Top PDF Meta-analysis of the association between COX-2 polymorphisms and risk of colorectal cancer based on case-control studies.

Meta-analysis of the association between COX-2 polymorphisms and risk of colorectal cancer based on case-control studies.

Meta-analysis of the association between COX-2 polymorphisms and risk of colorectal cancer based on case-control studies.

Based on the search criteria, 19 studies relevant to the role of COX-2 polymorphisms on CRC susceptibility were identified. Five of these articles were excluded: two were based on family or sibling pairs [24,25], two did not provide allele or genotyping data [26,27], and one was a meta-analysis [13]. Manual search of references cited in the published studies did not reveal any additional articles. As a result, a total of 14 relevant studies met the inclusion criteria for the meta-analysis [14,15,16,28,29,30,31,32,33,34,35,36,37,38] (Figure S1). Among them, two of the eligible studies contained data on two different ethnic groups, and we treated them independently [14,31]. Therefore, a total of 16 separate comparisons were finally included in the meta-analysis. The main characteristics of the 16 casecontrol comparisons are summarized in Table 1. Among them, 13 studies including 6,807 cases and 10,052 controls were available for 2765G.C polymorphism, 10 studies with 6,774 cases and 9,772 controls for 21195A.G polymorphism, and 8 studies containing 5,121 cases and 7,487 controls for 8473T.C polymorphism. The sample size of these studies varied consider- ably, ranging from 230 to 4,552 individuals. Of all the eligible studies, 9 were conducted in Caucasians and 4 were in Asians for 2765G.C polymorphism; 8 were conducted in Caucasians and 2 were in Asians for 21195A.G polymorphism; all the 8 studies were conducted in Caucasians for 8473T.C polymorphism. Seven studies were population–based and 9 were hospital–based studies. Nine studies in the present meta-analysis did not provide definite criteria for the CRC confirmation. Several genotyping methods were used, including PCR-RFLP, TaqMan assay, PCR- CTTP, and Pyrosequencing TM . The genotype distributions among the controls in two studies were not consistent with HWE for -1195A.G [16,32].
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Relevance of hMLH1 -93G>A, 655A>G and 1151T>A polymorphisms with colorectal cancer susceptibility: a meta-analysis based on 38 case-control studies

Relevance of hMLH1 -93G>A, 655A>G and 1151T>A polymorphisms with colorectal cancer susceptibility: a meta-analysis based on 38 case-control studies

generated conflicting results, which had insufficient power in the meta-analysis because the number of studies was considerably smaller than that needed for the achievement of robust conclusions. In addi- tion, due to small size meta-analysis, they could not rule out the possibility of publication bias. With more studies about hMLH1 polymorphisms and CRC have available recently, our updated meta-analysis, which has the largest sample size thus reported, we found that the 655A>G and 1151T>A polymorphisms were associated with risk of CRC. Moreover, we found that they wrongly calculated HWE test for both cases and controls in their meta-analysis. Therefore, cumula- tive meta-analyses have suggested that no significant association was observed between hMLH1 polymor- phisms and CRC, as evidence accumulated by time.
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Association between CD14 gene polymorphisms and cancer risk: a meta-analysis.

Association between CD14 gene polymorphisms and cancer risk: a meta-analysis.

In interpreting our results of the current meta-analysis, some limitations should be acknowledged. First, the controls were not uniformly defined. Some studies used a healthy population as the control group, whereas others selected patients without cancers in hospital as the reference group. Therefore, the controls may not always be truly representative in the underlying source popula- tions, especially when the polymorphism is also expected to affect the risk of other diseases. Second, the number of published studies was not sufficiently large for a comprehensive analysis, particularly for subgroup analysis by cancer type. Thus, we may fail to explore the real association between the polymorphism and specific cancer type (such as colorectal, ALL). Third, because of the lack of original data, our results were based on single-factor estimates without adjustment for age, gender and other risk factors (e.g. smoking, drinking status), which may cause serious confounding bias.
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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.

significant association was observed between MTHFR C677T polymorphism and susceptibility to ovarian cancer [37]. Besides, Niu et al suggested that no significant association between MTHFR A1298C polymorphism head and neck cancer [38], which were consistent with our results. These inconsistent and confusing conclusions can be attributed to several factors. Different selection criteria and selection bias might account for the diversity of the results. In addition, the reason might be the complexity of the folate metabolic pathway because MTHFR is only one of many enzymes involved in the pathway. Moreover, the studies with small sample size will have a lower statistical Table 2. Distribution of MTHFR C677T genotypes and allelic frequencies in acute myeloid leukemia patients.
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Association between the ERCC5 Asp1104His polymorphism and cancer risk: a meta-analysis.

