| HRA002815
(Controlled Access)
|
The molecular mechanism of relapse remains unclear for around half of the pediatric B-lineage acute lymphoblastic leukemia (B-ALL). Here, we interpreted the chromatin accessibility features of 61 relapsed B-ALL patients by incorporating whole-genome sequencing (WGS), transcriptome sequencing (RNA-seq) and chromatin immunoprecipitation sequencing (ChIP-seq) data. We showed the increased and rewired chromatin accessibility in B-ALL compared with normal B cells, which were associated with leukemogenesis. By analyzing for differential chromatin accessibility regions between diagnosis and relapse, we identified alterations in chromatin accessibility in response to drug treatment and those associated with relapse free survival. These data provide an integrative portrait of a pediatric B-ALL genome and emphasize the importance of chromatin accessibility alterations in tumorigenesis and drug responses. Totally, the new data set includes 79 ATAC-seq data, 37 RNA-seq data and 24 H3K27ac ChIP-seq data. |