WoS İndeksli Yayınlar Koleksiyonu / WoS Indexed Publications Collection
Permanent URI for this collectionhttps://hdl.handle.net/11147/7150
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Article Citation - WoS: 37Mechanisms of Cellular Resistance To Imatinib in Human Chronic Myeloid Leukemia Cells(Taylor and Francis Ltd., 2007) Baran, Yusuf; Ural, Ali Uğur; Gündüz, UfukA major advancement in the treatment of chronic myeloid leukemia (CML) has been the development of imatinib, which has shown striking activity in the chronic phase and the accelerated phase, but less so in the blast phase of the disease. Despite high rates of hematologic and cytogenetic responses to therapy, the emergence of resistance to imatinib has been recognized as a major problem in the treatment of patients with CML. Various cellular mechanisms may be involved in the nature of cellular resistance. Increased amount of target, alteration in structure of target proteins, decreased drug uptake and increased detoxification are well-known mechanisms of resistance. On the other hand, in some cases, even if anticancer drugs reach their sites of action, bypassing drug efflux system of the cells, some cells still may survive via the dysregulation of apoptotic signalling. In this study, mechanisms of resistance to imatinib-induced apoptosis in human Meg-01 CML cells were examined. Continuous exposure of cells to step-wise increasing concentrations of imatinib resulted in the selection of 200- and 1000 nM imatinib-resistant sub-lines referred to as Meg-01/IMA-0,2 and Meg-01/1MA-1, respectively. MTT cell proliferation, cell cycle analyses and trypan blue dye exclusion analyses showed that Meg-0l/IMA-1 cells were resistant to imatinib-induced apoptosis as compared to parental sensitive cells. There was an increased expression of BCR/ABL, Bcl-2 and an increase in mitochondrial membrane potential (MMP) detected in resistant cells comparing to parental sensitive cells. There was no mutation detected in imatinib binding site of ABL kinase region. Various diverse mechanisms have been reported for their involvement in the multidrug resistance. In this study, it has been shown that the degree of BCR/ABL expression appears to be directly proportional to the levels of imatinib resistance. In addition, there have been BCR/ABL-independent mechanisms reported for deriving resistance against imatinib. Our results revealed that besides BCR/ABL overexpression, imatinib resistance also depends on the inhibition of apoptosis as a result of up-regulation of anti-apoptotic stimuli and down-regulation of pro-apoptotic stimuli through MMP but does not depend on any mutation on imatinib binding site of ABL kinase.Conference Object Cytotoxic Effects of Apigenin on Multiple Myeloma Cells(Ferrata Storti Foundation, 2013) Baran, Yusuf; Yılmaz, S.; Cincin, Zeynep; Kozanoğlu, İlknur; Çakmakoğlu, Bedia; Özdoğu, Hakan[No abstract available]Conference Object Changes in Gene Expression Profiles in Response To Apigenin in Imatinib Sensitive and Resistant Chronic Myeloid Leukemia Cells(FERRATA STORTI FOUNDATION, 2013) Baran, Yusuf; Gökbulut, Aysun; Cincin, Zeynep; Çakmakoğlu, Bedia; Kozanoğlu, İlknur[No abstract available]Conference Object Determination of Cytotoxic and Apoptotic Effects of Caffeic Acid Phenethyl Ester and Gossypol in Combination With Fludarabine at a Molecular Level in Acute Lymphoblastic Leukemia Cells(Ferrata Storti Foundation, 2013) Baran, Yusuf; İskender, G.; Pişkin, Özden; Özcan, Mehmet Ali[No abstract available]Conference Object Diagnostic and Therapeutic Potentials of Expression Levels of Bioactive Sphingolipid Genes in Newly Diagnosed and Drug-Resistant Chronic Myeloid Leukemia Patients(Ferrata Storti Foundation, 2013) Baran, Yusuf; Yandım, Melis; Kozanoğlu, İlknur; Özdoğu, Hakan; Pişkin, Özden; Özcan, Mehmet Ali[No abstract available]Conference Object Immunologically Detection of Bcr/Abl Fusion Protein With Flow Cytometry in K562 Chronic Myeloid Leukemia Cells and Comparison With Rt-Pcr Results(Ferrata Storti Foundation, 2013) Kozanoğlu, İlknur; Aygün, B.; Boğa, I.; Cansun, C.; Üstündağ, N.; Baran, Yusuf; Özdoğu, Hakan[No abstract available]Conference Object Comparison of Ishage-Based Cd34 (+) Cell Enumeration Protocols on Bd Facs Canto Iı and Attune Flow Cytometers(Nature Publishing Group, 2014) Kozanoğlu, İlknur; Ünver, Gülşah; Sarıtürk, Çağla; Baran, Yusuf; Yeral, Mahmut; Boğa, Can; Özdoğu, Hakan[No abstract available]Conference Object Expression Levels of Ceramide-Metabolising Genes in Newly Diagnosed and Tyrosine Kinase Inhibitor-Resistant Chronic Myeloid Leukemia (cml) Patients: the Discovery of Novel Targets in Cml(Elsevier Ltd., 2014) Yandım, Melis Kartal; Kozanoğlu, İlknur; Özdoğu, Hakan; Pişkin, O.; Özcan, Mehmet Ali; Saydam, Göksel; Baran, Yusuf[No abstract available]Conference Object Jak/Stat Signalling Pathway Genes in the Regulation of Tyrosine Kinase Inhibitors Induced and Clinical Process in Chronic Myeloid Leukemia Patients(Elsevier, 2014) Kiraz, Yağmur; Kartal Yandım, Melis; Kozanoğlu, İlknur; Özdoğu, Hakan; Pişkin, I.; Özcan, Mehmet Ali; Saydam, Göksel; Şahin, Fahri; Avcu, Ferit; Ural, Ali Uğur; Ünal, Ali; Baran, Yusuf[No abstract available]Conference Object Effects of Apigenin on Imatinin-Sensitive and Resistant Chronic Myeloid Leukemia Cells(Ferrata Storti Foundation, 2013) Baran, Yusuf; Solmaz, Soner; Gökbulut, Aysun; Kozanoğlu, İlknur; Özdoğu, Hakan[No abstract available]