Molecular Biology and Genetics / Moleküler Biyoloji ve Genetik

Permanent URI for this collectionhttps://hdl.handle.net/11147/9

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Author: search.filters.author.Özcan, Mehmet Ali

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Now showing 1 - 6 of 6
  • 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
    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
    Antiproliferative and Apoptotic Effects of Resveratrol on Chronic Lymphocytic Leukemia Cells
    (Ferrata Storti Foundation, 2012) Baran, Yusuf; Gökbulut, Aysun; Özcan, Mehmet Ali; Pişkin, Özden; Ünlü, Miray
    [No abstract available]
  • Article
    Citation - WoS: 6
    Citation - Scopus: 7
    Nilotinib Does Not Alter the Secretory Functions of Carotid Artery Endothelial Cells in a Prothrombotic or Antithrombotic Fashion
    (SAGE Publications Inc., 2015) Katgı, Abdullah; Sevindik, Ömer Gökmen; Adan Gökbulut, Aysun; Özsan, Güner Hayri; Yüksel, Faize; Solmaz, Şerife Medeni; Alacacıoğlu, İnci; Özcan, Mehmet Ali; Demirkan, Fatih; Baran, Yusuf; Pişkin, Özden
    Background: There have been concerns about the possible prothrombotic effects of nilotinib, especially in patients having cardiovascular risk factors. The potential mechanism behind the increased risk of thromboembolic events is still not clear. Objectives: In this study, we aimed to evaluate possible harmful effects of nilotinib on endothelial cells. To this aim, we examined proliferative capacity and secretory functions of healthy human carotid artery endothelial cells (HCtAECs) in response to nilotinib. Methods: 3-(4,5-Dimethylthiazolyl-2)-2,5-diphenyltetrazolium bromide (MTT) cell proliferation method was used to determine antiproliferative effects of nilotinib on HCtAECs. The HCtAECs were incubated with 5, 10, and 100 nmol/L doses of nilotinib for 72 hours. Then, in order to assess the endothelial function, levels of nitric oxide (NO), von Willebrand factor (vWF), tissue plasminogen activator, plasminogen activator inhibitor 1 (PAI-1), and endothelin 1 (ET-1) were evaluated using enzyme-linked immunosorbent assay from tissue culture supernatants. Results: There were slight but statistically significant decreases in cell proliferation in response to nilotinib. Nilotinib increased the secretion of t-PA, PAI-1, and vWF in a dose-dependent manner when compared with the untreated control group. The ET-1 secretion was lower in 5 nmol/L and higher in 10 and 100 nmol/L nilotinib-treated cells as compared to untreated cells. Regarding NO secretion, lower levels were observed in 5 and 10 nmol/L, and higher levels were detected in 100 nmol/L nilotinib-treated cells as compared to untreated control group cells. Conclusion: Considering the results obtained in our study, nilotinib does not affect the functions of endothelial cells either in a prothrombotic or an antithrombotic fashion, despite a dose-dependent decline in cell viability.
  • Article
    Citation - WoS: 8
    Citation - Scopus: 8
    Multidrug Resistance in Chronic Myeloid Leukemia
    (TÜBİTAK, 2014) Ünlü, Miray; Kiraz, Yağmur; Kacı, Fatma Necmiye; Özcan, Mehmet Ali; Baran, Yusuf
    Chronic myeloid leukemia (CML) is characterized by the accumulation of Philadelphia chromosome-positive (Ph+) myeloid cells. Ph+ cells occur via a reciprocal translocation between the long arms of chromosomes 9 and 22 resulting in constitutively active Bcr-abl fusion protein. Tyrosine kinase inhibitors (TKIs) are used against the kinase activity of Bcr-abl fusion protein for the effective treatment of CML. However, the development of drug resistance, directed by different genetic mechanisms, is the major problem of clinical applications of TKIs. These mechanisms include mutations in the TKI binding site of Bcr-abl, overexpression of Bcr-abl, overexpression of ATP binding cassette transporters, aberrant ceramide metabolism, inhibition of apoptosis, and changes in expression levels of microRNAs. Recently, many studies have focused on understanding the molecular mechanisms of drug resistance in cancer while targeting therapies providing reversal of resistance. Cancer stem cells also have roles in tumor initiation, maintenance, progression, metastasis, and drug resistance. Uncovering the mechanisms of drug resistance can provide more efficient treatment of cancer since these findings may provide novel targets for a complete cure. In this review, we discuss recent findings on the mechanisms of multidrug resistance and its reversal in CML. © TÜBİTAK.