The long-term survival rate in paediatric acute lymphoblastic leukaemia (ALL) exceeds 80%; however, the outcome of adult ALL remains to be poor. Glucocorticoids (GCs) are the preferred drugs in the traditional treatment of ALL patients. In the anti-leukaemia molecular mechanisms of GCs, c-Myc inhibition serves a critical role. In the present study, a c-Myc inhibitor that increased the sensitivity to GCs in NALM6 cells of the B-cell-ALL cell line and CEM cells of the T-cell-ALL cell line was

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... stigated. The data demonstrated that 10058-F4, a c-Myc inhibitor, increased the growth inhibition, G 0 /G 1 phase arrest and apoptosis of the NALM6 and CEM cells as induced by dexamethasone (DXM), a type of GC. Additionally, 10058-F4 reinforced the decreased expressions of c-Myc, cyclin-dependent kinase (CDK)-4 and CDK6 in the NALM6 and CEM cells treated with DXM. These findings indicated that DXM in combination with the c-Myc inhibitor 10058-F4 may be a novel, potent therapeutic strategy for the treatment of ALL. Materials and methods Cell lines and reagents. NALM-6 (a B-ALL cell line) and CEM cells (a T-ALL cell line) were purchased from the