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. 2023 Oct 18;623(7985):157–166. doi: 10.1038/s41586-023-06623-2

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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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 5 — A total of 13 paired IDH^WTrGBMs with good-quality RNA was analysed by bulk RNA transcriptomics. Transcriptomic signatures for different biological programs were estimated for each sample, and these signatures were assessed for correlation with survival after CAN-3110 treatment either in all patients or only in patients who were HSV1 seropositive before or after CAN-3110 treatment. a, Example of two immune signatures (antitumour cytokine and T cell signatures) that are strongly correlated with survival after CAN-3110 treatment when analysed in HSV1 seropositive patients. Pearson’s r correlation coefficients and P values (two-sided, based on t-distribution) are shown above the plots. Importantly, these signatures did not appear to be significantly confounded by the tissue collection timepoint (Extended Data Fig. 12c). b, The change in Pearson’s correlation P (left) (two-sided, based on t-distribution) and r (right) values when correlations between post-treatment immune signatures and survival were performed in all patients (red points) or in only HSV1-seropositive patients (teal points). Only gene signatures that reached P ≤ 0.05 (dashed red line) in either analysis were plotted. DCs, dendritic cells; MDSCs, myeloid-derived suppressor cells; T_H1, T helper 1. c, The change in Pearson’s correlation P (left) (two-sided, based on t-distribution) and r (right) values for pre-treatment (red points) and post-treatment (teal points) samples from HSV1-seropositive patients. This panel includes all of the analysed RNA-seq gene signatures. The dashed red line indicates P = 0.05. CAFs, cancer-associated fibroblasts; EMT, epithelial–mesenchymal transition; NK cells, natural killer cells; TAMM, tumour-associated monocyte/macrophage; T_reg cells, regulatory T cells. d, Combined data for all of the patients in the study, including survival after CAN-3110 treatment, HSV1 serology, HSV1 tumour pathology, T cell fraction changes based on TCRβ DNA-seq, initial tumour volumes and bulk RNA-seq-based antitumour cytokine signature scores. The grey boxes indicate missing data. For b and c, HSV1 serology remained unchanged after CAN-3110 treatment for all of the patients, and one patient (045) was omitted from the analysis due to early non-GBM mortality.

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