Combination therapy of BCR-ABL-positive B cell acute lymphoblastic leukemia by tyrosine kinase inhibitor dasatinib and c-JUN N-terminal kinase inhibition.

ABSTRACT:

Background

The Philadelphia chromosome (Ph), which leads to the creation and expression of the fusion gene product BCR-ABL, underlines the pathogenesis of chronic myelogenous leukemia (CML) and a fraction of adult and pediatric acute B-lymphoblastic leukemia (B-ALL). The BCR-ABL tyrosine kinase inhibitors (TKIs) have shown a remarkable clinical activity in patients with CML, but their efficacy in treating Ph⁺ B-ALL is limited. Identifying additional therapeutic targets is important for the effective treatment of Ph⁺ B-ALL.

Methods

Activation of the JNK signaling pathway in human and mouse BCR-ABL⁺ B-ALL cells with or without dasatinib treatment was analyzed by Western blotting. JNK was inhibited either by RNA interference or chemical inhibito

SUBMITTER: Xiao X 

PROVIDER: S-EPMC7302132 | biostudies-literature | 2020 Jun

REPOSITORIES: biostudies-literature