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. 2024 Nov 28;43:311. doi: 10.1186/s13046-024-03231-4

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© The Author(s) 2024

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. 7 — A tailored combinatory approach to target the SMe and delay the onset of GBM recurrences. A) Heat maps representing the HSA synergy score obtained using a 3 × 4 matrix to test the GemC₁₂-LNC and GDC-0152 combination on GL261 (left panel), GBM9 (middle panel) and CT2A cells (right panel); B) Effect of GDC-0152, GemC₁₂-LNC and their combination on the immune cells expression of CD206, CD11b, CD11c, TMEM119, MHCII in tumoroids from three different patients as fold change versus untreated tumoroids; C) Schematic representation of the treatment regimen proposed to target the SMe and the post-mortem analysis performed on the extracted brains; D) Kaplan–Meier survival curves of the tumor-bearing C57BL/6 mice receiving tumor surgery and treatment at day 14 post-grafting (n = 8–9; ns = non-significant; *p < 0.05; **p < 0.01)