Shaela Wright

Bromo- and extra-terminal domain inhibitors (BETi) have exhibited therapeutic activities in many cancers. However, the mechanisms controlling BETi response and resistance are not well understood. We conducted genome-wide loss-of-function CRISPR screens using BETi-treated KMT2A-rearranged (KMT2A-r) cell lines.

Leukemia lines MOLM13, OCIAML2, THP1, U937, MV411, HL60, SEM, TF1, and HEL were maintained in RPMI-1640 medium (CORNING, 10–040-CV) containing 10% fetal bovine serum (FBS) (HyClone, 03.N16001DC). HEK293T cells were cultured in DMEM (HyClone, SH300022.01) supplemented with 10% FBS and 4.5-mM L-glutamine. The OCIAML2 and SEM cell lines were originally purchased from DSMZ. MOLM13 was originally purchased from ACCEGEN.