Fig. 1
From: Non ABL-directed inhibitors as alternative treatment strategies for chronic myeloid leukemia
Schematic representation of the BCR-ABL1 signaling pathways targeted by non ABL-directed inhibitors. FT-Is (a) and mTOR-Is (b) inhibit RAS and mTOR activation resulting in cell proliferation arrest; Smo-As (c) inhibit the Hedgeohg signaling and reduce self-renewal, survival and cell proliferation; JAK-Is (d) suppress JAK2/STATs pathway reducing cell survival; Hsp-90-Is (e) reduce BCR-ABL1 half-life inducing its degradation; HDAC-Is (f) modify the histone acetylation state regulating gene expression; Sirt-Is (g) suppress the deacetylation activity of SIRT1; BCL2-Is (h) block the pro-survival activity of BCL-2 family members increasing apoptosis; AURK-Is (i) block the mitotic process by inhibiting of AURKs