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Fig. 2 Inflammatory pathways with STAT1 as a key regulator are enriched in ICB responsive tumors in mouse models and patients. Inflammatory pathways with STAT1 as a key regulator are enriched in ICB responsive tumors in mouse models and patients. (A) GSEA top hallmark gene sets in responsive versus nonresponsive tumors. TNFα, tumor necrosis factor–α; NF-κB, nuclear factor κB. (B) GSEA of responsive versus nonresponsive tumors from the patient cohort (n = 192) (23). NES, normalized enrichment score; ES, enrichment score. (C) Overrepresented canonical pathways within responsive tumors. (D) WGCNA module enrichment for differentially expressed genes between responsive and nonresponsive tumors. Bars indicate standard deviation with outliers; horizontal dashed line, P = (E) Previous knowledge-based graphical reconstruction of the wiring diagram of module 1. (F) GSEA of responsive [complete response (CR)] versus nonresponsive [progressive disease (PD)] tumors from the patient cohort (n = 192) (23), using a STAT1 gene set (54). (G) Representative pSTAT1 immunohistochemistry in nonresponsive and responsive AB1 tumors. Scale bars, 100 μm. (H) Survival curves of mice with pSTAT1 high– and low ICB–treated tumors (n = 10 responsive and 8 nonresponsive; log-rank test, ***P < 0.001). Rachael M. Zemek et al., Sci Transl Med 2019;11:eaav7816 Copyright © 2019 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works
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