Nilotinib significantly induces apoptosis in imatinib resistant K562 cells with wild-type BCR-ABL, as effectively as in parental sensitive counterparts

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2010-02-01

Author

Ekiz, Huseyin Atakan
Can, Geylani
Gündüz, Ufuk
BARAN, YUSUF

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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.

Subject Keywords

İmatinib, Nilotinib, Drug resistance, BCR–ABL, CML

URI

https://hdl.handle.net/11511/30550

Journal

HEMATOLOGY

DOI

https://doi.org/10.1179/102453310x12583347009775

Collections

Graduate School of Natural and Applied Sciences, Article

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Citation Formats

H. A. Ekiz, G. Can, U. Gündüz, and Y. BARAN, “Nilotinib significantly induces apoptosis in imatinib resistant K562 cells with wild-type BCR-ABL, as effectively as in parental sensitive counterparts,” HEMATOLOGY, pp. 33–38, 2010, Accessed: 00, 2020. [Online]. Available: https://hdl.handle.net/11511/30550.