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. 2018 Mar 8;103(4):565–574. doi: 10.3324/haematol.2017.185603

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Figure 5. — IKZF1 alterations mediate therapy resistance. Overview of IKZF1-affected pathways contributing to tyrosine kinase inhibitor (TKI) resistance and glucocorticoid (GC) resistance. Enhanced cell adhesion due to loss of IKZF1 function has been shown to contribute to both TKI and GC resistance. Deregulation of metabolic pathways, such as LKB1/AMPK signaling and glucose metabolism, attenuated glucocorticoid receptor (GR) target gene regulation and upregulation of epithelial membrane protein 1 (EMP1) have been implicated in mediating GC resistance of IKZF1-deleted BCP-ALL. Green boxes indicate activated targets or pathways, while red boxes define attenuated pathways. Targets within the metabolic pathway can either promote or inhibit GC resistance.