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    Aldosterone Synthase CYP11B2 Gene Promoter Polymorphism in a Turkish Population With Chronic Kidney Disease
    (Iranian Soc Nephrolgy, 2015) Yilmaz, Meral; Sari, Ismail; Bagci, Binnur; Gumus, Erkan; Özdemir, Öztürk
    Introduction. It has been shown that gene polymorphisms influence the development and progression of chronic kidney disease (CKD). Many studies have indicated that aldosterone synthase CYP11B2 gene polymorphism (-344C>T) influences the aldosterone level, urinary aldosterone excretion, blood pressure, and left ventricular size and mass. We aimed to investigate whether there is an effect of CYP11B2 -344C>T polymorphism on the development of CKD in a Turkish population. Material and Methods. A total of 240 patients with stage 5 CKD and 240 age- and sex-matched healthy individuals were included in the study. Genotyping of CYP11B2 gene -344 T>C promoter polymorphism was carried out using polymerase chain reaction and restriction fragment length polymorphism methods. Results. No significant differences were found in the genotype distribution of CYP11B2 -344 C>T polymorphism between the patients and controls; however, -344 C>T polymorphism was significantly more frequent among the CKD patients with diabetes mellitus as compared to those with it (P = .02). Diabetic CKD patients with TC genotype had a 2-fold increased risk for development of the disease than the CKD patients without diabetes mellitus (odds ratio, 2.21; 95% confidence interval, 1.04 to 4.67). Conclusions. Our study suggests that the CYP11B2 gene -344 C>T polymorphism may have an effect on the development of CKD in diabetic patients.
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    Associations of fractalkine receptor (CX3CR1) and CCR5 gene variants with hypertension, diabetes and atherosclerosis in chronic renal failure patients undergoing hemodialysis
    (Springer, 2016) Bagci, Binnur; Bagci, Gokhan; Huzmeli, Can; Sezgin, Ilhan; Özdemir, Öztürk
    We aimed to investigate the associations of fractalkine receptor (CX3CR1) V249I, T280M and CCR5-59029 A/G gene polymorphisms in chronic renal failure (CRF) subjects undergoing hemodialysis and to evaluate possible associations of these polymorphisms with hypertension (HT), diabetes mellitus (DM) and atherosclerosis (AS). A total of 225 CRF subjects undergoing hemodialysis and 201 healthy controls were enrolled in the study. CRF subjects were divided into three major subgroups according to comorbidities including HT (n = 127), DM (n = 65) and AS (n = 33). Genotyping was done using polymerase chain reaction-restriction fragment length polymorphism method. The II genotype and I allele frequencies of CX3CR1 V249I polymorphism were found significantly more frequent in CRF subjects, CRF subjects with DM and CRF subjects with AS compared with controls (p < 0.05 for all comparisons). G allele frequency of CCR5 polymorphism was found significantly more prevalent in CRF subjects with DM than that of controls. Further, GG genotype and G allele frequencies of CCR5 polymorphism were significantly more prevalent in CRF subjects with AS compared with controls (p < 0.05). We also explored these polymorphisms among CRF subjects with and without following comorbidities: HT, DM, AS. We found significant association between CRF subjects with HT and without HT in terms of genotype and allele frequencies of V249I polymorphism (p < 0.05). CX3CR1 T280M polymorphism was not found significantly different in none of the comparisons. These data demonstrate possible associations between CX3CR1 V249I and CCR5-59029 A/G polymorphisms and/or HT, DM and AS in CRF subjects.
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    KRAS, BRAF oncogene mutations and tissue specific promoter hypermethylation of tumor suppressor SFRP2, DAPK1, MGMT, HIC1 and p16 genes in colorectal cancer patients
    (Ios Press, 2016) Bagci, Binnur; Sari, Musa; Karadayi, Kursat; Turan, Mustafa; Özdemir, Öztürk; Bagci, Gokhan
    BACKGROUND: Colorectal cancer is a serious disease that causes significant morbidity and mortality in developed countries. Genetic changes, such as mutations in proto-oncogenes and DNA repair genes, and loss of function in the tumor suppressor genes cause colorectal cancer development. Abnormal DNA methylation is also known to play a crucial role in colorectal carcinogenesis. OBJECTIVE: In this study, frequencies of KRAS and BRAF mutations, promoter hypermethylation profiles of SFRP2, DAPKI, MGMT, HIC1 and p16 genes, and possible associations between hypermethylation of these genes and KRAS and BRAF mutations were aimed to find out. METHODS: Ninety three colorectal cancer tissues and 14 normal colon mucosas were included in the study. Common twelve KRAS gene mutation were investigated with using reverse-hybridization strip assay method. BRAF V600E mutations were investigated with RFLP method. Hypermethylation status of five tumor suppressor genes were detected by using reverse-hybridization strip assay method after bisulfite modification of DNA. RESULTS: KRAS and BRAF mutation frequencies were determined as 54.84% and 12.9%, respectively. Promoter hypermethylation frequencies of tumor suppressor genes SFRP2, DAPK1, MGMT, HIC1 and p16 were determined as 66.7%, 45.2%, 40.9%, 40.9% and 15.1%, respectively. Statistically significant associations were found between BRAF mutation and SFRP2 and p16 tumor suppressor genes hypermethylation (SFRP2; p = 0.005, p16; p = 0.016). Compared to rectum, SFRP2 (p = 0.017) and MGMT (p = 0.013) genes have statistically significantly higher promoter hypermethylation in colon. CONCLUSIONS: Results of the current study have confirmed that KRAS mutations and SFRP2 hypermethylation can be used as genetic markers in colorectal cancer.
