattern and, consequently, the compounds in tobacco smoke may have different effects in female carriers of different ESR1 genotypes. Our data suggest that the +261G>C polymorphism might influence HDL-C levels in premenopausal women, but this effect seems to be modu- lated by smoking. Clearly, further studies are necessary before reaching definitive conclusions about the role of these polymorphisms on lipoprotein metabolism. Our re- sults indicate that environmental and genetic interactions should be considered in association studies of complex traits.
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Molecular analysis of three FUT3 gene single nucleotide polymorphisms

Molecular analysis of three FUT3 gene single nucleotide polymorphisms

The situation is even more complex due to the pres- ence of FUT3 single nucleotide polymorphisms (SNPs) which can result in nucleotide mutations that generate en- zymes which may have different catalytic activities or even be inactive (Nishihara et al., 1993, 1994; Kudo et al., 1996; Cakir et al., 2002; Cooling and Gu, 2003; Soejima et al., 2004; Jost et al., 2005). The most frequent FUT3 SNPs are the 202T > C, 314C > T, 508G > A and 1067T > A poly- morphisms (le genes) which affect and inactivate the cata- lytic domain of FucT III enzyme (Nishihara et al., 1993, 1994; Kudo et al., 1996), while a further SNP, 59T > G, is known to cause the substitution of an amino acid in the transmembrane region but its effect on enzymatic activity has not yet been defined (Elmgren et al., 1996).
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Association between Directly Observed Therapy and Treatment Outcomes in Multidrug-Resistant Tuberculosis: A Systematic Review and Meta-Analysis.

Association between Directly Observed Therapy and Treatment Outcomes in Multidrug-Resistant Tuberculosis: A Systematic Review and Meta-Analysis.

this disease [67]. Second, some confounders that may also affect treatment success rates were not included, such as patient drug resistance patterns and other patient support strategies. Third, similar as the previous systematic reviews [4, 68] of observational studies, this review observed a significant heterogeneity in study characteristics. Fourth, we were not able to exclude XDR-TB patients in articles published early that did not report XDR in their subjects. We performed a sensitivity analysis by removing these articles while this did not change the conclusion. Another potential bias could be language selection bias, as we had only included articles published in English. Moreover, incomplete data regarding DOT providers, DOT loca- tions, HIV prevalence, proportions of previously treated cases, and patient socio-economic characteristics were reported in several of our included studies, which may prevent us having a robust pooled treatment success rate.
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Single nucleotide polymorphisms of PIN1 promoter region and cancer risk: evidence from a meta-analysis.

Single nucleotide polymorphisms of PIN1 promoter region and cancer risk: evidence from a meta-analysis.

Peptidylprolyl cis/trans isomerase NIMA-interacting 1 (PIN1) belongs to the parvulin peptidyl-prolyl isomerase family. With a conserved WW (Trp-Trp) domain, which is responsible for binding to specific sequences of target proteins and recruiting these proteins into signaling complexes [1,2]. PIN1 has a high affinity to proteins with Ser/Thr-Pro (Proline) motifs and regulates the conformation of pro-directed phosphorylation sites [2,3]. Pro- directed phosphorylation is a critical signaling mechanism that regulates various biological processes, such as cell proliferation, differentiation, transcriptional regulation and tumorigenesis [4]. Thus, PIN1 can regulate a lot of signaling pathways including those responsible for tumorigenesis [5] by modulating pro-directed phosphorylation. It has been well demonstrated that numerous oncogenic and tumor suppressor proteins are regulated by PIN1, such as cyclin D1 [6], c-Jun [7], Bcl-2 [8], b-catenin [9] and p53 [10]. Therefore, PIN1 functions as a critical regulator during the process of tumorigenesis.
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Association between MTHFR polymorphisms and acute myeloid leukemia risk: a meta-analysis.

Association between MTHFR polymorphisms and acute myeloid leukemia risk: a meta-analysis.

Previous observational studies investigating the association between methylenetetrahydrofolate reductase (MTHFR) polymorphisms and acute myeloid leukemia risk (AML) have yielded inconsistent results. The aim of this study is to derive a more precise estimation of the association between MTHFR (C677T and A1298C) polymorphisms and acute myeloid leukemia risk. PubMed and Embase databases were systematically searched to identify relevant studies from their inception to August 2013. Odds ratios (ORs) with 95% confidence intervals (CIs) were the metric of choice. Thirteen studies were selected for C677T polymorphism (1838 cases and 5318 controls) and 9 studies (1335 patients and 4295 controls) for A1298C polymorphism. Overall, pooled results showed that C677T polymorphism was not significant associated with AML risk(OR, 0.98–1.04; 95% CI, 0.86–0.92 to 1.09–1.25). Similar results were observed for the A1298C polymorphism and in subgroup analysis. All comparisons revealed no substantial heterogeneity nor did we detect evidence of publication bias. In summary, this meta-analysis provides evidence that MTHFR polymorphisms were not associated with AML risk. Further investigations are needed to offer better insight into the role of these polymorphisms in AML carcinogenesis.
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