Investigation of TNFA 308G &gt; A and TNFB 252G &gt; A polymorphisms in genetic susceptibility to migraine

Ghosh, Jayashri; Joshi, Gunjan; Pradhan, Sunil; Mittal, Balraj

doi:10.1007/s00415-009-5430-x

Cited by 36 publications

(45 citation statements)

References 29 publications

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“…Our results also did not differ from those found for the Brazilian population without hemoglobinopathies (Cajado et al, 2011), suggesting that the inheritance of the polymorphisms studied is independent of the β S gene inheritance. In re-lation to the Indian population, the frequencies found in our population did not differ (Ghosh et al, 2010), probably due to the ethnic heterogeneity of both.…”

Section: Discussioncontrasting

confidence: 43%

Frequencies of -308G/A (TNFA) and -509C/T (TGFB1) polymorphisms in sickle cell anemia patients from Brazil

Torres¹,

Junior²,

Silva³

et al. 2013

Genet. Mol. Res.

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ABSTRACT. Sickle cell anemia is an affection that causes chronic inflammation, with consequences for vaso-occlusion, oxidative stress and cytokine production. Genetic polymorphisms in markers involved in this process can modulate the inflammatory response, including polymorphisms -308G/A of TNFA (tumor necrosis factor alpha) and -509C/T of TGFB1 (transforming growth factor beta 1), reported to increase TNF-α and TGF-β1 production, respectively. Changes in the cytokine balance are important risk factors for clinical events; consequently, we examined the frequencies of these polymorphisms in 240 Brazilian sickle cell anemia patients from southeast Brazil. PCR-RFLP was used to detect these polymorphisms. The -509C/T (TGFB1) polymorphism was more frequent than -308G/A (TNFA), with allelic frequency of 0.3 for the mutant allele T (TGFB) agaist 0.1 for the mutant TNFA and TGFB polymorphism frequencies allele A (TNFA). These allelic frequencies are similar to those known from populations with ethnicity similar to the Brazilian population. Inheritance of these polymorphisms does not seem to be associated with that of the Hb S mutation; however, this information could be useful in analyses of specific clinical characteristics of sickle cell anemia.

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Section: Discussioncontrasting

confidence: 43%

Frequencies of -308G/A (TNFA) and -509C/T (TGFB1) polymorphisms in sickle cell anemia patients from Brazil

Torres¹,

Junior²,

Silva³

et al. 2013

Genet. Mol. Res.

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“…In addition, among the included studies, one concerned only MO (12) and another only MA (13), three (15)(16)(17) clarified the clinical type of migraine and one (14) did not clarify the clinical type.…”

Section: Study Inclusion and Characteristicsmentioning

confidence: 99%

“…The genotype distribution of the included studies and the P-values for HWE testing are shown in Tables I and II. Main results, subgroup analyses. Six studies concerning the correlation between the TNF-α -308G/A polymorphism and migraine are shown in Table I (14) and Ghosh et al (15) revealed a significant association between the TNF-α -308G/A polymorphism and migraine risk. However, Hasan et al (16) revealed no significant association between the polymorphism and migraine and the results of Lee et al (17) were uncertain.…”

Section: Study Inclusion and Characteristicsmentioning

confidence: 99%

“…Distribution of TNF-α genotype and alleles between the cases and controls. The meta-analysis consisted of three case-control studies concerning MA (15)(16)(17) and four case-control studies concerning MO (12,(15)(16)(17). The summary result of the subgroup analysis revealed a significant correlation between the TNF-α -308G/A polymorphism and MA risk.…”

Section: Study Inclusion and Characteristicsmentioning

confidence: 99%

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The TNF-α-308G/A polymorphism is associated with migraine risk: A meta-analysis

