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. 2025 May 4;15:15592. doi: 10.1038/s41598-025-00222-z

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© The Author(s) 2025

Open Access This article is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License, which permits any non-commercial use, sharing, 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 you modified the licensed material. You do not have permission under this licence to share adapted material derived from this article or parts of it. 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-nc-nd/4.0/.

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Fig. 6 — Immune infiltration and pathway enrichment of UNC13 A mutations. (A) Kaplan-Meier survival curves stratified by wild-type and mutated UNC13 A. (B) Multivariate Cox regression model of UNC13 A mutations with clinical confounding factors taken into account. (C) Heatmap representation of infiltration abundance differences of 28 immunocyte subtypes between UNC13 A two subgroups. Immunocytes highlighted with red were significantly enriched in UNC13 A mutated patients, whereas green immunocytes were enriched in UNC13 A wild-type patients. GSEA analyses of UNC13 A mutations based on the signaling pathways from (D) KEGG and (E) GO BP databases. Pathways highlighted with purple were immune response relevant. (F) Distinct TMB levels between UNC13 A wild-type and mutated groups. (G) T cell-inflamed signature, (H) cytolytic activity, and (I) WNT TGFβ signature enrichment scores between UNC13 A wild-type and mutated groups.