Genetic evaluation of the TNF-α −238G&gt;A and −308G&gt;A promoter polymorphisms in Croatian patients with type I diabetes

Korolija, Marina; Medvidović, Edita Pape; Pavković, Pajica; Kapitanović, Sanja; Renar, Ivana Pavlić; Hadžija, Mirko

doi:10.1016/j.humimm.2010.09.003

Cited by 7 publications

(9 citation statements)

References 21 publications

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“…An evaluation of the multiple polymorphisms in the TNF region revealed that these are in good fit with Hardy-Weinberg equilibrium in this population. In addition to the positive association of TNF Ϫ238G and/or TNF Ϫ308A alleles with T1D, as reported in other populations [37,45,50,51], we also observed a significant positive association of the TNFa5 allele in the North Indian population. The fact that TNF Ϫ308A allele is a "high expressor" allele [35,52] explains the immunological basis of its association with the inflammatory stage of pathogenesis of T1D to some extent.…”

Section: Discussionsupporting

confidence: 90%

“…The localization of TNF genes in the MHC class III region between HLA-B and HLA-DR loci suggests that genetic polymorphisms in TNF might be in strong LD with HLA class I and class II genes as a part of the conserved MHC haplotype. Although several studies have reported an independent association of the TNF polymorphism with T1D in variable populations [38,[42][43][44][45], others failed to replicate the same in their studies [46]. These results highlight possible populationbased variations in TNF association with T1D, although other factors that include discordance in study design, statistical evaluations, sample size, and methods of genotyping employed in different studies can also affect ethnic discrepancies.…”

Section: Discussionmentioning

confidence: 88%

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Tumor necrosis factor–associated susceptibility to type 1 diabetes is caused by linkage disequilibrium with HLA-DR3 haplotypes

et al. 2012

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Section: Discussionsupporting

confidence: 90%

Section: Discussionmentioning

confidence: 88%

Tumor necrosis factor–associated susceptibility to type 1 diabetes is caused by linkage disequilibrium with HLA-DR3 haplotypes

et al. 2012

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“…The Protein Tyrosine Phosphatase Non‐receptor type 22 (PTPN22) T1D risk allele was associated with HbA1c level, but this finding was not replicated in an independent study that used the insulin dose‐adjusted HbA1c measure (IDAAC), defined by Mortensen et al in 2009 . Associations reported for the candidate genes interleukin‐6 (IL‐6), T lymphocyte‐associated antigen‐4 (CTLA4), and tumour necrosis factor‐Alpha (TNF‐α) genes did not remain significant after correcting for multiple testing. Another study reported suggestive TLR3 association with HbA1c level, but these results are inconclusive considering that a difference of age at onset of 7 years was noted between the two studied groups and so was possibly responsible for the effect …”

Section: Resultsmentioning

confidence: 99%

“…These candidate gene association studies have never been or have been poorly replicated, except for angiotensin I converting enzyme (ACE) gene . Five of the 13 selected studies reported significant or suggestive associations, which were however never replicated …”

Section: Resultsmentioning

confidence: 99%

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A systematic review of non‐genetic predictors and genetic factors of glycated haemoglobin in type 1 diabetes one year after diagnosis

Gloaguen

Bendelac

Nicolino

et al. 2018

Diabetes Metabolism Res

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Type 1 diabetes (T1D) results from autoimmune destruction of the pancreatic βcells. Although all T1D patients require daily administration of exogenous insulin, their insulin requirement to achieve good glycaemic control may vary significantly. Glycated haemoglobin (HbA1c) level represents a stable indicator of glycaemic control and is a reliable predictor of long-term complications of T1D. The purpose of this article is to systematically review the role of non-genetic predictors and genetic factors of HbA1c level in T1D patients after the first year of T1D, to exclude the honeymoon period. A total of 1974 articles published since January 2011 were identified and 78 were finally included in the analysis of non-genetic predictors. For genetic factors, a total of 277 articles were identified and 14 were included. The most significantly associated factors with HbA1c level are demographic (age, ethnicity, and socioeconomic status), personal (family characteristics, parental care, psychological traits...) and features related to T1D (duration of T1D, adherence to treatment …). Only a few studies have searched for genetic factors influencing HbA1c level, most of which focused on candidate genes using classical genetic statistical methods, with generally limited power and incomplete adjustment for confounding factors and multiple testing. Our review shows the complexity of explaining HbA1c level variations, which involves numerous correlated predictors. Overall, our review underlines the lack of studies investigating jointly genetic and non-genetic factors and their interactions to better understand factors influencing glycaemic control for T1D patients.

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Associations between TNF gene polymorphisms (−308 A/G, −238 A/G, −1031 C/T and −857 T/C) and genetic susceptibility to T1D: a meta-analysis

et al. 2014

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The aim of this study was to estimate the associations between tumor necrosis factor (TNF) gene polymorphisms and type 1 diabetes (T1D) using meta-analysis. Relevant studies were searched using PubMed and Embase up to August 2013. A total of 32 comparisons from 21 studies examining the associations between TNF polymorphisms and T1D were included in the present meta-analysis. Our meta-analysis identified a significant association between TNF -308 A/G polymorphism A allele and T1D in all subjects [odds ratio (OR) 2.001, 95 % confidence interval (CI) 1.732-2.312). Significant associations of AA and AA+AG genotype of TNF -308 A/G polymorphism with genetic susceptibility to T1D were also found (OR 3.203, 95 % CI 2.373-4.324; OR 2.232, 95 % CI 1.881-2.649). After stratification by ethnicity, significant associations of T1D with TNF -308 A/G polymorphism under all genetic models (A allele and AA, AA+AG genotype) were still detected in European (OR 1.952, 95 % CI 1.675-2.274; OR 3.108, 95 % CI 2.169-4.455; OR 2.249, 95 % CI 1.870-2.706, respectively) and non-European populations (OR 2.152, 95 % CI 1.488-3.112; OR 3.439, 95 % CI 2.000-5.914; OR 2.207, 95 % CI 1.496-3.257, respectively). Our meta-analysis also revealed an association of TNF -857 T/C polymorphism T allele with T1D risk (OR 1.647, 95 % CI 1.431-1.896). Furthermore, analysis of TT and TT+TC genotype indicated the same result patterns as shown by the TNF -857 T/C polymorphism T allele (OR 2.206, 95 % CI 1.467-3.317; OR 1.762, 95 % CI 1.490-2.083). In conclusion, our meta-analysis results indicate that TNF -308 A/G and -857 T/C polymorphisms are involved in the genetic background of T1D.

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Genetic evaluation of the TNF-α −238G>A and −308G>A promoter polymorphisms in Croatian patients with type I diabetes

Cited by 7 publications

References 21 publications

Tumor necrosis factor–associated susceptibility to type 1 diabetes is caused by linkage disequilibrium with HLA-DR3 haplotypes

Tumor necrosis factor–associated susceptibility to type 1 diabetes is caused by linkage disequilibrium with HLA-DR3 haplotypes

A systematic review of non‐genetic predictors and genetic factors of glycated haemoglobin in type 1 diabetes one year after diagnosis

Associations between TNF gene polymorphisms (−308 A/G, −238 A/G, −1031 C/T and −857 T/C) and genetic susceptibility to T1D: a meta-analysis

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