Gu¹,

Yan²,

Long

et al. 2012

Experimental and Therapeutic Medicine

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Abstract. Migraine is a neurasthenia and the genetic etiology has not been determined. Several studies concerning the correlation between the tumor necrosis factor (TNF)-α -308G/A polymorphism and migraine have been published, but their results remain controversial and the small samples in each study do not allow sufficient statistical power. In the present study, odds ratios (ORs) with 95% confidence intervals (CIs) were used to assess the strength of the association between the polymorphism and migraine. An inverse-variance method was applied to estimate the frequency of the putative risk allele in the controls. Heterogeneity was determined using Cochran's Q test and the inconsistency index (I 2 ). Begg's test and the inverted funnel plot were used to assess the publication bias. Five studies on Asian populations, comprising 985 cases and 958 controls, were included in the meta-analysis. The overall results revealed that the TNF-α -308G/A polymorphism was associated with migraine risk in Asians. The ORs were 1.735 (95% CI, 1.129-2.666) for A vs. G; 1.781 (95% CI, 1.166-2.718) for GA vs. GG; 1.821 (95% CI, 1.153-2.874) for AA+GA vs. GG. The subgroup analysis was based on migraine with aura (MA) and migraine without aura (MO) and there was a statistically significant result for MA [the OR was 1.728 (95% CI, 1.095-2.726) for GA vs. GG and 1.651 (95% CI, 1.049-2.598) for AA+GA vs. GG] but not for MO. In conclusion, the TNF-α -308G/A polymorphism was associated with migraine risk. IntroductionMigraine is a common, chronic, recurrent and neurovascular disorder which is associated with digestive system and autonomic nervous system symptoms (1). The two main clinical types are MA (migraine with aura) and MO (migraine without aura). In the general population, 10% of males and 24% of females suffer from migraine (2,3). A review (4) reported that the global incidence of adult migraine is over 10%. It has been confirmed that migraine is associated with other diseases. Research has shown that MA may increase the risk of cardiovascular disease (CVD), myocardial infarction and ischemic stroke in female patients (5). The mortality rate of patients with MA who have CVD and stroke is higher than that of those who do not suffer from migraine (6).However, the pathophysiology of migraine remains unclear. Previously, the vascular hypothesis (7) proposed that migraine was caused by intracranial and extracranial vascular dysfunction. However, this hypothesis did not address neurogenic changes and did not explain the typical migraine (MA) and common migraine (MO) phenomena. Neurogenic inflammation may be a key mechanism in stimulating the trigeminal system and causing the headache.Tumor necrosis factor (TNF) is a pro-inflammatory molecule and a polypeptide effector of the inflammatory reaction which also appears to play a role in migraine. TNF-α activates the transcription of calcitonin gene-related peptide (CGRP) and plays a key role in migraine pathophysiology (8). A study (9) revealed that levels of CGRP in the external jugular vei...

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“…Since then, several follow-up studies have been continuously carried out in an effort to replicate the initial finding. Some were successful [16], [17], whereas others failed [18], [19]. Multiple factors including selection of diverse populations, different control sources, and misclassification of genotypes may individually or jointly result in the controversy, but the main source can attribute to the various numbers of subjects used in each study.…”

Section: Introductionmentioning

confidence: 99%

Effects of Tumor Necrosis Factor-β (TNF-β) 252A>G Polymorphism on the Development of Migraine: A Meta-Analysis

Liu

Cui

et al. 2014

PLoS ONE

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Background and ObjectiveGenetic factors including TNF-β have been considered as important components in the aetiology of migraine. Many studies have investigated the association between TNF-β 252A>G polymorphism and migraine risk, with debatable results. This study was designed to examine whether the TNF-β 252A>G polymorphism confers genetic susceptibility to migraine in diverse populations.MethodStudies eligible for this meta-analysis were searched in the PubMed, Embase, and CNKI by using the keywords “tumor necrosis factor”, “TNF”, “252A>G”, “rs909253”, “polymorphism”, “polymorphisms”, “variant”, “SNP”, combined with “migraine” or “migraine with aura (MA)” or “migraine without aura (MO)”. Pooled ORs and 95% CI were appropriately calculated using the fixed-effect model.ResultsWe finally included a total of seven studies, providing 5 557 migraineurs and 20 543 unrelated healthy controls. Meta-analysis results showed no statistical evidence of a significant association between TNF-β 252A>G polymorphism and overall migraine risk. Stratified analyses by type of migraine and gender revealed similar results. Interestingly, an OR with 95% CI representing an increased migraine risk was indicated in Asians under the recessive model (GG vs. AG + AA: OR, 1.38; 95%CI, 1.04–1.84; P for heterogeneity, 0.665).ConclusionsOur findings appear to support the hypothesis that genetic variability of 252A>G polymorphism in TNF region may modulate risk of migraine in the population of Asian ancestry.

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Investigation of TNFA 308G > A and TNFB 252G > A polymorphisms in genetic susceptibility to migraine

Cited by 36 publications

References 29 publications

Frequencies of -308G/A (TNFA) and -509C/T (TGFB1) polymorphisms in sickle cell anemia patients from Brazil

Frequencies of -308G/A (TNFA) and -509C/T (TGFB1) polymorphisms in sickle cell anemia patients from Brazil

The TNF-α-308G/A polymorphism is associated with migraine risk: A meta-analysis

Effects of Tumor Necrosis Factor-β (TNF-β) 252A>G Polymorphism on the Development of Migraine: A Meta-Analysis

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