Basal-to-inflammatory transition enhances basal cell carcinoma (BCC) therapy resistance via crosstalk with a pro-inflammatory stromal niche [ATAC-Seq]
Ontology highlight
ABSTRACT: 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
ORGANISM(S): Mus musculus
PROVIDER: GSE248313 | GEO | 2024/07/26
REPOSITORIES: GEO
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