p21Cip1 Confers resistance to imatinib in human chronic myeloid leukemia cells
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چکیده
منابع مشابه
Analysis of Expression Of SIRT1 Gene In Patients With Chronic Myeloid Leukemia Resistant To Imatinib Mesylate
Background: Chronic myeloid leukemia is a clonal myeloproliferative disease which is characterized by bcr/abl translocation. With the emergence of tyrosine kinase inhibitors such as imatinib mesylate, significant improvement has been made in treatment of this disease. However, drug resistance against this medicine is still an obstacle. SIRT1 is a gene with deacetylase activity which has been de...
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Imatinib mesylate is the leading compound to treat chronic myeloid leukemia (CML) and other cancers, through its inhibition of Bcr-Abl tyrosine kinases. However, resistance to imatinib develops frequently, particularly in late-stage disease and has necessitated the development of new Bcr-Abl inhibitors. The synthesis of a new series of phenylaminopyrimidines, structurally related to imatinib, s...
متن کاملUse of deferasirox, an iron chelator, to overcome imatinib resistance of chronic myeloid leukemia cells.
BACKGROUND/AIMS The treatment of chronic myeloid leukemia (CML) has achieved impressive success since the development of the Bcr-Abl tyrosine kinase inhibitor, imatinib mesylate. Nevertheless, resistance to imatinib has been observed, and a substantial number of patients need alternative treatment strategies. METHODS We have evaluated the effects of deferasirox, an orally active iron chelator...
متن کاملImatinib in chronic myeloid leukemia elderly patients
Leukemia (CML) reported in clinical trials is generally of 50-55 years; it is higher (more than 60 years) in epidemiologic registries and in observational studies [1]. Therefore, a significant proportion of CML patients are " elderly " , according to the most widely accepted definition of " old person " (age > 65 years). Prior to imatinib (IM) introduction, an orally taken tyrosine kinase inhib...
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ژورنال
عنوان ژورنال: Cancer Letters
سال: 2010
ISSN: 0304-3835
DOI: 10.1016/j.canlet.2009.11.017