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• W1968120167 startingPage "592" @default.
• W1968120167 abstract "Bcr-Abl is one of the most potent antiapoptotic molecules and is the tyrosine-kinase implicated in Philadelphia (Ph) chromosome-positive leukemia. It is still obscure how Bcr-Abl provides the leukemic cell a strong resistance to chemotherapeutic drugs. A rational drug development produced a specific inhibitor of the catalytic activity of Bcr-Abl called STI571. This drug was shown to eliminate Bcr-Abl-positive cells both in vitro and in vivo, although resistant cells may appear in culture and relapse occurs in some patients. In the study described here, Bcr-Abl-positive cells treated with tyrosine-kinase inhibitors such as herbimycin A, genistein or STI571 lost their phosphotyrosine-containing proteins, but were still extremely resistant to apoptosis. Therefore, in the absence of tyrosine-kinase activity, Bcr-Abl-positive cells continue to signal biochemically to prevent apoptosis induced by chemotherapeutic drugs. We propose that secondary antiapoptotic signals are entirely responsible for the resistance of Bcr-Abl-positive cells. Precise determination of such signals and rational drug development against them should improve the means to combat Ph chromosome-positive leukemia." @default.
• W1968120167 created "2016-06-24" @default.
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• W1968120167 date "2003-05-01" @default.
• W1968120167 modified "2023-10-07" @default.
• W1968120167 title "Bcr-Abl-mediated resistance to apoptosis is independent of constant tyrosine-kinase activity" @default.
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• W1968120167 doi "https://doi.org/10.1038/sj.cdd.4401210" @default.
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