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Browsing by Author "Srzentić, Sanja (57204289670)"

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    Publication
    -174G/C interleukin-6 gene promoter polymorphism predicts therapeutic response to etanercept in rheumatoid arthritis
    (2013)
    Jančić, Ivan (24721867100)
    ;
    Arsenović-Ranin, Nevena (59662809600)
    ;
    Šefik-Bukilica, Mirjana (8118591400)
    ;
    Živojinović, Sladjana (35754184300)
    ;
    Damjanov, Nemanja (8503557800)
    ;
    Spasovski, Vesna (26655022200)
    ;
    Srzentić, Sanja (57204289670)
    ;
    Stanković, Biljana (35785023700)
    ;
    Pavlović, Sonja (7006514877)
    To examine whether -174G/C interleukin-6 (IL-6) gene polymorphism, previously reported to correlate with IL-6 level, influences response to etanercept therapy in patients with rheumatoid arthritis. Seventy-seven patients with active RA were studied, at baseline and 6- and 12-month follow-up after etanercept therapy. Treatment response was estimated according to the European League Against Rheumatism response criteria. RA patients were genotyped for -174G/C IL-6 gene polymorphism by the PCR-RFLP method, and influence of genotype at this polymorphism to clinical response to etanercept was assessed. After 12 months of treatment, the percentage of responders (patients who had DAS28 improvement >1.2) was significantly increased in patients carrying the IL-6 -174G/G genotype (95.7 %) compared with those with the G/C (75.6 %) or CC (44.4 %) genotype (p = 0.006 by Chi-square test). No significant difference in the mean values of DAS28 improvement was observed between groups with different genotype. RA patients with an IL-6 -174GG genotype respond to etanercept better than patients with GC or CC genotype. This finding, if confirmed in future studies, suggests that the -174G/C IL-6 polymorphism may be a genetic marker of responsiveness to tumor necrosis factor-alpha (TNF-α) blockers in RA. © 2012 Springer-Verlag Berlin Heidelberg.
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    Publication
    -174G/C interleukin-6 gene promoter polymorphism predicts therapeutic response to etanercept in rheumatoid arthritis
    (2013)
    Jančić, Ivan (24721867100)
    ;
    Arsenović-Ranin, Nevena (59662809600)
    ;
    Šefik-Bukilica, Mirjana (8118591400)
    ;
    Živojinović, Sladjana (35754184300)
    ;
    Damjanov, Nemanja (8503557800)
    ;
    Spasovski, Vesna (26655022200)
    ;
    Srzentić, Sanja (57204289670)
    ;
    Stanković, Biljana (35785023700)
    ;
    Pavlović, Sonja (7006514877)
    To examine whether -174G/C interleukin-6 (IL-6) gene polymorphism, previously reported to correlate with IL-6 level, influences response to etanercept therapy in patients with rheumatoid arthritis. Seventy-seven patients with active RA were studied, at baseline and 6- and 12-month follow-up after etanercept therapy. Treatment response was estimated according to the European League Against Rheumatism response criteria. RA patients were genotyped for -174G/C IL-6 gene polymorphism by the PCR-RFLP method, and influence of genotype at this polymorphism to clinical response to etanercept was assessed. After 12 months of treatment, the percentage of responders (patients who had DAS28 improvement >1.2) was significantly increased in patients carrying the IL-6 -174G/G genotype (95.7 %) compared with those with the G/C (75.6 %) or CC (44.4 %) genotype (p = 0.006 by Chi-square test). No significant difference in the mean values of DAS28 improvement was observed between groups with different genotype. RA patients with an IL-6 -174GG genotype respond to etanercept better than patients with GC or CC genotype. This finding, if confirmed in future studies, suggests that the -174G/C IL-6 polymorphism may be a genetic marker of responsiveness to tumor necrosis factor-alpha (TNF-α) blockers in RA. © 2012 Springer-Verlag Berlin Heidelberg.
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    Publication
    Predictive genetic markers of coagulation, inflammation and apoptosis in Perthes disease—Serbian experience
    (2015)
    Srzentić, Sanja (57204289670)
    ;
    Nikčević, Gordana (6602344117)
    ;
    Spasovski, Duško (25028865800)
    ;
    Baščarević, Zoran (6506868841)
    ;
    Živković, Zorica (57224757364)
    ;
    Terzic-Šupić, Zorica (15840732000)
    ;
    Matanović, Dragana (21739989500)
    ;
    Djordjević, Valentina (7005657086)
    ;
    Pavlović, Sonja (7006514877)
    ;
    Spasovski, Vesna (26655022200)
    Perthes disease is one of the most common forms of pediatric femoral head osteonecrosis with an unknown etiology. Coagulation factors were the first genetic factors suspected to have a role in the pathogenesis of this disease, but studies showed inconsistent results. It is described that inflammation is present during early stages of Perthes disease, but its genetic aspect has not been studied extensively. Little is known regarding the status of apoptotic factors during the repair process that leads to the occurrence of hip deformity in patients. Therefore, the aim of this study was to analyze major mediators involved in coagulation, inflammation, and apoptotic processes as possible causative factors of Perthes disease. The study cohort consisted of 37 patients. Gene variants of TNF-α, FV, FII, and MTHFR genes were determined by PCR-RFLP, while IL-3 and PAI-1 were genotyped by direct sequencing. The expression level of Bax, Bcl-2, Bcl2L12, Fas and FasL was analyzed by quantitative reverse-transcriptase polymerase chain reaction (qRT-PCR) technique. Our results showed a significantly increased level of expression of pro-apoptotic factor Bax along with significantly higher Bax/Bcl-2 ratio in the patient group. Conclusion: The results presented indicate that apoptosis could be one of the factors contributing to the lack of balanced bone remodeling process in Perthes patients. © 2015, Springer-Verlag Berlin Heidelberg.

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