TR-Dizin
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Browsing TR-Dizin by Journal "Turkish Journal of Hematology"
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Review The importance of protein profiling in the diagnosis and treatment of hematologic malignancies(Galenos Yayincilik, 2011) Sanli-Mohamed, Gulsah; Turan, Taylan; Ekiz, Huseyin Atakan; Baran, Yusuf; Baran, YusufProteins are important targets in cancer research because malignancy is associated with defects in cell protein machinery. Protein profiling is an emerging independent subspecialty of proteomics that is rapidly expanding and providing unprecedented insight into biological events. Quantitative assessment of protein levels in hematologic malignancies seeks a comprehensive understanding of leukemia-associated protein patterns for use in aiding diagnosis, follow-up treatment, and the prediction of clinical outcomes. Many recently developed high-throughput proteomic methods can be applied to protein profiling. Herein the importance of protein profiling, its exploitation in leukemia research, and its clinical usefulness in the treatment and diagnosis of various cancer types, and techniques for determining changes in protein profiling are reviewed. (Turk J Hematol 2011; 28: 1-14)Article Optimization of transfection of green fluorescent protein in pursuing mesenchymal stem cells in vivo(2008) Avcu, Ferit; Baran, Yusuf; Ural, Uğur; Elçi̇, Pınar; Sarper, Meral; Baran, YusufAmaç: Yeşil floresan proteini (YFP), günümüzde hücre biyolojisi çalışmalarında tanımlayıcı gen ve hücre işaretleyici olarak kullanılmaktadır. YFP’nin oldukça önemli kullanım alanları farklı genlerin içerisine eklenerek bu genlerin farklı organizmalardaki ekspresyonlarının miktar tayininde ve canlı hücreler içerisinde işaretleyici olarak kullanılabilmesidir. Bu çalışmamızda doku tamiri amacıyla ve hayvanlara aktardığımız mezankimal kök hücrelerini (MKH) in vivo takip edebilmek amacı ile YFP genini içeren plazmid vektörünün MKH’lara aktarılmasını optimize etmeye çalıştık. Yöntem ve Gereçler: Bu amaçla YFP geni taşıyan phM-YFP plazmid vektörü ve MKH’lara plazmid vektörün aktarılması amacı ile Effectene Transfeksiyon kiti kullanılmıştır.Bulgular: Elde edilen sonuçlar, MKH’ların phM-YFP ile iki defa transfekte edilmelerinin tek bir defa transfekte edilmelerine göre daha yüksek oranda ve daha uzun süreli YFP ekspresyonu sağladığını göstermiştir.Sonuç: MKH’ların YFP ile işaretlenmesi çalışmalarında transfeksiyon kimyasallarının yeterli bir inkübasyondan sonra uzaklaştırılmasının ve transfeksiyon işleminin 48 saat arayla iki defa yapılmasının MKH’ların aktarıldığı doku veya canlılarda daha uzun süreli ve daha etkin bir şekilde takibine olanak sağlayacağı gösterilmiştirArticle Therapeutic Potentials of Inhibition of Jumonji C Domaincontaining Demethylases in Acute Myeloid Leukemia(2020) Engür, Selin; Koca, Duygu; Ki̇raz, Yağmur; Ulu, Tuğçe; Baran, Yusuf; Çekdemi̇r, Demet; Baran, YusufObjective: Acute myeloid leukemia (AML) is a complex disease affected by both genetic and epigenetic factors. Histone methylation and demethylation are types of epigenetic modification in chromatin remodeling and gene expression. Abnormal expression of histone demethylases is indicated in many types of cancer including AML. Although many commercial drugs are available to treat AML, an absolute cure has not been discovered yet. However, inhibition of demethylases could be a potential cure for AML. Methylstat is a chemical agent that inhibits the Jumonji C domain-containing demethylases. Materials and Methods: The cytotoxic and apoptotic effects of methylstat and doxorubicin on HL-60 cells were detected by MTT cell viability assay, double staining of treated cells with annexin-V/ propidium iodide, and caspase-3 activity assay. Mitochondrial activity was analyzed using JC-1 dye. The expression levels of the BCL2 and BCL2L1 anti-apoptotic genes in HL-60 cells were determined using real-time polymerase chain reaction (PCR). Lastly, the cytostatic effect was determined by cell cycle analysis. Results: In our research, cytotoxic, cytostatic, and apoptotic effects of methylstat on human HL-60 cells were investigated. Cytotoxic and cytostatic analyses revealed that methylstat decreased cell proliferation in a dose-dependent cytotoxic manner and arrested HL60 cells in the G2/M and S phases. Methylstat also induced apoptosis through the loss of mitochondrial membrane potential and increases in caspase-3 enzyme activity. The expression levels of BCL2 and BCL2L1 were also decreased according to real-time PCR results. Finally, the combination of methylstat with doxorubicin resulted in synergistic cytotoxic effects on HL-60 cells. Conclusion: Taken together, these results demonstrate that methylstat may be a powerful candidate as a drug component of AML treatment protocols.