SRA

Acute myeloid leukemia (AML) is a hematological malignancy that is characterized by the expansion of immature myeloid precursors and poor patient survival outcomes. As such there is a need for the evaluation of potential therapeutic candidates that can be used in combination with current treatment regimens to improve patient outcomes. In this study, we investigated the efficacy of DSA on AML cells in vitro and performed gene expression profile analysis of DSA-treated AML cells to identify genes that are regulated by DSA. Here we report DSA-induced differentially expressed genes and cellular pathways that are associated with the functional changes that are observed in DSA-treated AML cells. Our data provides, for the first time, DSA's unique gene signature and provides a mechanistic rationale for DSA-induced functional effects in AML cells. Overall design: To determine the gene expression profile of DSA-treated human AML cells, human AML cell lines (Molm 14 and HL-60) were cultured with two different concentrations of DSA for 36 hours. At 36 hours, cells were harvested and RNA was isolated from the cells using Qiagen's RNeasy mini kit. RNA concentration and quality was determined using the nanodrop. Gene sequencing was performed by the Hartwell Center for Biotechnology (St. Jude Children's Research Hospital) and gene expression profiling analysis by the Center for Applied Bioinformatics (St. Jude Children's Research Hospital) and Loma Linda University.