LAUSR

Aberrations in transcription and epigenetic factors lead to neoplastic transformation such as acute myeloid leukemia (AML), which is characterized by accumulation of hyperproliferative blasts originating from leukemic stem cells. The use of therapeutic agents designed to lift the differentiation block and reinforce terminal cellular differentiation and growth arrest is 1 way to manage AML pathophysiology. Therefore, understanding these critical regulatory switches is essential for designing selective and effective drug tar-gets for AML. The ATP-dependent SWItch/sucrose non-fermentable (SWI/SNF) chromatin remodeling complex has been implicated in 20% cancers, including AML. 1 The catalytic subunit, SMARCA4, drives leukemogenesis by facilitating constitutive Myc expression via enhancer remodeling. 2,3 The loss of auxiliary subunits such as ACTL6A leads to proliferation defects in stem cells and bone marrow failure, whereas defects in SMARCD2 affect neutrophil development. 4-6 This prompted us to investigate the differential expression of SWI/SNF