Browsing by Author "Goker, B"

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    EPIGALLOCATECHIN-3-GALLATE TRIGGERS AUTOPHAGY MEDIATED CELL DEATH VIA UP-REGULATION OF TMEM74 GENE EXPRESSION IN CHRONIC MYELOID LEUKEMIA CELLS
    Goker, B; Caliskan, C; Mutlu, Z; Tepedelen, BE; Korkmaz, M; Saydam, G; Gunduz, C; Avci, CB
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    Synergistic effect of ponatinib and epigallocatechin-3-gallate induces apoptosis in chronic myeloid leukemia cells through altering expressions of cell cycle regulatory genes
    Goker, B; Caliskan, C; Caglar, HO; Kayabasi, C; Balci, T; Tepedelen, BE; Aygunes, D; Susluer, SY; Mutlu, Z; Gunel, NS; Korkmaz, M; Saydarn, G; Gunduz, C; Avci, CB
    Purpose: Ponatinib (P) has been used for the treatment of chronic myeloid leukemia (CML) and it is known that inhibition of BCR-ABL fusion protein by ponatinib induces apoptosis of CML cells. Epigallocatechin-3-gallate (EGCG), which is a poly phenol in green tea, induces apoptosis in different types of cancer cells. The purpose of this study was to determine the cytotoxic and apoptotic effects of ponatinib and EGCG combination in K562 CML cell line. This study also aimed to detect alterations of the expression levels of cell cycle-regulation related genes after ponatinib and EGCG combination in K562 CML cell line. Methods: The cytotoxic effects of the compounds on K562 cells were determined in a time-and dose-dependent manner by using WST-1 analysis. The combination index (CI) isobologram was used to analyze the data. Apoptotic effects of P-EGCG were defined by flow cytometry and gene expressions were detected by RT-qPCR. Results: IC50 values of ponatinib and EGCG were 87.13 nM and 50 mu M, respectively. CI value of the P-EGCG was 0.658 and the combination showed synergistic effect (ED90 value: 28.39 nM ponatinib, 117.12 mu g/ml EGCG). Ponatinib, EGCG and P-EGCG induced apoptosis compared to control cells. CyclinD1 and CDC25A were downregulated by P-EGCG by 2.49 and 2.63-fold, respectively. TGF-beta 2 was upregulated by 4.57-fold. Conclusion: EGCG possesses cytotoxic and apoptotic properties and may cooperate with the growth inhibiting activity of ponatinib synergistically against CML cells. P-EGCG mediated apoptosis might be associated with upregulation of TGF-/32 gene and downregulation of cyclinD1 and CDC25A genes.
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    The Efficacy and Safety of CT-P13 as First-line and Subsequent-line Therapy in Patients with Ankylosing Spondylitis: Real-life Data from TURKBIO Cohort
    Uslu, S; Gulle, S; Can, G; Senel, S; Capar, S; Dalkilic, HE; Akar, S; Koca, SS; Tufan, A; Yazici, A; Yilmaz, S; Inanc, N; Birlik, M; Solmaz, D; Cefle, A; Goker, B; Yolbas, S; Krough, NS; Yilmaz, N; Erten, S; Bes, C; Soysal, O; Ozturk, MA; Haznedaroglu, S; Yavuz, S; Direskeneli, H; Onen, F; Sari, I
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    Efficacy and Safety of CT-P13 as First- and Second-Line Treatment in Patients with Ankylosing Spondylitis
    Uslu, S; Gülle, S; Sen, G; Capar, S; Senel, S; Dalkilic, E; Akar, S; Koca, SS; Tufan, A; Yazici, A; Yilmaz, S; Inanc, N; Birlik, M; Solmaz, D; Cefle, A; Goker, B; Direskeneli, H; Yolbas, S; Krogh, NS; Yilmaz, N; Erten, S; Bes, C; Gündüz, OS; Oztürk, MA; Haznedaroglu, S; Yavuz, S; Onen, F; Sari, I
    Background/Objectives: CT-P13 is a biosimilar version of infliximab, a monoclonal antibody. In individuals with ankylosing spondylitis (AS), CT-P13 has been shown to be effective and to have a well-tolerated safety profile. The aim of this study was to evaluate the long-term drug persistence, safety, and efficacy of infliximab biosimilar CT-P13 in patients with AS undergoing first-line (1st-line) and later (>= 2nd-line) treatment in clinical practice. Methods: We performed an observational cohort study that included AS patients based on the biological drug database in the TURKBIO Registry between 2014 and 2021. The patients were divided into two groups: those receiving CT-P13 as first-line treatment or as a switch (>= 2nd-line) from another TNF inhibitor (TNFi). Standard disease activity metrics were used to assess the effectiveness of CT-P13, and drug retention rates were investigated. Results: There were 179 AS patients using CT-P13 (47.4% male, mean age: 42.9 +/- 11.3 years). Of these patients, 123 (68.7%) were receiving CT-P13 as a first-line treatment. The mean length of treatment was 3.5 years. CT-P13 drug retention rates in the general patient population were 58.6% and 48.2% in the first-line and >= second-line treatment, respectively, after 3 years of follow-up. The most common reason for CT-P13 treatment discontinuation was lack of efficacy. The first-line CT-P13 group had statistically substantially higher ASAS20/40 response rates at three and six months. Nonetheless, both groups' response rates at one year were comparable. Conclusions: In this real-world data analysis, AS patients who were TNFi na & iuml;ve (1st-line) and subsequently treated (>= 2nd-line) with CT-P13 showed encouraging drug retention rates with acceptable long-term effectiveness and safety.
