Overexpression of Tpl2 is linked to imatinib resistance and activation of MEK-ERK and NF-jB pathways in a model of chronic myeloid leukemia NF-jB signaling attenuates the survival of IM-resistant CML cells and CML CD34+ cells. Therefore, combination of SFK, MEK, and NF-jB inhibitors may offer a new therapeutic approach to overcome TKI resis- tance in CML patients

内容摘要

Overexpression of Tpl2 is linked to imatinib resistance and activation of MEK-ERK and NF-jB pathways in a model of chronic myeloid leukemia NF-jB signaling attenuates the survival of IM-resistant CML cells and CML CD34+ cells. Therefore, combination of SFK, MEK, and NF-jB inhibitors may offer a new therapeutic approach to overcome TKI resis- tance in CML patients