Association between the ERCC5 Asp1104His polymorphism and cancer risk: a meta-analysis.

As a structure-specific endonuclease and also a 59-39 exo- nuclease, the ERCC5 protein is required for two sub-pathways in NER. One is TCR, which preferentially removes DNA damage in the transcribed DNA strand of active genes; the other is global genomic repair (GGR), which removes lesions throughout the genome [15,16]. Additionally, ERCC5 also possesses some secondary functions independent of its cleavage activity in supporting a role of TFIIH in receptor-mediated transcription [17,18]. Furthermore, data from S. cerevisiae studies demonstrate a role for Rad2 (the ERCC5 homolog) in RNA polymerase II- mediated transcription [19]. In addition, ERCC5 is thought to have a possible role in the removal of oxidative damage by BER and possibly other pathways [20,21]. Numerous studies using various tumor cell lines or tissues indicates that ERCC5 plays a key role in carcinogenesis and that its deficiency leads to DNA repair defects, genomic instability, failure of modulation of gene transcription [22–26]. Genetic disorders resulting from mutations in the ERCC5 gene, such as xeroderma pigmentosum (XP), Cockayne syndrome (CS), and tri-chothiodystrophy (TTD), un- derscore the biological importance of this gene [14], and most of these syndromes follow a recessive genetic model, in which heterozygotes are unaffected, but mutant homozygotes manifest the disease [27].
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Association between the PARP1 Val762Ala polymorphism and cancer risk: evidence from 43 studies.

Association between the PARP1 Val762Ala polymorphism and cancer risk: evidence from 43 studies.

In the current meta-analysis, the PARP1 Val762Ala polymor- phism seemed to exert opposite effects on the risks of gastric and brain cancer. It remains unclear whether the PARP1 Val762Ala polymorphism affects cancer risk through the same biological mechanism across different types of cancer or ethnic group. Nevertheless, it was noteworthy that the opposing results on gastric and brain cancer risks were derived from different ethnic groups. Studies on brain tumor were exclusively performed from Caucasians. In contrast, all studies on gastric cancer were from Asians. Nonetheless, a few evidence suggested the PARP1 Val762Ala polymorphism might play differential roles in Asians and Caucasians. First, frequencies of the minor allele of the PARP1 Val762Ala polymorphism among controls were about 0.423 and 0.166 for Asians and Caucasians, respectively [65]. The discrep- ancy in the MAF of PARP1 Val762Ala polymorphism between ethnicity may slightly shed light on the observation that this polymorphism differentially modulates cancer susceptibility be- tween Asians and Caucasians. The protective effect of PARP1 Val762Ala polymorphism on brain cancer risk in Caucasian may be associated relative higher Val (T) allele frequency in this ethnic group. Second, we found that PARP1 Val762Ala polymorphism significantly altered mRNA expression levels of PARP1 gene in Asians, but not in Caucasians or Africans. The PARP1 762Ala (C) allele can significantly decrease poly (ADP-ribo-syl)action activity in a dosage-dependent manner. Moreover, alteration in the catalytic domain of Ala allele may impair enzymatic activity [7].
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MUC1 Predicts Colorectal Cancer Metastasis: A Systematic Review and Meta-Analysis of Case Controlled Studies.

MUC1 Predicts Colorectal Cancer Metastasis: A Systematic Review and Meta-Analysis of Case Controlled Studies.

metastasis of CRC, which was consistent with the conclusions of most included studies. Present evidence from the meta-analysis indicated that MUC1 might be a promising biomarker to pre- dict the status of CRC metastasis at the time of diagnosis. The expression of MUC1 in CRC tis- sue can be determined by IHC method with monoclonal antibody against MUC1, which can be done simultaneously when pathologists conduct pathological diagnosis with tumor tissue obtained from surgery or biopsy. It is relatively easy to realize and popularize in clinical prac- tice, which is of great significance to help surgeons determine treatment strategy. The establish- ment of the relationship between MUC1 expression and CRC metastasis may also help to clarify the metastasis risk of CRC patients at the time of diagnosis, especially those without symptoms or signs of metastasis. If MUC1 is highly expressed in a CRC patient without meta- static manifestation, it is worthy to do more detailed examination in search for any existing small metastasis. Patients with over expressed MUC1 may need more radical or aggressive treatment after diagnosis and more rigorous care after tumor resection due to a relatively high risk of metastasis. However, present study only proved the correlation between MUC1 expres- sion and CRC metastasis. The positive rate of MUC1 expression in CRC patients with metasta- sis differed greatly in previous retrospective studies, and the sensitivity and specificity of MUC1 in predicting CRC metastasis have not been validated in prospective studies. Besides,
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Association between CTLA-4 60G/A and -1661A/G polymorphisms and the risk of cancers: a meta-analysis.

