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. 2023 Apr 6;55(5):807–819. doi: 10.1038/s41588-023-01355-5

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© The Author(s) 2023

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 3 — a, Overview of M signature generation using B-NMF. b, H-matrix of SU2C-MARK samples and normalized M signature activity from semisupervised B-NMF. c, Dot plot of hallmark GSEA results for B-NMF-derived M signatures. Nominal P values from the one-sided hypergeometric test are shown. d, Swarmplots of selected tumor-associated immune cell signatures by M clusters. Myeloid cells were generally enriched in the wound healing (M-1, n = 52 RNA samples) subtype, while most immune cell types were enriched in the immune-activated (M-2, n = 56 RNA samples) subtype and depleted in the immune desert (M-3, n = 44 RNA samples) subtype (P < 0.001 for all signatures, Kruskal–Wallis test). e, Response rate by M subtype. The immune-activated (M-2) subtype was enriched for responders compared to the wound healing (M-1) and immune desert (M-3) subtypes (P = 0.06, one-sided Fisher’s exact test).