A novel function of STAT3β in suppressing interferon response improves outcome in acute myeloid leukemia. A novel function of STAT3β in suppressing interferon response improves outcome in acute myeloid leukemia

To elucidate the role of STAT3β in acute myeloid leukemia (AML), we established a mouse model of STAT3β-deficient, MLL-AF9-driven AML. STAT3β-deficiency significantly shortened survival of leukemic mice confirming its role as a tumor suppressor. Furthermore, RNA sequencing revealed enhanced STAT1 expression and interferon (IFN) signaling upon loss of STAT3β. Overall design: To investigate the differences in gene expression in STAT3β expressing and deficient leukemia cells, MLL-AF9-transformed fetal liver cells were generated and transplanted into immunocompromised mice. Leukemic blasts were isolated from bone marrow (n=3 per group) and spleen (n=3 per group) of diseased animals by sorting Venus+ cells using a BD FACSymphonyTM S6 Cell Sorter (BD Bioscience) and subjected to RNA sequencing.