Association between CTLA-4 60G/A and -1661A/G polymorphisms and the risk of cancers: a meta-analysis.

In this meta-analysis, we investigated the association between CTLA-4 60G/A (rs3087243) and CTLA-4 -1661A/G (rs4553808) and cancer risk. The subgroup analysis stratified by ethnicity, source of controls and cancer types were also performed. For CTLA-4 60G/A polymorphism, a total of 18 studies, comprising 5571 cases and 5567 controls, our meta-analysis on the available studies suggested no significant increased cancer risk in all of the genetic comparison models. The results were robust, which did not vary materially after we excluded the study with controls not in HWE. When we performed subgroup analysis by cancer type, we found the CTLA-4 60G/A (rs3087243) polymorphism is corre- lated to significant increased skin cancer. It was reported that CTLA-4 gene palys an important role in UV-induced immune suppression as well as in development of skin cancer, transgenic mice that express a skin-specific CTLA-4 antagonist, developed fewer skin tumors after chronic exposure to UV [42]. The CTLA- 4 60G/A polymorphism is a key susceptibility locus for autoimmune and cancer, previous results indicated that presence of G alleles in polymorphic sites 60G/A polymorphism was associated with lower levels of membrane and cytoplasmic CTLA- 4 in CD4+ T lymphocytes [43]. Moreover, in the subgroup analysis of source of controls, hospital-based group showed significant increased risk of cancers, and the results did not vary materially after we performed the sensitivity analysis. The remaining pooled ORs from this analysis were insignificant (all P.0.05).
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Association of +331G/A PgR polymorphism with susceptibility to female reproductive cancer: evidence from a meta-analysis.

Association of +331G/A PgR polymorphism with susceptibility to female reproductive cancer: evidence from a meta-analysis.

The statistical analysis for the current meta-analysis study was performed by using the comprehensive meta-analysis (CMA) V2 software (Biostat, USA). Meta-analysis is a powerful tool which combines results of independent similar studies and derive a definitive conclusion [12]. CMA V2 has several advantages over other software available for computing meta-analyses (http:// www.meta-analysis.com/pages/comparisons.html). The strength of the association between the PgR +331G/A polymorphism and risk of cancer was measured by odd ratios (ORs) with 95% confidence intervals (CIs). We examined the association between the allele A of the PgR +331G/A polymorphism and cancer risk, and made comparisons with the dominant genetic model (AA+AG vs. GG). A recessive genetic model was not performed as the data were not available for the homozygous mutant (AA) in the studied cases. The heterogeneity assumption was evaluated with an I 2 - based Cochran’s Q statistic test. A significant p value (,0.10) was used to indicate heterogeneity among studies, and the combined OR was calculated by using a random effect model [13]. In contrast, a fixed effect model [14] was used for the calculation of the combined OR for homogeneity among the studies. In addition, the I 2 statistic was used to quantify inter-study variability. This statistic ranged from 0 to 100%, where a value of 0% indicated no observed heterogeneity, and as the values increased the degree of heterogeneity increased (cut-off points include: I 2 = 0–25%, no heterogeneity; I 2 = 25–50%, moderate heteroge- neity; I 2 = 50–75%, large heterogeneity; I 2 = 75–100%, extreme heterogeneity) [15]. The funnel plot was employed to examine the publication bias. Egger’s regression analysis was used for re- evaluation of publication bias, and a P value less than 0.10 was considered to be significant. Funnel plots and Egger’s linear regression tests were used to provide a diagnosis of the potential publication bias.
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The modification process of AlSi21CuNi silumin and its effect on change of mechanical properties of the alloy

The modification process of AlSi21CuNi silumin and its effect on change of mechanical properties of the alloy

Pouring temperature belongs to very important factors in obtainment of correct results of the modification. Hypereutectoid silumins are characteristic of good castability even in temperatures close to liquidus curve, what suggests implementation of low temperature of casting. However, such method of casting creates conditions to easy coarsening of primary crystals of silicon and their non-uniform distribution on microstructure of the casting. Rate of cooling of the alloy poured into mould has also an effect on results of the modification.
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An updated meta-analysis on the association of MDM2 SNP309 polymorphism with colorectal cancer risk.

