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Öğe Significant association between SCGB1D4 gene polymorphisms and susceptibility to adenoid hypertrophy in a pediatric population(Tubitak Scientific & Technological Research Council Turkey, 2017) Ozdas, Talih; Ozdas, Sibel; Babademez, Mehmet Ali; Muz, Sami Engin; Atilla, M. Hunturk; Bastimur, Sibel; Izbirak, AfifeBackground/aim: Adenoid hypertrophy (AH) is chronic enlargement of the adenoid tissue. The pathophysiology of the disease is unclear. We analyzed SCGB1D4 gene polymorphisms in order to determine the effect of the variants or their genetic combinations on AH. Materials and methods: We genotyped the SCGB1D4 (IIS) gene in 167 participants (95 children with AH and 72 controls) by performing DNA sequencing in blood samples. Results: We genotyped three single nucleotide polymorphisms (SNPs). In the analysis, we found that in the presence of those SNPs and the minor alleles of individual SNPs four haplotypes were associated with an increased risk of AH. In addition, those SNPs were significantly associated with asthma, allergy, sleep-disordered breathing, AH grade + 4, and a high level of IgE. As indicated on multifactor dimensionality reduction analysis, single-locus (rs35328961), two-locus (rs35328961_rs56196602), and three-locus models (rs200327820_rs35328961_rs56196602) had the highest synergistic interaction effect on AH. The three-factor model was also significantly associated with some genotypes of rs35328961 and allergic-asthmatic AH. Conclusion: SNPs of SCGB1D4 and their combinations are associated with an increased risk for developing AH. We highlighted the importance of genetic factors on AH and AH-related clinical phenotypes.Öğe The common genetic variants of toll-like receptor and susceptibility to adenoid hypertrophy: a hospital-based cohort study(Tubitak Scientific & Technological Research Council Turkey, 2016) Babademez, Mehmet Ali; Ozdas, Talih; Ozdas, SibelBackground/aim: Adenoid hypertrophy (AH) is one of the most frequent pediatric disorders. The aim of this study was to investigate the effects of TLR2-R753Q, TLR4-T399I, and TLR4-D299G polymorphisms in children with AH. Materials and methods: The variants of the TLR gene were determined by restriction fragment length polymorphism (PCR-RFLP) analysis in 60 patients with AH and in 50 healthy children. Data were analyzed with SNPStats and multifactor dimensionality reduction (MDR) software. Results: We found that the presence of the G allele, the AG+GG and AG genotypes at TLR4-D299G, and the GGT haplotype were associated with AH in children (P = 0.013, P = 0.02, P = 0.038, and P = 0.001, respectively). On the contrary, no association was found between TLR2-R753Q and predisposition to AH. The CT genotype at TLR4-T399I showed a sex-specific association with AH, occurring only in boys with allergies (P = 0.0048). In addition, MDR analysis indicated a strong synergy between TLR gene markers contributing to AH. Allergic children with the diplotypes that included minor alleles of TLR4-D299G or TLR4-T399I had about a 4-fold increased risk for AH. Conclusion: Common genetic variants of the gene encoding the TLR4 protein may have differential effects on AH and the presence of sex-specific allergy.Öğe The common genetic variants of toll-like receptor and susceptibilityto adenoid hypertrophy: a hospital-based cohort study(2016) Babademez, Mehmet Ali; Özdaş, Talih; Özdaş, SibelBackground/aim: Adenoid hypertrophy (AH) is one of the most frequent pediatric disorders. The aim of this study was to investigate the effects of TLR2-R753Q, TLR4-T399I, and TLR4-D299G polymorphisms in children with AH. Materials and methods: The variants of the TLR gene were determined by restriction fragment length polymorphism (PCR-RFLP) analysis in 60 patients with AH and in 50 healthy children. Data were analyzed with SNPStats and multifactor dimensionality reduction (MDR) software. Results: We found that the presence of the G allele, the AG+GG and AG genotypes at TLR4-D299G, and the GGT haplotype were associated with AH in children (P = 0.013, P = 0.02, P = 0.038, and P = 0.001, respectively). On the contrary, no association was found between TLR2-R753Q and predisposition to AH. The CT genotype at TLR4-T399I showed a sex-specific association with AH, occurring only in boys with allergies (P = 0.0048). In addition, MDR analysis indicated a strong synergy between TLR gene markers contributing to AH. Allergic children with the diplotypes that included minor alleles of TLR4-D299G or TLR4-T399I had about a 4-fold increased risk for AH. Conclusion: Common genetic variants of the gene encoding the TLR4 protein may have differential effects on AH and the presence of sex-specific allergy.