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

Date

2010-02-01

Author

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

Metadata

Show full item record

This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.

Item Usage Stats

1
views

0
downloads

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

Collections

Graduate School of Natural and Applied Sciences, Article