HDAC7 induction combined with standard-of-care chemotherapy provides a therapeutic advantage in t(4;11) infant B-ALL (Dataset)

Infants diagnosed with B cell acute lymphoblastic leukemia (B-ALL) and t(4;11) chromosomal rearrangements represent a subset of patients with poor therapeutic response. t(4;11) B-ALL cells exhibit low levels of HDAC7, which is essential for optimal B lymphocyte differentiation. Here, we show that HDAC7 silencing in this malignancy is mediated by epigenetic mechanisms involving the chromatin remodeler EZH2 and the KMT2A-AFF1 fusion protein. This dataset contains the processed ChIPseq data files (bigwig and narrowpeaks) from the publication.