Figure 3 from Long-term Multimodal Recording Reveals Epigenetic Adaptation Routes in Dormant Breast Cancer Cells

Adaptation is driven by divergent transcriptional reprogramming. A, Tamoxifen resistance analysis of the TAM TEPs (late progression) to increasing doses of 4-OHT is depicted in the left. Growth rates of –E2 (AI) TEPs in response to treatment with different drugs: Tamoxifen (Tam, 4-OHT), fulvestrant (Fulv), CDK7 inhibitor (CDK7i), CDK4/6i (palbociclib) are depicted on the right. Representative graphs are shown as normalized confluency fold change upon 7 days of compound treatment (n = 3). B, Principal component analysis (PCA) of bulk RNA-seq expression data for all MCF7 TRADITIOM samples (POT (pretreatment), latency (time between onset of treatment and dormancy), dormancy, awakening (early progression), and TEP (late progression) of both treatment arms [TAM and –E2(AI)] and their counterpart untreated (UT) samples cultured in parallel for 170 days. C, Heat map from bulk RNA-seq data depicting a subset of TRADITIOM MCF7 dormancy signature with top 50 significantly up- and downregulated genes in TAM and –E2 (AI) treated samples during dormancy in comparison with POT (pretreatment). D, GSEA for TRADITIOM dormancy signature.