RESEARCH Open Access Sp1 and c-Myc modulate g

Acute myeloid leukemia (AML) is an aggressive malignancy with a-5 year overall survival rate of approximately 30%-45 % in adults and nearly 70 % in children [1]. Although the survival rate in children is quite high, recurrence and acquired drug-resistance remain the leading causes of death, occurring in over 60 % of cases by 1 year after complete remission [2]. AML is typically a stem cell-driven disease, and the existence of leukemia stem cells (LSCs) was first identified (CD34 +CD38-) by JE Dick in 1994; these cells extremely promote AML progression, chemo-resistance and recurrence [3,4]. Therefore, identifying molecules or pathways that are preferentially expressed in LSCs and determining the principles controlling AML pathogenesis are critical and may facilitate the optimization of clinical treatments for AML patients