Please use this identifier to cite or link to this item: https://hdl.handle.net/11147/2861
Title: Docetaxel enhances the cytotoxic effects of imatinib on Philadelphia positive human chronic myeloid leukemia cells
Authors: Güçlüler, Gözde
Baran, Yusuf
Güçlüler, Gözde
Baran, Yusuf
Izmir Institute of Technology. Molecular Biology and Genetics
Keywords: Imatinib
Docetaxel
Apoptosis
Chronic myeloid leukemia
BCR/ABL
Issue Date: Jun-2009
Publisher: Taylor and Francis Ltd.
Source: Güçlüler, G., and Baran, Y. (2009). Docetaxel enhances the cytotoxic effects of imatinib on Philadelphia positive human chronic myeloid leukemia cells. Hematology, 14(3), 139-144. doi:10.1179/102453309X426164
Abstract: Chronic myelogenous leukemia (CML) results from a translocation between chromosomes 9 and 22 which generates BCR/ABL fusion protein and characterized by uncontrolled proliferation of immature white blood cells. Imatinib, a molecularly targeting anticancer agent, is used widely for the treatment of CML and showed significant activity in chronic and accelerated phases but much less in blast crisis phase. The resistance to imatinib especially in blast crisis phase is recognized as a major problem in the treatment of CML patients. Docetaxel is shown to arrest cells in G2/M phase of the cell cycle which makes cells more sensitive to chemo- and radiotherapy. In this study, we aimed to increase chemosensitivity of human K562 CML cells to imatinib in combination with docetaxel. Taken together, our results showed that the combination of imatinib and docetaxel decreased cellular proliferation and increased apoptosis in human K562 chronic myeloid leukemia cells as compared to any agent alone. Imatinib and docetaxel induced apoptosis through caspase-3 enzyme activity and mitochondrial membrane potential.
URI: http://doi.org/10.1179/102453309X426164
http://hdl.handle.net/11147/2861
ISSN: 1024-5332
1024-5332
Appears in Collections:Molecular Biology and Genetics / Moleküler Biyoloji ve Genetik
Scopus İndeksli Yayınlar Koleksiyonu / Scopus Indexed Publications Collection
WoS İndeksli Yayınlar Koleksiyonu / WoS Indexed Publications Collection

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