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Antiapoptotic proteins Bcl2 and BclX do not protect chronic myeloid leukemia cells from imatinib-mediated growth arrest

AuthorsGómez-Casares, M. Teresa; Vaqué, José P.; Lemes, Angelina; Molero, Teresa; Ferrándiz, Nuria ; León, Javier
Issue Date2006
PublisherInstituto de España
CitationAnales - Real Academia Nacional de Farmacia 72: 27-36 (2006)
AbstractImatinib (Glivec, Gleevec, STI571), a Bcr-Abl kinase inhibitor, is the most used drug in chronic myeloid leukemia. Imatinib induces apoptosis in a number of CML-derived cell lines, including K562. However, in order to achieve hematological remissions it is required chronic treatment with the drug, a fact inconsistent with a cytotoxic mechanism of imatinib in vivo. In this work we have analysed the effects of imatinib on the proliferation and apoptosis of K562-derived cell lines with constitutive expression of the anti-apoptotic genes Bcl2 and BclX. We found that imatinib-mediated apoptosis was completely abrogated in both Bcl2- and BclX-cell lines. However, imatinib inhibited proliferation, although growth rate was higher than in parental K562. We conclude that, besides its apoptotic effect, imatinib acts through an apoptosis-independent mechanism to arrest cell growth.
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