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The roles of epigenetic modifications of proapoptotic BID and BIM genes in imatinibresistant chronic myeloid leukemia cells
(Taylor & Francis, 2013-07)
In chronic myeloid leukemia (CML), epigenetic modifications such as promoter hypermethylation and inactive histone modification are known mechanisms of drug resistance. In our study, we investigated the roles of promoter ...
A novel mechanism of dasatinib-induced apoptosis in chronic myeloid leukemia; Ceramide synthase and ceramide clearance genes
(Springer, 2011-11)
Sphingolipids are bioeffector molecules that control various aspects of cell growth, proliferation, apoptosis, and drug resistance. Ceramides, the central molecule of sphingolipid metabolism, are inducer of apoptosis and ...
Imatinib induces autophagy through BECLIN-1 and ATG5 genes in chronic myeloid leukemia cells
(Taylor & Francis, 2011-03)
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Hematology
Volume 16, Issue 2, March 2011, Pages 95-99
Imatinib induces autophagy ...
miR-17 in imatinib resistance and response to tyrosine kinase inhibitors in chronic myeloid leukemia cells
(Zerbinis Medical Publications, 2013-04)
In this study we examined the expression levels of miR-17 which possesses oncogenic activities through downregulation of CDKN1A, p21 and E2F1 tumor suppressor genes, in imatinib sensitive and resistant chronic myeloid ...
Docetaxel enhances the cytotoxic effects of imatinib on Philadelphia positive human chronic myeloid leukemia cells
(Taylor & Francis, 2009-06)
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, ...
Suppression of STAT5A increases chemotherapeutic sensitivity in imatinib-resistant and imatinib-sensitive K562 cells
(Informa Healthcare, 2010-10)
STAT proteins are cytoplasmic transcription factors that are involved in the regulation of numerous cellular activities such as cell growth, differentiation, and survival. In this study, we aimed to identify the expression ...
Nilotinib significantly induces apoptosis in imatinib resistant K562 cells with wild-type BCR-ABL, as effectively as in parental sensitive counterparts
(Taylor & Francis, 2010-02)
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 ...
Dishevelled proteins and CYLD reciprocally regulate each other in CML cell lines
(Springer, 2017-10)
Dishevelled (Dvl) proteins are activated by Wnt pathway stimulation and have crucial roles in the regulation of β-catenin destruction complex. CYLD is a tumor suppressor and a deubiquitination enzyme. CYLD negatively ...
Combination of fludarabine and imatinib induces apoptosis synergistically through loss of mitochondrial membrane potential and increases in caspase-3 enzyme activity in human K562 chronic myleloid leukemia cells
(Informa Healthcare, 2010-06)
In this study, we aimed to show the synergistic apoptotic effects of imatinib/fludarabine combination in human K562 chronic myleloid leukemia (CML) cells. There was a significant increase in cytotoxicity of combination of ...
Therapeutic potential of apigenin, a plant flavonoid, for imatinib-sensitive and resistant chronic myeloid leukemia cells
(Routledge, 2014-05)
Despite the presence of many therapeutic regimens like imatinib and other tyrosine kinase inhibitors, the development of resistance, intolerance, and side effects makes chronic myeloid leukemia (CML) therapy challenging. ...