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    Efficacy and Safety of Secukinumab in the Treatment of Axial Spondyloarthritis: Real-Life Data from TURKBIO Cohort
    Gulle, S; Karakas, A; Can, G; Senel, S; Capar, S; Dalkilic, HE; Akar, S; Koca, SS; Tufan, A; Yazici, A; Yilmaz, S; Inanc, N; Birlik, M; Solmaz, D; Cefle, A; Goker, B; Yolbas, S; Krough, NS; Yilmaz, N; Erten, S; Bes, C; Soysal, O; Ozturk, MA; Haznedaroglu, S; Yavuz, S; Direskeneli, H; Onen, F; Sari, I
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    The impact of smoking on response to tumor necrosis factor-α inhibitor treatment in patients with ankylosing spondylitis
    Tugsal, HY; Kenar, G; Can, G; Çapar, S; Zengin, B; Akar, S; Dalkiliç, E; Senel, S; Koca, SS; Goker, B; Yazici, A; Inanç, N; Ellidokuz, H; Akkoç, N; Önen, F
    Background/aim: To investigate the impact of smoking on disease activity, treatment retention, and response in patients with ankylosing spondylitis (AS) treated with their first tumor necrosis factor-alpha inhibitor (TNFi). Materials and methods: AS patients who started their first TNFi treatment for the active axial disease (BASDAI >= 4) from TURKBIO Registry were included. Treatment response of smoker (current and ex-smokers) and nonsmoker (never smoker) patients were primarily evaluated as achievement of BASDAI50 or improvement in BASDAI at least 20 mm at 3 months and 6 months compared to baseline. Results: There were 322 patients with AS (60% male, 59% smoker, mean age: 38.3 years). The median follow-up time was 2.8 years (Q1-Q3: 1.3-3.8), and disease duration was 3.5 years (Q1-Q3: 0.7-8.2). Smokers had male predominance (p < 0.001), lower ESR (p = 0.03), higher BASDAI (p = 0.02), BASFI (p = 0.05), HAQ-AS (p = 0.007), and ASDAS-CRP (p = 0.04) compared with nonsmokers at baseline. In the multivariate analysis, male gender [OR 2.7 (95%CI 1.4-5), p = 0.002], and concomitant conventional synthetic disease-modifying antirheumatic drug use [OR 2.4 (95%CI 1.1-5.2), p = 0.03] were associated with better treatment response. There was an association of male gender [HR 2.4 (95%CI 1.6-3.7), p < 0.001], older age (>= 30years) [HR 1.8 (95%CI 1.1-2.8), p = 0.01], and response to treatment [HR 1.8 (95%CI 1.2-2.9), p = 0.008] with better treatment retention. No impact of smoking status was found on treatment retention and response in univariate and multivariate analyses. Conclusion: This study suggested that smoking was associated with poorer patient-reported outcomes in biologic naive AS patients initiating their first TNFi treatment, but it had no impact on the TNFi treatment response and retention rate.
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    DO COMORBIDITIES IMPACT PERSISTENCE OF FIRST TUMOR NECROSIS FACTOR INHIBITOR TREATMENT IN RHEUMATOID ARTHRITIS? DATA FROM TURKBIO
    Inel, TY; Kocaer, SB; Erez, Y; Gulle, S; Karakas, A; Avsar, AK; Uslu, S; Can, G; Sari, I; Birlik, M; Dalkiliç, E; Pehlivan, Y; Akar, S; Goker, B; Cetin, GY; Haznedaroglu, S; Yavuz, S; Pirildar, T; Direskeneli, H; Akkoc, N; Onen, F