An updated meta-analysis on the association of MDM2 SNP309 polymorphism with colorectal cancer risk.

This study was performed according to the proposal of Meta- analysis of Observational Studies in Epidemiology group (MOOSE) [13]. We conducted a comprehensive literature search in PubMed, Embase, and Chinese Biomedical Literature database (CBM) databases up to July 01, 2013 using the following search strategy: (“colorectal cancer”, “CRC”, “colon cancer” or “rectum cancer”) and (“Murine double minute 2”, or “MDM2”) and (“polymorphism”, “variation”, “mutation”, “genotype”, or “genetic polymorphism”). There was no restriction on time period, sample size, population, language, or type of report. All eligible studies were retrieved and their references were checked for other relevant studies. The literature retrieval was performed in duplication by two independent reviewers (Xue Qin and Qiliu Peng). When multiple publications reported on the same or overlapping data, we chose the most recent or largest population. When a study reported the results on different subpopulations, we treated it as separate studies in the meta-analysis.
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Buying Behavior Of Organic Vegetables Product The Effects Of Perceptions Of Quality And Risk

Buying Behavior Of Organic Vegetables Product The Effects Of Perceptions Of Quality And Risk

Quality is defined as the degree of excellence or superiority that an organization’s product possesses (Khan, 2005:28). Consumers judge or perceive the quality of the products and it also called perception of quality, because perception of quality derived from the analysis of consumers on product quality (Sanyal & Datta, 2011:605). Customer perceived value of product quality is a consumer opinion as ability of the product who suitable with expectation of consumer (Terenggana et al., 2013:326). Perception of quality is formed on consumers can be affected by several things including past experience, education, purchasing and consumer community (Yaseen et al., 2011:834), and perception of quality is important in improving the quality of products in the view of consumers (Parrol et al., 2013:603). Since knowledge and consumer needs change time by time, it taken an understanding related consumer perception of quality in evaluated to be known how big influence on purchase intention (Sanyal & Datta, 2011:607). Reviewing consumer behavior in foods, in previous research is often studied through perception of quality (Carrasco et al., 2012:1414). On last studied, perceived quality is the consumer’s judgment about a product’s overall excellence or superiority (Zeithaml, 1988). Meanwhile perceived quality is the judgment a consumer of product which refers to the physical characteristics of the product, and is related more to engineering and food technology (Carrasco et al., 2012). Several things that concern on perception of quality, first are spoke on the advantages related to the assessment of consumer products and the second on the technology applied to products that are both better than similar products. That matter is a critical element for consumer decision making, consequently, consumers will compare the
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Ciênc. saúde coletiva  vol.16 número9

Ciênc. saúde coletiva vol.16 número9

The results of this study, which pooled the results of seven published studies, suggest a pos- itive relationship between formaldehyde exposure and childhood asthma. To place the observed re- sults (OR of 1.17 per 10-µg/m3 increase) in con- text, when compared with indi-viduals with no formaldehyde exposure, those with the highest levels of exposure reported in the seven studies (i.e., 80 µg/m3) would have 3.5-times higher odds of asthma. The results reported herein are consis- tent with much of the previously published litera- ture regarding the association between formalde- hyde exposure and childhood asthma. This should not be surprising in that many of these studies serve as the foundation of our meta-analysis. However, in addition to the seven studies includ- ed in the meta-analysis, two additional studies, each reporting a positive association, could not be included, yet they provide further support for the observed quantitative results (Pati and Parida 2005; Tavernier et al. 2006). Tavernier et al. (2006) reported elevated but not statistically significant ORs for specific levels of formaldehyde exposure; unfortunately, the authors did not provide the actual, quantitative values associated with those levels. Similarly, Pati and Parida (2005) simply reported that, indoor exposure to formaldehyde . . . signifi-cantly increased the risk of having asthma. Additionally, Symington et al. (1991) compared the prevalence of respiratory symptoms exhibit- ed by children living within 1 mile of a formalde- hyde-emitting foundry with that of children liv- ing in other areas and reported no differences (Symington et al. 1991). Franklin et al. (2000) de- termined that individuals with a home formalde- hyde concentration of at least 50 ppb had a signif-
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Influence of tungsten and titanium on the structure of chromium cast iron

