Enclosed is scBLender: a suite of quantitative measures of plasticity using the Basal-Luminal mixed phenotype as a proxy for plasticity based on time-course single-cell RNA sequencing data. We used these plasticity scores to identify gene programs enriched in cells with high plasticity. We followed this strategy to identify JAK-STAT inflammatory signaling as a driver of plasticity in prostate cancer; however, we envision generalizability in other cancer settings.
Additionally, we provide notebooks to generate figures in the submission for "Lineage plasticity in prostate cancer depends on JAK/STAT inflammatory signaling." This paper merges two bioRxiv pre-prints:
"Reversal of lineage plasticity in RB1/TP53-deleted prostate cancer through FGFR and Janus kinase inhibition" at https://www.biorxiv.org/content/10.1101/2021.11.01.466615v1 "Multilineage plasticity in prostate cancer through expansion of stem–like luminal epithelial cells with elevated inflammatory signaling" at https://www.biorxiv.org/content/10.1101/2021.11.01.466599v1.