Deconvolution of healthy and diseased epithelial clusters highlights the malignant stem cell nature of C0epi and C4epi. A, UMAP cluster distribution of epithelial cells from healthy lungs (n = 3, dark blue), Vehicle- (n = 10, red), and Unesbulin-treated tumors (n = 3, light blue), up to 30 days. B, Split distribution of the 17 epithelial transcriptional clusters (C0–C16) identified in healthy lungs (left), Vehicle- (middle), and Unesbulin-treated tumors (right). Each color represents a defined transcriptomic cluster. C, Histograms representing C0–C16 percentage distribution per sample (healthy lungs, Vehicle-, and Unesbulin-treated tumors). D, Histograms representing the percentage contributions of C0–C16 clusters per sample (healthy lungs, Vehicle-, and Unesbulin-treated tumors). E, UMAP cluster annotation of epithelial cells from healthy lungs, and Vehicle- and Unesbulin-treated tumors. Each color represents a different epithelial subpopulation. F, STREAM analysis on the AT2/AT1 subpopulations identifies states S0–S11. G, STREAM analysis on the AT2/AT1-annotating clusters depicts trajectories of differentiation. H, Heat map showing GSEA of Vehicle- and Unesbulin-treated C0epi-C4epi identifies signaling pathways enriched in each sample and affected upon treatment.
No takes yet. Share an insight, caveat, or question.
Maroni et al. (2024) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: