PubMed İndeksli Yayınlar Koleksiyonu / PubMed Indexed Publications Collection

Permanent URI for this collectionhttps://hdl.handle.net/11147/7645

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  • Article
    Citation - WoS: 33
    Citation - Scopus: 35
    Imatinib Induces Autophagy Through Beclin-1 and Atg5 Genes in Chronic Myeloid Leukemia Cells
    (Taylor and Francis Ltd., 2011) Can, Geylani; Ekiz, Hüseyin Atakan; Baran, Yusuf
    Locate full-text(opens in a new window)|Full Text(opens in a new window)|View at Publisher| Export | Download | Add to List | More... Hematology Volume 16, Issue 2, March 2011, Pages 95-99 Imatinib induces autophagy through BECLIN-1 and ATG5 genes in chronic myeloid leukemia cells (Article) Can, G., Ekiz, H.A., Baran, Y. Department of Molecular Biology and Genetics, Faculty of Science, Izmir Institute of Technology, 35430 Urla, Izmir, Turkey View references (35) Abstract Imatinib is a chemotherapeutic drug used for the treatment of chronic myeloid leukemia (CML). Recent data showed imatinib-induced cell death in various types of cancers. Autophagy is the physiological process in which cellular components are broken down by the lysosomal activation. In this study, we aimed to examine the effects of imatinib on autophagy in addition to apoptosis in CML cells. Results suggested that imatinib induces autophagy in CML cells through inducing over-expression of BECLIN-1 and ATG5 genes with the statistical significance. Our results demonstrated that autophagy might be involved in imatinib-induced cell death.
  • Article
    Citation - WoS: 31
    Citation - Scopus: 36
    Quercetin-Induced Apoptosis Involves Increased Htert Enzyme Activity of Leukemic Cells
    (Taylor and Francis Ltd., 2011) Avcı, Çığır Biray; Yılmaz, Sunde; Doğan, Zeynep Özlem; Saydam, Güray; Dodurga, Yavuz; Ekiz, Hüseyin Atakan; Kartal, Melis; Şahin, Fahri; Baran, Yusuf; Gündüz, Cumhur
    We aimed to examine the growth suppressive effects of quercetin on acute promyelocytic and lymphoblastic leukemia and chronic myeloid leukemia, and to find out whether the growth suppression is related to the blocking of telomerase enzyme activity. Cytotoxic effects of quercetin were shown by trypan blue analyses. Apoptotic effects of quercetin were examined by acridine orange and ethidium bromide staining by fluorescence microscopy. The effects of quercetin on telomerase enzyme activity were shown by hTERT Quantification Kit. Our results demonstrated that quercetin has antiproliferative and apoptotic effects on T-cell acute lymphoblastic leukemia (ALL), acute promyelocytic leukemia, and chronic myeloid leukemia (CML) cells. We also showed for the first time by this study that quercetin suppresses the activity of telomerase in ALL and CML cells. The results of this study show the importance of quercetin for its therapeutic potential in treatment of leukemias.
  • Article
    Citation - WoS: 7
    Citation - Scopus: 7
    Nilotinib Significantly Induces Apoptosis in Imatinib Resistant K562 Cells With Wild-Type Bcr-Abl, as Effectively as in Parental Sensitive Counterparts
    (Taylor and Francis Ltd., 2010) Ekiz, Hüseyin Atakan; Can, Geylani; Gündüz, Ufuk; Baran, Yusuf
    Chronic myeloid leukemia (CML) is a hematological malignancy characterized by high levels of immature white blood cells. CML is caused by the translocation between chromosomes 9 and 22 (which results in the formation of the Philadelphia chromosome) creating BCR-ABL fusion protein. Imatinib and nilotinib are chemotherapeutic drugs which specifically bind to the BCR-ABL and inhibit cancer cells. Nilotinib is more effective in this respect than imatinib. We have shown that nilotinib induces apoptosis in imatinib-resistant K562 CML cells which have the wild-type BCR-ABL fusion gene almost to the same extent as it does in the parental sensitive cells by the increase in caspase-3 enzyme activity and the decrease in mitochondrial membrane potential. This effect of nilotinib, even in low concentrations, may indicate the efficacy of the usage of nilotinib in imatinib-resistant CML with less risk of undesired cytotoxic effects in the remaining cells of the body. © 2010 W. S. Maney & Son Ltd.