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.Gündüz, UfukInstitution Author: search.filters.institutionAuthor.Ekiz, Hüseyin Atakan

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Now showing 1 - 2 of 2
  • 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; Baran, Yusuf; Baran, Yusuf; Ekiz, Hüseyin Atakan; 04.03. Department of Molecular Biology and Genetics; 04. Faculty of Science; 01. Izmir Institute of Technology
    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.
  • Article
    Citation - WoS: 18
    Citation - Scopus: 16
    Suppression of Stat5a Increases Chemotherapeutic Sensitivity in Imatinib-Resistant and Imatinib-Sensitive K562 Cells
    (Informa Healthcare, 2010) Kosova, Buket; Tezcanlı, Burçin; Baran, Yusuf; Çakır, Zeynep; Selvi, Nur; Ekiz, Hüseyin Atakan; Yandım, Melis Kartal; Gündüz, Ufuk; Baran, Yusuf; 04.03. Department of Molecular Biology and Genetics; 04. Faculty of Science; 01. Izmir Institute of Technology
    STAT proteins are cytoplasmic transcription factors that are involved in the regulation of numerous cellular activities such as cell growth, differentiation, and survival. In this study, we aimed to identify the expression pattern of STAT genes in imatinib-sensitive and-resistant K562 cells, and further, to reveal the effects of STAT5A siRNA knockdown on cell growth and apoptosis induction. The XTT cell proliferation assay showed that both sensitive and resistant K562 cells were sensitized to imatinib upon transfection with STAT5A siRNA. Caspase-3 enzyme activity was increased significantly in both cells. These results may open up new opportunities to overcome chemotherapeutic resistance in leukemia. © 2010 Informa UK, Ltd.