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. 2025 Aug 22;14:109. doi: 10.1186/s40164-025-00700-0

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© The Author(s) 2025

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/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 1 — The role of the adaptive immune system in the anticancer activity of Triapine. (A) Top 20 upregulated GO-terms in a transcriptomic dataset (SW480, 1 µM Triapine, 15 h) compared to control. (B) Impact of immune status on the anticancer activity of Triapine in murine allograft models. Mean tumor volume (mm³) ± SEM is given. (C) Flow cytometry analysis on day seven of CT-26 tumor-infiltrating immune cells of female Balb/c mice. Mean percent cells of the (grand)parental gate ± SD is given. Effect of a CD8-blocking antibody on (D) tumor growth (mean tumor volume (mm³) ± SEM) of Triapine-treated CT-26 allografts and (E) overall survival. Pink lines indicate Triapine treatment. (F) Representative confocal microscopy images of CT-26 cells stained for CALR (green) and DAPI (blue) after 24 h Triapine treatment (10 µM, scale bar: 50 μm). (G) Flow cytometry analysis of CALR (24 h). (H) Representative fluorescence images and (I) associated quantification of CT-26 cells stained for HMGB1(green) and DAPI (blue) after 24 h Triapine treatment (10 µM; scale bar: 15 μm). Triapine induced (J) HMGB1 and (K) ATP release into the supernatant after 24 h treatment. Values given are the mean ± SD of at least three independent experiments, normalized to untreated control. (L) Percentage of tumor-free mice at the site of re-challenge site after vaccination with Triapine-treated cancer cells. The control group received freezed/thawed (F/T)-lysed cells. Significant differences were calculated by mixed-effects analysis corrected for multiple comparisons by Sidak, unpaired T-test, one-way, two-way ANOVA corrected for multiple comparisons by Sidak or Dunnett, or Log-rank and Mantel-Cox post-test (**** p < 0.0001, *** p < 0.001, **p < 0.01; *p < 0.05, n.s. = not significant)