Genome wide mapping of IKAROS binding (ChIP-Seq) in human patient-derived BCR-ABL1+ (Ph+) pre-B ALL xenograft cells

IKAROS is an important tumor suppressor in human pre-B ALL and is mutated or deleted in a high percentage of human BCR-ABL1+ (Ph+) pre-B ALL. We here report the genome-wide binding of IKAROS in two independent patient-derived BCR-ABL1+ (Ph+) pre-B ALL xenograft cells that express wild type full-length IKAROS. Two different patient-derived human BCR-ABL1+ (Ph+) pre-B ALL xenograft cells (ICN1 and LAX2), both expressing wild type full-length IKAROS, and no detectable level of dominant negative (DN) IKAROS isoform. Three IKAROS ChIP-Seq from each cell type: Two biological replicates with same Ab (H-100, Santa Cruz, sc-13039 X), and one sample with a separate Ab used for the ChIP (Ik-C, Smale lab, Hahm et al., 1998). One input control from each cell type (input-ICN1 and input-LAX2).