Imatinib reverses doxorubicin resistance by affecting activation of STAT3-dependent NF-κB and HSP27/p38/AKT pathways and by inhibiting ABCB1.

In either event, our data are highly significant because they demonstrate that imatinib converts a master survival regulator, NF-κB, from a pro-survival into a pro-apoptotic factor, thereby rendering a conventional chemotherapeutic agent more effective for treating metastatic disease.

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