Basal-to-inflammatory transition enhances basal cell carcinoma (BCC) therapy resistance via crosstalk with a pro-inflammatory stromal niche [ATAC-Seq]
The goal of these ATAC-seq experiments was to determine changes in chromatin accesiblity caused by Il1a and Osm ligand treatment of mouse BCC cells at 48h timepoint versus PBS control Overall design: There were two experimental conditions in this ATACseq experiment: (1) PBS control and (2) ligand-treated mouse BCC cells. All samples were performed in biological replicates.