Influence of tungsten and titanium on the structure of chromium cast iron

stage, the content of manganese was made up with an addition of ferromanganese and the melt was held for 3 minutes. During holding of the melt and before tapping, the temperature of liquid iron was measured with a thermocouple. The melt was transferred to a ladle, which was next transported to the casting stand and molten metal was poured into the previously prepared moulds. Test bars with a φ 15 mm diameter and castings were made following the production regime adopted by HARDKOP Foundry at Trzebinia. As a next step, specimens were prepared for metallographic examinations. Chemical composition of the cast iron phase constituents was examined using a JEOL 500LV scanning electron microscope with attachment for X-ray microanalysis (EDS).
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Genetic polymorphisms of GSTM1, GSTT1, and GSTP1 with prostate cancer risk: a meta-analysis of 57 studies.

Genetic polymorphisms of GSTM1, GSTT1, and GSTP1 with prostate cancer risk: a meta-analysis of 57 studies.

restrictions were placed on language, time period, sample size, type of study and population. All eligible articles were retrieved and their references were checked for other relevant studies. The inclusion criteria were: (1) studies which evaluated associations between GSTM1, GSTT1, GSTP1 polymorphisms and PCa risk; (2) control population did not contain malignant tumor patients. The exclusion reasons of studies were: (1) insufficient original data for the calculation of odds ratios (ORs) with corresponding 95% confidence intervals (95%CIs); (2) when multiple reports were available for the same study population, we included only the most recent or the largest report. Two investigators independently reviewed the titles, abstracts to determine if an individual study was eligible for the inclusion and exclusion criteria and all disagreements were resolved during a consensus meeting among all reviewers.
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Association of Interleukin-10 -1082A>G (rs1800896) Polymorphism with Predisposition to Breast Cancer: a Meta-Analysis based on 17 Case- Control Studies

Association of Interleukin-10 -1082A>G (rs1800896) Polymorphism with Predisposition to Breast Cancer: a Meta-Analysis based on 17 Case- Control Studies

We have also carried out subgroup analyses that were stratified by ethnicity. Overall, no obvious ev- idence of associations between the IL-10 -1082A>G (rs1800896) polymorphism and susceptibility to the breast cancer were found in Caucasian, Asian and Af- rican populations under all genetic models (Figure 2B). Moreover, subgroup analysis of studies with high quali- ty (HWE status) did not show significant association be- tween IL-10 -1082A>G (rs1800896) polymorphism and increased risk of breast cancer (Figure 2C). The results of these analyses are shown in Table 2 and Figure 2.
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Myeloperoxidase polymorphism, menopausal status, and breast cancer risk: an update meta-analysis.

Myeloperoxidase polymorphism, menopausal status, and breast cancer risk: an update meta-analysis.

Myeloperoxidase (MPO) is a metabolic/oxidative lysosomal enzyme secreted by reactive neutrophils at the sites of inflamed organs and tissues during phagocytosis. MPO has been either directly or indirectly linked to neoplasia, which is a well- established risk factor for many types of cancer. A large number of studies have reported the role of MPO G-463A polymorphism regarding breast-cancer risk. However, the published findings are inconsistent. Therefore, we conducted a meta-analysis to determine more precise estimations for the relationship. Eligible studies were identified by searching several electronic databases for relevant reports published before June 2012. According to the inclusion criteria and exclusion criteria, a total of five eligible studies were included in the pooled analyses. When the five eligible studies concerning MPO G-463A polymorphism were pooled into this meta-analysis, there was no evidence found for a significant association between MPO G-463A polymorphism and breast-cancer risk in any genetic model. We also categorized by ethnicity (Caucasian or Asian) for subgroup analysis; according to this subgroup analysis, we found no significant association between MPO G-463A polymorphism and breast-cancer risk in any genetic model. However, in the stratified analysis for the premenopausal group, women carrying the AA genotype were found to have a significantly reduced risk (OR = 0.56, 95% CI 0.34–0.94, p = 0.027). Under the recessive model, there was a significant association between MPO G- 463A polymorphism and breast-cancer risk (OR = 0.57, 95% CI 0.34–0.93, p = 0.025). We conclude that MPO-G463A polymorphism might not be a good predictor of breast-cancer risk, though menopausal status modified women’s risk of developing breast cancer.
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Alcohol consumption and the neoplastic progression in Barrett's esophagus: a systematic review and meta-analysis.

