Fig. 2: Diversity of short-term ER modulator transcriptomic response.

A Boxplots depicting the log10 (coefficient variations)^2 as a measurement of data set variation within all the tamoxifen and fulvestrant comparisons. Mann–Whitney U test was used. B Distribution of log10 p values of each variable from mixed effect multivariant linear regression model of gene regulatory percentiles tile from −100% to 100% with short-term tamoxifen or fulvestrant treatment experiments, among all genes. C Scatter plot showing Pearson correlation of average regulatory percentiles of each gene from tamoxifen and fulvestrant treatment experiments. Highlighted dots include consistently regulated genes with average fold change percentile ≥25 and ≤−25 in both tamoxifen or fulvestrant treatment experiments (‘Tam-up & Fulv-up’, blue and ‘Tam-down & Fulv-down’, green) as well as inconsistently regulated genes with average regulatory percentile ≥25 and ≤−25 in one of the compounds (‘Tam-up & Fulv-down’, red and ‘Tam-down & Fulv-up’, yellow). D–G Dot plots showing enriched pathways in genes which were ‘Tam-up & Fulv-up’ (D), ‘Tam-down & Fulv-down’ (E), ‘Tam-up & Fulv-down’ (F), and ‘Tam-down & Fulv-up’ (G), using five different databases. H, K Heatmaps illustrating the Pearson correlation coefficients of global gene regulatory percentile between each of the two compounds (H) and cell lines (K) with unsupervised clustering. I A heatmap showing the regulatory percentile of 11,191 genes in each of the indicated experiments and average values of fulvestrant and tamoxifen. Cell lines and compound names are labeled with color coded experiments and drug types. J A heatmap showing GSEA normalized enrichment score (NES) of average drug-caused enrichment changes from 50 MSigDB Hallmark signatures with unsupervised clustering. L Left: Venn diagram showing the overlapping of ER interactors from RIME experiment (log2FC > 5, padj < 0.05 to IgG) between CAMA1 and union of MCF7, T47D, BT483, BT474 and EFM19. Right: Overlapping of CAMA1 unique ER interactors and predicted regulators from CAMA1-specific up- and down-reglated genes. Consistent targets are labeled.