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    The Analysis of GJB2, GJB3, and GJB6 Gene Mutations in Patients with Hereditary Non-Syndromic Hearing Loss Living in Sivas
    (Aves, 2019) Kurtulgan, Hande Kucuk; Altuntas, Emine Elif; Yildirim, Malik Ejder; Özdemir, Öztürk; Bagci, Binnur; Sezgin, Ilhan
    OBJECTIVES: The aim of the present study was to investigate the presence of GJB2, GJB3, and GJB6 gene mutations in non-syndromic sensorineural hearing loss (NSHL) cases living in Sivas region, to provide appropriate genetic counseling for cases who were found to have mutation, and to contribute to decrease the frequency of mutant allele in the next generation and plan treatment and rehabilitation with early diagnosis. MATERIALS and METHODS: The study included 53 unrelated cases that were diagnosed with congenital NSHL between June 2009 and March 2010. Multiplex ligation-dependent probe amplification method was used for genotyping of GJB2, GJB3, and GJB6 gene mutations. RESULTS: Heterozygous 35delG variant was determined in 1,9% (n=1) of cases, homozygous 35delG in 15.1% (n=8), heterozygous IVS1+1G>A mutation in 1.9% (n=1), compound heterozygous in 3.8% (n=2), and homozygous IVS1+1G>A variant in 3.8% (n=2). None of the cases had mutation in GJB3 and GJB6 genes. Mutated allele frequencies in the present study were found to be 17.9% for 35delG and 6,6% for IVS1+1G>A. CONCLUSION: The present study showed that 35delG mutation is the most common variant in the Sivas region, and that IVS1+1G>A mutation should be investigated in hearing loss. Another result of the present study was that genetic analyzes would allow early diagnosis of hearing impairments particularly when infants whose parents have consanguinity do not pass the newborn hearing screening.
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    The protective effect of MCP-1-2518 A>G promoter polymorphism in Turkish chronic renal failure patients requiring long-term hemodialysis
    (Springer, 2015) Bagci, Binnur; Bagci, Gokhan; Candan, Ferhan; Özdemir, Öztürk; Sezgin, Ilhan
    Monocyte chemoattractant protein-1 (MCP-1) plays a major role in the pathogenesis and progression of different types of human renal disease. Therefore, in this study, we aimed to investigate the effect of MCP-1 gene -2518 A > G promoter polymorphism in chronic renal failure (CRF) patients requiring long-term hemodialysis. The study population consisted of 201 adult CRF patients requiring long-term hemodialysis and 194 healthy controls. The polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) technique was used for genotyping of MCP-1 -2518 A > G polymorphism in the CRF patients and healthy controls. There were statistically significant differences in terms of genotypic (chi (2) = 12.69, p = 0.02) and allelic (chi (2) = 5.72, p = 0.02) frequencies of MCP-1 -2518 A > G between CRF patients and control subjects. According to our results, in the patient group MCP-1 -2518 AA genotype frequency was significantly higher than that of control group. On the other hand, heterozygous AG genotype frequency in the control group was significantly higher than that of the study group. Three different main disease subgroups of CRF (hypertension, diabetes mellitus, and atherosclerosis) patients were also evaluated, and significant associations were found between hypertension (genotype: chi (2) = 9.28, p = 0.01; allele: chi (2) = 6.00, p = 0.01), atherosclerosis (genotype: chi (2) = 5.37, p = 0.02; allele: chi (2) = 4.13, p = 0.04), and distributions of MCP-1 -2518 A > G genotypes and alleles. However, no significant association was found between diabetes mellitus and distributions of MCP-1 -2518 A > G genotype and allele frequencies (genotype: chi (2) = 2.37, p = 0.3; allele: chi (2) = 1.88, p = 0.17). Current data show that MCP-1 -2518 AA genotype may cause susceptibility to CRF, while G allele may have a protective effect against development of CRF. In addition, MCP-1 -2518 AA genotype seems to associate with CRF originated from hypertension and atherosclerosis in our study population.