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. 2023 Nov 29;7:126. doi: 10.1038/s41698-023-00476-8

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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. 1 — Primary gliomas contain non-senescent microglia, tumor-associated macrophages, and minimal abundance of the senescence associated secretory phenotype (SASP). After chemoradiation, the latent glioma microenvironment is characterized by senescence of each of these components of the tumor microenvironment (TME) as well as the injured glioma cells, along with increased SASP components. Currently, no treatments exist for latent glioma, leading to inevitable tumor recurrence characterized by abundant tumor-associated macrophages, tumor invasion, and aggressivity. Senolytics in latent glioma may be of use to ablate these latent tumor cells and the microenvironment that contribute to aggressive glioma recurrence. Created using BioRender.