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dc.contributor.authorÜnlü, Miray
dc.contributor.authorKiraz, Yağmur
dc.contributor.authorKacı, Fatma Necmiye
dc.contributor.authorÖzcan, Mehmet Ali
dc.contributor.authorBaran, Yusuf
dc.date.accessioned2017-04-24T08:25:01Z
dc.date.available2017-04-24T08:25:01Z
dc.date.issued2014
dc.identifier.citationÜnlü, M., Kiraz, Y., Kacı, F. N., Özcan, M. A., and Baran, Y. (2014). Multidrug resistance in chronic myeloid leukemia. Turkish Journal of Biology, 38(6), 806-816. doi:10.3906/biy-1405-21en_US
dc.identifier.issn1300-0152
dc.identifier.urihttp://doi.org/10.3906/biy-1405-21
dc.identifier.urihttp://hdl.handle.net/11147/5382
dc.description.abstractChronic myeloid leukemia (CML) is characterized by the accumulation of Philadelphia chromosome-positive (Ph+) myeloid cells. Ph+ cells occur via a reciprocal translocation between the long arms of chromosomes 9 and 22 resulting in constitutively active Bcr-abl fusion protein. Tyrosine kinase inhibitors (TKIs) are used against the kinase activity of Bcr-abl fusion protein for the effective treatment of CML. However, the development of drug resistance, directed by different genetic mechanisms, is the major problem of clinical applications of TKIs. These mechanisms include mutations in the TKI binding site of Bcr-abl, overexpression of Bcr-abl, overexpression of ATP binding cassette transporters, aberrant ceramide metabolism, inhibition of apoptosis, and changes in expression levels of microRNAs. Recently, many studies have focused on understanding the molecular mechanisms of drug resistance in cancer while targeting therapies providing reversal of resistance. Cancer stem cells also have roles in tumor initiation, maintenance, progression, metastasis, and drug resistance. Uncovering the mechanisms of drug resistance can provide more efficient treatment of cancer since these findings may provide novel targets for a complete cure. In this review, we discuss recent findings on the mechanisms of multidrug resistance and its reversal in CML. © TÜBİTAK.en_US
dc.language.isoengen_US
dc.publisherTÜBİTAKen_US
dc.relation.isversionof10.3906/biy-1405-21en_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectTyrosine kinase inhibitoren_US
dc.subjectDrug resistanceen_US
dc.subjectChronic myeloid leukemiaen_US
dc.subjectCancer cellsen_US
dc.subjectBCR-ABL proteinen_US
dc.titleMultidrug resistance in chronic myeloid leukemiaen_US
dc.typereviewen_US
dc.contributor.authorIDTR119193en_US
dc.contributor.iztechauthorÜnlü, Miray
dc.contributor.iztechauthorKiraz, Yağmur
dc.contributor.iztechauthorKacı, Fatma Necmiye
dc.contributor.iztechauthorBaran, Yusuf
dc.relation.journalTurkish Journal of Biologyen_US
dc.contributor.departmentİYTE, Fen Fakültesi, Moleküler Biyoloji ve Genetik Bölümüen_US
dc.identifier.volume38en_US
dc.identifier.issue6en_US
dc.identifier.startpage806en_US
dc.identifier.endpage816en_US
dc.identifier.wosWOS:000345431100011
dc.identifier.scopusSCOPUS:2-s2.0-84911397975
dc.relation.publicationcategoryDiğeren_US


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