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. Author manuscript; available in PMC: 2020 Sep 2.
Published in final edited form as: Nat Cancer. 2020 Mar 9;1(3):329–344. doi: 10.1038/s43018-020-0037-3

Extended Data Fig. 6. NetBID identifies regulatory nodes of prednisolone resistance.

Extended Data Fig. 6

(a.) Enrichment of previously reported resistance genes (n=40 genes and miRNAs; Wilcoxon two-tailed p-value) in NetBID results. (b.) Heatmap of top 48 NetBID-predicted drivers (‘symbol’_’regulon size’) are ranked by integrated NetBID p-value. Left: color-coded by z-score and labeled by p-value of NetBID results in TOTXVI, TOTXV, and combination (Comb); Right: differential expression of each driver itself, color-coded by z-score and labeled by signed fold-change in TOTXVI, TOTXVI and combination (Comb; (Stouffer’s combined Bayesian generalized linear model “NetBID” p-value; n=203 patients). (c.) CELSR2 regulon from B-ALLi (n=399 genes). Legends of node and edge follow Figure 6c. (d.) Enrichment of NetBID-inferred CELSR2 regulon (n=399 genes) in differentially expressed genes of CELSR2 knockdown vs. NTC in Nalm-6 human ALL cell lines (n=222 genes; Wilcoxon two-tailed p-value) upon prednisolone treatment for 24hr (top) Blue lines inside the box indicate the down-regulation of CELSR2 itself, labeled p-value and signed foldchange. (e.) Enrichment of previously reported resistance genes (n= 40 genes and miRNAs; Wilcoxon two-tailed p-value) in differentially expressed genes of CELSR2 knockdown vs. NTC in NALM-6 ALL cell lines without prednisolone treatment.