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. 2023 Dec 14;28:590. doi: 10.1186/s40001-023-01576-8

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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 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. 4 — ACBD3 expression in different molecular subtypes of various TCGA cancers. brain lower grade glioma (LGG), breast invasive carcinoma (BRCA), prostate adenocarcinoma (PRAD), pheochromocytoma and paraganglioma (PCPG), colon adenocarcinoma (COAD), ovarian serous cystadenocarcinoma (OV), lung squamous cell carcinoma (LUSC), liver hepatocellular carcinoma (LIHC), stomach adenocarcinoma (STAD), skin cutaneous melanoma (SKCM), kidney renal papillary cell carcinoma (KIRP), head and neck squamous cell carcinoma (HNSC). ACBD3 expressed the highest in the molecular subtype of A G-CIMP-high in LGG, B LunA in BRCA, C 1-ERG in PRAD, D Kinasesignaling in PCPG, E CIN in COAD, F Immunoreactive and Proliferative in OV, G classical in LUSC, H iCluster:1 in LIHC, I CIN in STAD, J BRAF_Hotspot_Mutants in SKCM, K C1in KIRP, and L Basal in HNSC