Please use this identifier to cite or link to this item: https://hdl.handle.net/11147/2791
Title: Nilotinib significantly induces apoptosis in imatinib resistant K562 cells with wild-type BCR-ABL, as effectively as in parental sensitive counterparts
Authors: Ekiz, Hüseyin Atakan
Can, Geylani
Gündüz, Ufuk
Baran, Yusuf
Keywords: Nilotinib
Imatinib
Drug resistance
Chronic myeloid leukemia
BCR-ABL protein
Issue Date: Feb-2010
Publisher: Taylor and Francis Ltd.
Source: Ekiz, H. A., Can, G., Gündüz, U., and Baran, Y. (2010). Nilotinib significantly induces apoptosis in imatinib resistant K562 cells with wild-type BCR-ABL, as effectively as in parental sensitive counterparts. Hematology, 15(1), 33-38. doi:10.1179/102453310X12583347009775
Abstract: 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.
URI: http://doi.org/10.1179/102453310X12583347009775
http://hdl.handle.net/11147/2791
ISSN: 1024-5332
1024-5332
Appears in Collections:Molecular Biology and Genetics / Moleküler Biyoloji ve Genetik
PubMed İndeksli Yayınlar Koleksiyonu / PubMed Indexed Publications Collection
Scopus İndeksli Yayınlar Koleksiyonu / Scopus Indexed Publications Collection
WoS İndeksli Yayınlar Koleksiyonu / WoS Indexed Publications Collection

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