Alcohol consumption and the neoplastic progression in Barrett's esophagus: a systematic review and meta-analysis.

this might produce no serious problem. Secondly, even the categories of alcohol consumption are reported in some studies; however, the data were varied and broad. Thus, we were unable to determine the dose-response association between alcohol con- sumption and progression of Barrett’s esophagus. Third, it has been argued that because meta-analyses of observational studies may produce very precise, but spurious, results, a statistical combination of these data should not be the prominent component. However, considering that as an etiology exploring nature of this study, the pooled results of the observational studies would also provide certain improvement of the knowledge of the neoplastic development. The end, a combination of prognostic factors has been suggested to be required to define subgroups of patients at an increased risk of progression. However, the data of the included studies reported no sufficient data for an advanced research, which demonstrated the potential breakthrough. The forth, the understanding of the Barrett’s esophagus has developed in the recent years. The old conception says that although several different kinds of columnar epithelium can be found in the lower esophagus, it is only specialized intestinal metaplasia (SIM), distinguished by the presence of goblet cells, which increased the cancer risk. However, nowadays recent studies revealed that cardiac-type mucosa, columnar lined esophagus without goblet cells, also have the posibility of cancer development. With the development of understanding of Barrett’s esophagus, the older papers might provide results based on inaccurate definitions and
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Rev. Soc. Bras. Med. Trop.  vol.50 número2

Rev. Soc. Bras. Med. Trop. vol.50 número2

In spite of the publication of several genetic association studies, no clear consensus on the effect of TLR4 or TLR9 variants on the clinical manifestation of malaria has thus far been obtained. This could be attributed to the inclusion of incorrectly deined or partially matched controls, different study designs, relatively small sample sizes, population stratiication, or genetic heterogeneity. Therefore, it is essential to perform a comprehensive search and meta-analysis of these studies in order to verify whether these SNPs are associated with the risk or severity of malaria. Meta-analysis is a powerful tool that has been employed to reach a consensus by analyzing data addressing the same research problem in global malarial settings with different ethnic populations. Although in the majority of previous studies, TLR variants have been compared between healthy controls and either severe malaria (SM) or uncomplicated malaria (UM) patients to determine the severity of or susceptibility to malaria, respectively, there have been limited studies comparing variants in severe cases of malaria with P. falciparum-infected controls [mild or asymptomatic (reviewed in ref. 2)]. However, in regions hyper-endemic for malaria it is hard to obtain endemic controls for two reasons. First, although an individual may be healthy at the time of blood draw, he/she might have had previous infections with the malaria parasite and suffered from clinical symptoms; in fact, repeated antigen exposure from infective bites might have led to premunition. Second, because of the strategic control of mosquito-human contact (use of insecticides, bed-nets, etc.), individuals who appear to be healthy are not essentially endemic controls because they may not have been exposed to malaria at all; there remains the possibility that they may develop clinical symptoms upon exposure. The screening of mutations in these apparently healthy individuals and the inclusion of their data, therefore, may not truly fulill the requirements for controls. Therefore, in order to obtain more precise estimates of the pooled effects of TLR variants with increased statistical power, we carried out a meta-analysis combining relevant data from several independent P. falciparum-infected case-control studies conducted to evaluate the association between the TLR4 D299G and TLR9T- 1237C and T-1486C polymorphisms and the risk of severe malaria.
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A meta-analysis of PTGS1 and PTGS2 polymorphisms and NSAID intake on the risk of developing cancer.

A meta-analysis of PTGS1 and PTGS2 polymorphisms and NSAID intake on the risk of developing cancer.

In these studies, the types of NSAIDs (e.g., aspirin, ibuprofen, and other NSAIDs), dose methods (e.g., dosage and duration), study design (e.g., case control study or cohort study), population (e.g., age, gender, type of cancer, and ethnic), and study power are different. In addition, there was the lack of specificity for cancer type in our analysis because few studies have investigated the effect of associations between polymorphisms in PTGS1 and PTGS2 genes and NSAID use on cancer risk. Thus, it is difficult to draw any conclusion about the relationship between PTGS genotype and NSAID use on the risk of developing cancer. Nonetheless, our results provide limited evidence. Drug response is a complex phenomenon dependent on inherited and environmental factors. To carry more credibility, further analyses with study design formulation are required in several countries.
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