Transcriptomic and epigenetic profiling of adrenergic and mesenchymal neuroblastomas with cell state conversion [ATAC-Seq]

Neuroblastoma accounts for 15% cancer related deaths in children, largely due to the disease relapse after multimodal therapy. Understanding the mechanism by which cancer cells acquire therapy resistance is critical to develop therapies for eradicating all cancer cells. Neuroblastoma are composed of two major cell states, adrenergic (ADRN) and mesenchymal (MES), which are presumed to interconvert and contribute to therapy resistance. To better understand the cell plasticity of neuroblastoma in chemoresistance, we repeatedly treated human and murine neuroblastoma models with indisulam, a molecular glue drug that selectively degrades RBM39, a splicing factor critical to neuroblastoma cell survival. until these tumors developed full resistance. We then generated transcriptomic data, ATAC-seq data, CUT&Tag for H3K27Ac from these tumors, and defined their cell state features. These datasets provided a comprehensive transcriptomic and epigenetic profiling on ADRN and MES neuroblastoma cells after they developed therapy resistance. Here, we provided a detailed description of these unique datasets to facilitate their reusing. We anticipate that these datasets are useful resources to understand the role of cell lineage switching in therapy resistance. To explore chromatin accessibility in vechile treated and indisulan resistant neuroblasoma xenograft. This study represents a re-analysis of all of the raw data generated for GSE164504. *************************************************************** The table below lists GEO accessions reused/reanalyzed for this study. ***************************************************************